Osteoarthritis

Osteoarthritis is defined by the hallmarks of osteophytes, joint narrowing, subchondral cysts and subchondral sclerosis (Fig. 4-1). However, these hallmarks are not specific for osteoarthritis.

Figure 4-1 Hallmarks of osteoarthritis. The cortex thickens because of slow periosteal apposition, called “buttressing.” Similarly, osteophyte formation and subchondral sclerosis are responses to internal derangement and instability or altered stress, an adaptive phenomenon that secondarily may help support the joint.

In primary osteoarthritis, joint degeneration occurs as a result of a primary abnormality of the articular cartilage, usually due to overuse or old age. In weight-bearing joints, distribution of joint narrowing typically reflects the line of force (e.g., superomedial in the hip). Joints that undergo chronic stress or overuse such as the joints of the hand also commonly exhibit primary osteoarthritis. Patients with acromegaly experience premature primary osteoarthritis related to lack of nutrition of abnormally thickened cartilage. Similarly, paralyzed patients may acquire degenerated joints, which result from chondrolysis or decreased pumping action of nutrient-filled synovial fluid into the avascular hyaline cartilage. Patients with developmental joint conditions (e.g., epiphyseal dysplasias) are also more susceptible to hyaline cartilage wear.

Secondary osteoarthritis is seen as a delayed consequence of some joint insult (Box 4-1). This includes diverse mechanisms such as (1) fibrocartilage or ligament injury (e.g., medial meniscal tear with medial compartment osteoarthritis; anterior cruciate ligament tear with osteoarthritis; glenoid labral tear with instability and subsequent osteoarthritis; acetabular labral tear with superolateral hip osteoarthritis); (2) articular incongruity (e.g., intra-articular fracture with malunion and articular stepoff; avascular necrosis with articular surface collapse; developmental deformity such as hip dysplasia; progressive deformity of bone as with Paget disease; malalignment such as scapholunate advanced collapse of the wrist); or (3) cartilage destruction (e.g., septic arthritis, rheumatoid arthritis or hemophilia with primary chondrolysis and subsequent osteoarthritis) (Fig. 4-2). Secondary osteoarthritis due to cartilage destruction may cause confusion because there are signs of the primary process as well as the hallmarks of osteoarthritis. A common example is chronic rheumatoid arthritis with marginal erosions and diffuse joint narrowing due to hyaline cartilage destruction and with superimposed osteophytes.

Figure 4-2 Osteoarthritis (OA) can be separated into primary and secondary forms. Secondary osteoarthritis can be from mechanical causes such as joint incongruity or instability or other acute or chronic joint insult. Sequelae of inflammatory conditions (e.g., septic arthritis, rheumatoid arthritis) result in diffuse loss of cartilage. These chondrolytic processes as well as other processes resulting in diffuse cartilage loss (e.g., chemical, recurrent joint hemorrhage) are distinguished by diffuse (concentric) joint narrowing; mechanical causes of osteoarthritis often result in joint narrowing distributed asymmetrically in the joint.

Cartilage Descriptors and MR Imaging Protocol

Detecting hyaline cartilage defects can be a challenge in certain joints even with high-field MRI. Low-field scanners are at a great disadvantage owing to low resolution, signal, and limited fat suppression. Cartilage is bright on most imaging sequences in which fat suppression is used (without fat suppression, hyaline cartilage appears intermediate to dark); the key is using a sequence with high resolution and signal-to-noise ratio (SNR) with sufficient contrast between joint fluid and cartilage. On high-field scanners the most common sequences used are protein density (PD) or T2-weighted sequences with fat suppression and two- or three-dimensional fat-suppressed T1-weighted spoiled gradient-recalled echo (GRE) sequences. The T2-weighted sequence should optimally have a PD-like echo time (TE) of around 40 to 60 msec to increase SNR while retaining high fluid conspicuity. The GRE sequence can be acquired with a flip angle of 40 to 60 degrees, using the same value for time to repetition (TR) (40–60 msec) and minimum TE, combined with fat suppression. This yields a T1-weighted sequence in which cartilage is bright and fluid is dark. Both are sensitive for cartilage loss, but the PD T2-weighted sequence is more versatile and is also useful for ligaments, tendons, and marrow. The GRE sequence is very useful in situations in which cartilage is thin or the joint is small, as in the wrist and elbow. Intra-articular contrast can be useful to demonstrate cartilage defects, but there is often insufficient difference in signal between cartilage and joint fluid containing gadolinium. Newer sequences improve detection of cartilage defects; these generally involve steady-state GRE techniques and their nomenclature is vendor-specific. Physiologic imaging techniques including T2-mapping, T1-rho imaging, spectroscopy, and delayed gadolinium-enhanced MR imaging of cartilage (dGEMRIC) can be used to map areas of dehydration and proteoglycan depletion indicative of early cartilage degeneration. These techniques are used mainly for research studies but may be incorporated into routine MR protocols in the future as treatments for early cartilage damage evolve.

