Bone marrow oedema and erosions

BMO, while nonspecific, is often present in early and active rheumatologic diseases. It is characterized by high signal intensity on fluid-sensitive sequences (Figures 2, 4, 7A, 12A, 13A, 15C, 16, 22) and enhancement on post-contrast T1W images with fat saturation (Figures 13B, 15D), and it may demonstrate low to intermediate signal on T1W images (Figures 2C, 15B).

An erosion is defined as an intra-articular discontinuity of the bone surface that is visible in 2 perpendicular planes. Acute erosions will enhance and may have irregular margins with adjacent enhancing active synovitis (Figures 2, 16) [14]; chronic erosions may appear more well-marginated with cortication, frequently without adjacent active synovitis (Figures 3D, 8A-B, 23A) [10].

Synovial fluid (joint effusion, synovitis, tenosynovitis)

Joint effusion is defined as distention of the joint capsule with either simple or complex fluid. On MRI, simple joint effusion is characterized by uniform low signal intensity on T1W images and high signal on fluid-sensitive sequences, with only thin peripheral synovial enhancement following intravenous contrast administration. Complex joint effusions show more heterogeneous signal intensity and enhancement (Figures 2, 3B, 4, 13A). Comparing adjacent joints can help to detect and characterize effusions in small joints [9].

In inflammatory arthropathies, joint effusion is often associated with synovial proliferation, which is abnormal thickening of the synovial lining (Figures 3A-C, 4, 7A, 12A, 13A, 14, 15D). Synovial inflammation, or synovitis, occurs when periarticular vasodilatation is followed by synovial proliferation and neoangiogenesis [10,15]. These new vessels promote continued synovial hyperplasia by providing nutrition and inflammatory cells [15]. On MRI, synovial proliferation appears as increased synovial volume [8,9]. Active synovitis is characterized by low to intermediate signal intensity on T1W images, and high signal intensity on fluid-sensitive images [9,11,16,17], which enhances following contrast administration (Figures 14, 15D). Chronic synovitis is lower in signal intensity (Figures 3A-C, 4, 8A-B) and demonstrates little to no enhancement following contrast enhancement. Contrast-enhanced MRI allows easier differentiation between enhancing synovium and fluid; synovium will enhance, while simple joint fluid will not. Enhancement of the synovium following intravenous contrast administration indicates hyperaemia and implies active inflammation and synovitis, similar to the presence of Doppler signal in the synovial tissues at colour Doppler or power Doppler ultrasound (US) [8,10,18]. However, if imaging is delayed more than 10 minutes after intravenous contrast administration, gadolinium may diffuse into the joint fluid, mimicking synovitis, creating an intravenous arthrogram effect [9,11,19].

In DCE MRI, T1W acquisitions are repeated several times following the intravenous injection of gadolinium-based contrast to assess the dynamics of synovial enhancement and thus estimate the degree of synovial vascularity, used more often in research than in clinical practice [7,8,16,20] (Figures 14A-E). In DCE MRI, early enhancement has been shown to reflect the inflammatory activity of the joint [8]. DCE MRI has been shown to be helpful in differentiating RA from OA [8,21]. Synovial volume can be assessed using manual and computer-assisted techniques [8,9,16]. Many semi-quantitative scoring schemes exist for the evaluation of synovitis; however, quantification of synovitis remains predominantly a research tool rather than of current clinical use [1,8,20].

Tenosynovitis and bursitis are defined as distention of the tendon sheath or bursa with either fluid and/or hypertrophied synovial tissue [10,18]. Contrast-enhanced MRI can help differentiate tendon sheath and bursal fluid from synovial hypertrophy, which may be inactive when there is no associated synovial enhancement to suggest hyperaemia, or it may be active when there is associated hyperaemia and inflammation [10,18].

Enthesitis

Entheses are the osseous insertion sites of ligaments, tendons, and joint capsules [22,23]. In active enthesitis, fluid-sensitive sequences will show subenthesial BMO and adjacent soft tissue oedema, which will enhance on post-contrast sequences. In more chronic disease, erosive changes and enthesopathy may be present [2]. Erosions form at the sites of the entheses [24].

Rheumatoid arthritis

Rheumatoid arthritis (RA) is a chronic, progressive, systemic autoimmune disease characterized by proliferative synovitis and inflammatory arthritis, resulting in disability and systemic complications [25]. It affects 1% of the world’s population; women are affected 2 to 3 times more than men [9-11,14,16,26]. This disease has a peak age of onset between 45 and 65 years [10,11] and has both genetic and environmental risk factors [4,11,25,26]. The main symptoms of RA are joint pain, stiffness, and impaired function.

In 2010 the American College of Rheumatology and the European League Against Rheumatism (EULAR) revised the classification criteria for RA, with priority placed on findings that occur early in RA, including joint symptoms and duration (< or > 6 weeks duration), serology (rheumatoid factor and anti-citrullinated protein antibodies), and acute-phase reactants (C-reactive protein and erythrocyte sedimentation rate), to predict which patients would eventually develop erosive disease [27].

Synovitis occurs early in RA, leading to the development of pannus, a focal tumourlike proliferation of hypertrophic, inflamed synovium [9,11,14,16] (Figure 1B). This synovial proliferation eventually leads to marginal erosions along the bare areas of the joints (Figures 2, 3B-C). If left untreated, there is eventual fibrous and osseous ankylosis of the affected joints [10]. Involvement of tendons, tendon sheaths, and bursae is common and can occur early or late in the course of the disease [10,11] (Figures 2-4).

RA most commonly involves the proximal small joints of the hands and feet in a bilateral, symmetric distribution without bone proliferation [10,22]. Symmetric arthritis of the hands is the initial presentation in more than 60% of patients presenting with RA [7,16]. Other commonly involved joints include the ankle, knee, hip, glenohumeral, and sacroiliac joints.

In the hands, RA often involves the metacarpophalangeal (MCP), proximal interphalangeal (PIP), midcarpal, radiocarpal, and distal radioulnar joints, and the ulnar styloid process [22]. Ulnar deviation of the fingers occurs at the MCP joints [22]. Deformities of the fingers include swan neck deformity, with hyperextension at the PIP joints and flexion at the distal interphalangeal (DIP) joints, and boutonnière deformity, with flexion at the PIP joints and hyperextension at the DIP joints. Tenosynovitis of the hands and wrists is highly specific for early RA [7,28,29]. Hand and wrist tendon rupture occurs spontaneously in at least 1% of patients with chronic RA [30]. Finger extensor tendons are more commonly torn compared with flexor tendons [30,31]. Tendon rupture can occur due to tendons rubbing along the eroded bone, or due to ischaemia from tenosynovitis or a change in tendon collagen [30].

In the feet, RA often involves the metatarsophalangeal (MTP), PIP, and tarsal joints. The lateral plantar aspect of the fifth metatarsal head is often the first site of bone erosion in the foot [4,22]. A recent postmortem study has shown that the presence of tenosynovitis at the level of the MTP joints is highly specific for RA [28,32]. The retrocalcaneal bursa is a common site of RA involvement, leading to eventual erosive change of the adjacent calcaneus [22].

In the spine, RA may lead to erosions of the odontoid process, resulting in widening of the anterior atlantodens interval (> 3 mm in adults), accentuated with neck flexion [22]. This can lead to instability and subluxation that can result in spinal cord compression [11].

In the pre-erosive stage of RA, radiographs are usually normal; additionally, synovitis can be difficult to appreciate both clinically and on radiographs [16,33]. It is thought that treatment should be initiated within 