Radiologists interpreting MRI should use a common language with referring doctors and strive to be accurate and precise in describing cartilage damage. A commonly used grading system in the orthopedic nomenclature is the Outerbridge system (Box 4-2), which dates back to the late 1950s and was subsequently modified in 1975. The system was based on probing of the cartilage surface at surgery: grade 1 is cartilage softening; grade 2 is a cartilage defect smaller than half-inch wide (the width of the probe end; later changed to 1.5 cm); grade 3 is a defect greater than or equal to half-inch wide; and grade 4 is a full-thickness defect with exposed bone (Fig. 4-3). This system is awkward to apply to MRI because a combination of grades is usually present, and the surgical grading is based on surface analysis.

BOX 4-2 POPULAR GRADING SYSTEMS FOR DEGENERATIVE ARTHRITIS

Kellgren-Lawrence Radiographic Grading Scale of Osteoarthritis of the Tibiofemoral Joint

Grade 0: No radiographic findings of osteoarthritis

1: Minute osteophytes of doubtful clinical significance

2: Definite osteophytes with unimpaired joint space

3: Definite osteophytes with moderate joint space narrowing

4: Definite osteophytes with severe joint space narrowing and subchondral sclerosis

Outerbridge Arthroscopic Classification of Chondrosis (Modified)

Grade 0: Normal cartilage

1: Cartilage with softening and swelling

2: A partial-thickness defect with fissures on the surface that do not reach subchondral bone or exceed 1.5 cm in diameter

3: Fissuring to the level of subchondral bone in an area with a diameter more than 1.5 cm

4: Exposed subchondral bone

Noyes Arthroscopic Classification of Chondrosis

Grade 0: Normal articular cartilage

1a: Mild softening or discoloration of articular cartilage

1b: Severe softening or discoloration of articular cartilage

2a: Partial-thickness defect of <50% of the total thickness of articular cartilage

2b: Partial-thickness defect of >50% of the total thickness of articular cartilage

3a: Full-thickness articular cartilage defect with normal subchondral bone

3b: Full-thickness articular cartilage defect with erosion of subchondral bone

Figure 4-3 Examples of different Noyes grades of chondromalacia (see Box 4-2).

Other classification systems have subsequently been developed (see Box 4-2). The commonly used term chondromalacia is particularly useless and nondescriptive. The most useful method of characterizing cartilage loss is to be descriptive in location, size, and depth of cartilage defects seen. Cartilage loss can be divided into diffuse and focal lesions (Figs. 4-4 and 4-5). Some useful descriptors are listed in Box 4-3.

Figure 4-4 Cartilage descriptors (see Box 4-3).

Figure 4-5 Cartilage descriptors (see Box 4-3).

BOX 4-3 USEFUL CARTILAGE DESCRIPTORS FOR MRI

Diffuse

Diffuse surface irregularity

Diffuse partial-thickness cartilage loss

Diffuse severe cartilage loss

Focal

Fissuring/fraying (vertical linear defect)

Flap (oblique linear defect)

Delamination (fluid underneath otherwise intact cartilage)

Partial-thickness defect (some cartilage signal left); measure size

Full-thickness defect (no more cartilage signal); measure size

Cartilage flaps and delamination deserve special consideration. These represent unstable cartilage lesions and should be described separately. A cartilage flap is an oblique linear defect (see Fig. 4-4), causing the fragment to be potentially mobile; this can result in pain and locking, and the fragment can break off to form a body. Delamination is separation of the hyaline cartilage from underlying bone (Figs. 4-6 and 4-7). Fluid undermines the cartilage, and although the lesion may not be observed on arthroscopy, the “bubble” of fluid can propogate and form a flap.

Figure 4-6 Delamination is separation of the hyaline cartilage from underlying bone. Fluid undermines the cartilage, and although the lesion may not be observed on arthroscopy, the “bubble” of fluid can propogate and form a flap.

Figure 4-7 Acute cartilage delamination in a 13-year-old boy following patellar dislocation.

Cartilage lesions of all types can exhibit subchondral edema on MRI; this may occur only on one side of the joint in the early stages, later progressing to cyst formation (Fig. 4-8). Cartilage lesions almost always progress but occasionally spontaneously fill in with dark fibrocartilage or bone (Fig. 4-9). In the knee, a typical progression of cartilage loss is observed. A common presentation is tearing of the medial meniscus with extrusion; the altered forces cause diffuse cartilage loss in the medial compartment and osteophyte formation. Lateral compartment spurs form, with cartilage loss beginning near the tibial spines and eventually distributed throughout the compartment with a degenerative tear of the lateral meniscus following thereafter (Fig. 4-10). Meniscal extrusion and unstable meniscal tears (especially complex tears and radial tears) can result in rapid compartmental cartilage loss (Figs. 4-11 and 4-12) and should be described in the radiology report. Impingement and instability in other joints are also associated with osteoarthritis. Early osteoarthritis can also occur at the hip related to impingement and labral tear, for example.

Figure 4-8 Subchondral changes associated with cartilage lesions of different stages.

Figure 4-9 Cartilage is avascular and has an intricate internal collagen architecture; therefore, it does not heal with the same structural makeup. However, cartilage defects can “fill in” naturally, with disorganized dark signal fibrocartilage or with bone. A similar outcome is seen after surgical microfracture technique.

Figure 4-10 Subchondral cyst formation and progression are important to recognize on MRI, so as not to confuse findings with bone bruise, avascular necrosis, or other process.

Figure 4-11 Meniscal extrusion. Disruption of circular central meniscal fibers destabilizes the meniscus and leads to extrusion. Complex tears, large radial tears, and tears at the root attachments are associated with major (>3 mm) meniscal extrusion. Extrusion leads to compartmental osteoarthritis.

Figure 4-12 Rapid development of arthritis due to meniscal tear and extrusion.

Erosive Osteoarthritis

Erosive osteoarthritis, also called EOA or inflammatory osteoarthritis, is seen in patients with underlying osteoarthritis of the hands. Patients are typically elderly and often female. Arthritic interphalangeal joints (especially the distal interphalangeal joints) become tender, painful, and swollen. Central erosions occur and lead to the classic “seagull” pattern of the joint surface (Fig. 4-13). The joint may eventually undergo ankylosis.

Figure 4-13 Erosive osteoarthritis (OA).

Neuropathic Osteoarthropathy

Neuropathic osteoarthropathy, also known as Charcot arthropathy, can be considered a severe, aggressive form of osteoarthritis with a component of instability. Some features of osteoarthritis are often present, including sclerosis, osteophytes, and bodies. However, often subluxation, erosion, and joint destruction are seen, which may be extreme and deforming. The arthropathy begins as a sensory neuropathy, which may be from diabetes, syringomyelia, tabes dorsalis, leprosy, or other conditions (Box 4-4). Joints in the insensate region undergo unrecognized injury with ligament damage, osteochondral and capsular disruption and even fracture. The joint injury persists and progresses as a result of continued stress, and the arthropathy ensues. Loss of sympathetic control with neuropathy, or hypovascularity in the case of diabetic vasculopathy, may also play a role in disease progression.

Neuropathic osteoarthropathy can be described in three forms: atrophic, hypertrophic, and mixed (Figs. 4-14 and 4-15). The atrophic form appears as well-defined osteolysis with a “surgical–like” appearance. Proliferative response is absent, but the remaining bones are normally mineralized and the margins may be sclerotic. This pattern is classically seen in the shoulders associated with a spinal cord syrinx. The hypertrophic form appears as a severe osteoarthritis with new bone production, sclerosis, fragmentation, and often subluxation. The mixed form has features of bone destruction and production.

Figure 4-14 Atrophic neuropathic disease of the shoulder in a patient with a syrinx that was lost to follow-up for a period after ventriculoperitoneal shunting and subsequent shunt malfunction.

Figure 4-15 Hypertrophic and mixed forms of neuropathic disease, common in feet of diabetic patients.

Neuropathic disease can also be described in terms of acute, chronic, or acute-on-chronic (Fig. 4-16). In acute neuropathic osteoarthropathy, the patient presents with diffuse swelling and erythema; clinically this can simulate infection. The involved joints in this early stage of disease often show little deformity or malalignment, and radiographs may show just soft tissue swelling. On MRI, joint effusions are common, with prominent subchondral edema that may extend far into the medullary cavity. Signal intensity changes in the bone marrow consisting of low signal intensity on T1-weighted images and high signal on T2-weighted images may be identical to those observed in septic arthritis and osteomyelitis. Erosions may be seen at the margins of the joint. On gadolinium-enhanced images, marrow enhancement is typically present, with predominantly subchondral distribution. Periarticular soft tissue enhancement may also be seen. Recent fractures related to neuropathic osteoarthropathy may create intense bone marrow edema, which lead to potential diagnostic pitfalls. In chronic neuropathic osteoarthropathy, radiographic features have been summarized by words beginning with “D”: destruction, debris, preserved bone density, disorganization, and dislocation (or subluxation) (Box 4-5).

Figure 4-16 Neuropathic disease can also be described in terms of acute, chronic, or acute-on-chronic forms. OA, osteoarthritis.

The most commonly involved articulation is the Lisfranc joint. Involvement here causes the metatarsal bases to migrate dorsally, and the longitudinal arch collapses, resulting in a rocker-bottom deformity. MR imaging features are more typical of osteoarthritis, with bone production and subchondral cystic change. Acute clinical presentation may be superimposed on chronic neuropathic disease, resulting in features of both on radiographs and MRI. In any phase of neuropathic disease, in the setting of diabetes there is often underlying diffuse soft tissue edema or diffuse muscle atrophy, which in the absence of contrast can appear similar to diffuse cellulitis. Marrow changes can simulate infection.

In addition, osteomyelitis is frequently associated with neuropathic disease of the foot. Chronic neuropathic deformity causes osseous protuberances that can produce increased friction with ill-fitting footwear and results in adjacent skin callus formation, breakdown, and ulceration; osteomyelitis ensues from contiguous spread. Typical locations for this to occur are the metatarsal heads, midfoot, and calcaneus. Differential features between neuropathic disease and infection are discussed in detail in Chapter 5.

Septic Arthritis

Infection should always be considered when a monarticular arthropathy is seen. Imaging can appear identical to other inflammatory arthropathies such as rheumatoid arthritis or gout. Specific findings are discussed in more detail in Chapter 5.

Rheumatoid Arthritis

Rheumatoid arthritis (Figs. 4-17 through 4-22) affects females more often than males at a ratio of 2–3 to 1. Typically, adult-onset rheumatoid arthritis occurs in the 20s to 40s. Symptoms at presentation classically include joint stiffness, especially in the morning, with pain and swelling—most commonly polyarticular and symmetric. Systemic manifestations include fatigue and weight loss. Clinical criteria for diagnosis include at least four of the following (criteria 1 through 4 must have been present for at least 6 weeks): (1) morning joint stiffness lasting at least 1 hour; (2) soft tissue swelling of at least three joints; (3) swelling of the proximal interphalangeal, metacarpophalangeal, or wrist joints; (4) symmetric involvement; (5) subcutaneous nodules; (6) positive rheumatoid factor; (7) radiographic evidence of erosions of the joints of the hand or wrist. Most patients (approximately 85%) have positive serum rheumatoid factor.

Figure 4-17 Rheumatoid arthritis—progression of disease. Involved joints generally demonstrate concentric or uniform joint narrowing related to diffuse cartilage loss.

Figure 4-18 Hand deformities in rheumatoid arthritis. Boutonnière deformity is flexion at the proximal interphalangeal (PIP) joint and extension at the distal interphalangeal (DIP) joint; swan-neck deformity is extension at the PIP and flexion at the DIP. Deformities are due to stretching or erosion of joint cartilage and capsular structures and supporting ligaments with imbalance of forces across the regions. Also not pictured are dorsal intercalated segmental instability and volar intercalated segmental instability deformity and other carpal malalignments that occur with intercarpal and capsular ligament insufficiency (see Chapter 9). Ulnar translocation occurs when the extrinsic ligaments erode, allowing the carpus to shift over the ulna.

Figure 4-19 MRI is useful for evaluation of rheumatoid arthritis, to detect early erosions and track extent of synovial proliferation; MRI findings have been used to document response to treatment objectively. Intravenous contrast is helpful in that synovial pannus enhances brightly and is easily evaluated. Dynamic contrast can be used to document degree of synovial hyperemia by plotting the time-uptake curve. MRI is also helpful in diagnosing various complications of the disease and its treatment, including ligament tears and avascular necrosis.

Figure 4-20 Rheumatoid arthritis of the shoulder depicting how inflammatory synovial pannus can erode through intra-articular and capsular ligaments as well as periarticular structures. A, acromion; G, glenoid; H, humeral head; SS, supraspinatus.

Figure 4-21 Rheumatoid arthritis (RA) of the hips with masslike pannus and symmetric involvement.

Figure 4-22 Rheumatoid arthritis involving the cervical spine. There are five separate synovial compartments at C1-C2, any of which can be involved by the inflammatory pannus. Resulting erosion of the dens and ligamentous insufficiency causes atlantoaxial instability and even axial migration.

The basic pathology of rheumatoid arthritis is inflammation and proliferation of synovium (pannus), which leads to the various radiographic appearances. Periarticular swelling is due to a combination of pannus and joint effusion. Fusiform soft tissue swelling is characteristic at the proximal interphalangeal joints of the hands, with focal soft tissue swelling at the metacarpophalangeal joints, at the dorsum of the wrist, and over the ulnar styloid. In the feet, soft tissue swelling is common at the metatarsophalangeal joints, especially the fifth. Rheumatoid arthritis can affect any synovial structure, including bursae and tendon sheaths. Bursitis can cause areas of ill-defined soft tissue planes or focal soft tissue prominence; this is most evident radiographically in the retrocalcaneal bursa and olecranon bursa. Tenosynovitis is evident radiographically as diffuse or longitudinally oriented soft tissue swelling, commonly involving the tendons of the wrist. Inflammatory nodular soft tissue lesions may occur, called “rheumatoid nodules.” Rheumatoid nodules can occur in patients with rheumatoid arthritis and appear as focal soft tissue masses, usually at sites of chronic friction, such as the extensor surfaces of the forearm, as well as the hands and feet.

Periarticular osteopenia is a classic radiographic feature, especially in early stages of rheumatoid arthritis of the hands and feet, although a generalized pattern of osteopenia can also occur. Involved joints generally demonstrate concentric or uniform joint narrowing related to diffuse cartilage loss. However, in weight-bearing joints there may be more severe narrowing at the weight-bearing surface. Axial migration can occur at the hips because of bone remodeling at the central portion of the acetabulum, with inward bowing of the iliopectineal line, called protrusio acetabuli. Characteristic marginal erosions result from thickened, inflammatory synovial tissue (pannus) eroding the bone at the bare area adjacent to the margin of the articular cartilage. Osseous proliferation is not a feature of rheumatoid arthritis; however, osteophyte formation can occur in longstanding rheumatoid arthritis as a result of superimposed secondary osteoarthritis.

Deformities of the hands and feet are common in rheumatoid arthritis for a variety of reasons: laxity and distention of the joint capsule, ligamentous laxity or disruption, tendinopathy or tendon tears, and altered muscle tone. The “swan neck” deformity is hyperextension at the proximal interphalangeal joint and flexion at the distal interphalangeal joint. The “boutonière” deformity is flexion at the proximal interphalangeal joint and hyperextension at the distal interphalangeal joint. These deformities result from imbalance of the flexor and extensor tendons. Subluxations at the metacarpophalangeal and metatarsophalangeal joints are also common: The digits of the hands deviate in an ulnar direction (“windswept hand” appearance); in the foot, hallux valgus is very common and may be severe, leading to overlap of the first and second toes. In the hands, the carpal bones commonly erode (carpal-dominant involvement), with ligamentous disruption and laxity causing carpal instability patterns. In more severe cases, the process of erosion and instability may reach a point at which there is “carpal collapse,” with the metacarpal bases nearly apposed to the radius. The entire carpus and hand may slip in an ulnar direction, referred to as “ulnar translocation.” Carpal collapse and dissociation, in addition to mass effect from pannus, can cause impingement on the median nerve as it passes through the carpal tunnel, resulting in carpal tunnel syndrome.

Rheumatoid arthritis is most commonly recognized in the hands and feet; in fact, if there is a finding on a foot exam that is of questionable significance, it is often useful to evaluate radiographs of the hands, and vice versa. Distribution in the hands is characteristically more proximal than distal, commonly involving the carpus, as well as the metacarpophalangeal and proximal interphalangeal joints. In the feet/ankles, the distribution mimics that of the hands/wrists, with the metatarsophalangeal joints most commonly involved. Distribution is bilateral and symmetric; however, extent of involvement may not be the same from side to side.

Juvenile Chronic Arthritis (Fig. 4-23)

Juvenile chronic arthritis (JCA), more often called JRA, or juvenile rheumatoid arthritis, actually includes a number of subsets of articular disease with the common characteristic that they present before adulthood. These subcategories include juvenile-onset adult-type (seropositive) rheumatoid arthritis, seronegative chronic arthritis (Still disease), juvenile-onset ankylosing spondylitis, psoriatic arthritis, arthritis associated with inflammatory bowel disease, and miscellaneous categories. All tend to occur in an adolescent population and mimic the manifestations of the adult-onset disease except for Still disease, which typically occurs in younger children and is the most common form of JCA (approximately 70%). People affected with JCA at a young age have certain manifestations on radiographic examinations related to the chronic inflammation and hyperemia that occurs in growing joints; these manifestations are particularly associated with Still disease, likely in part related to the earlier age of onset of this disease.

Figure 4-23 Juvenile chronic arthritis. Chronic hyperemia during development can lead to overgrowth of the epiphyses in the appendicular skeleton as well as spinal deformity. Fusion is often seen, unlike in adult rheumatoid arthritis.

Patients with Still disease can present with a variety of forms: systemic (10%), polyarticular (40%), and pauci- or monarticular (50%). Onset of the systemic form is acute and often occurs in children younger than 5 years old. Systemic manifestations of the disease include fever, anorexia, rash, lymphadenopathy, hepatosplenomegaly, pericarditis/myocarditis, arthralgias and myalgias, and anemia/leukocytosis with increased sedimentation rate. Symmetric articular involvement is typical in the polyarticular form, with wrist joints, metacarpophalangeal and proximal interphalangeal joints of the hands, knee and ankle joints, intertarsal, metatarsophalangeal and interphalangeal joints of the feet, and the cervical spine articulations commonly involved. A monarticular or pauciarticular (four or fewer joints) pattern is often seen initially, which may progress to the polyarticular form. There are early-onset and late-onset subtypes; early-onset may occur in a child as young as 1 to 5 years of age. Joints commonly involved include the knee, ankle, elbow, wrist, and cervical spine. Systemic involvement is infrequent.

Some radiographic findings mimic the adult form of rheumatoid arthritis and include fusiform periarticular soft tissue swelling, periarticular osteoporosis, and concentric or uniform joint narrowing (although joint narrowing is typically seen only late in the disease course). However, unlike adult-onset rheumatoid arthritis, erosions are not a prominent feature. Also, in Still disease there is often periostitis adjacent to affected joints, whereas proliferation is uncommon in adult rheumatoid arthritis. Because the disease affects growing joints, other radiographic characteristics become prominent.

Hyperemia leads to overgrowth and an enlarged appearance of the epiphyses compared with the metaphyses and diaphyses (hemophilia can result in the same pattern). The hyperemic effect can also result in early fusion of the growth plate, causing an abrupt transition between the epiphysis and diaphysis. Early physeal fusion can cause growth disturbance, with bone shortening if the plate fuses uniformly or with deformity if the fusion affects only part of the growth plate. The diaphyses of affected extremities may be gracile, and the combination of thin diaphyses and epiphyseal overgrowth with abrupt transition results in an overtubulated pattern.

Juvenile chronic arthritis causes joint ankylosis much more frequently than does adult-onset rheumatoid arthritis. Any affected joints can fuse; in the cervical spine fusion of the facet joints may lead to a growth disturbance of the vertebral bodies. Because of the lack of space for the vertebral bodies to grow, they may become broad and flat or small and miniaturized. Fusion of the carpal or tarsal bones is also common. The deformity and effects of cartilage damage often result in development of secondary osteoarthritis in early adulthood.

As in adults, MR imaging of a joint affected with JCA shows a joint effusion that may be large, as well as synovial proliferation, which is best seen after contrast administration. Even without demonstration of synovial proliferation, a Baker cyst of the knee or ganglion cyst in other joints in a child should raise concern for JCA, since this finding is associated with chronic or recurrent effusion. Although synovial proliferation in a child should automatically prompt consideration of JCA, a careful history should be obtained because infection can look similar. For instance, Lyme disease can cause a chronic synovitis and is common in the spring in the northeastern United States. Of course, internal derangement can also result in synovial proliferation and is being seen increasingly as athletic activities are emphasized.

The rheumatoid factor–positive polyarticular form of JCA tends to occur later in life and behaves like adult rheumatoid arthritis. Other manifestations of JCA include a pattern resembling psoriatic arthritis and a chronic arthropathy associated with inflammatory bowel disease. Imaging characteristics of these forms of JCA are similar to the corresponding adult forms.

Psoriatic Arthritis (Figs. 4-24 and 4-25)

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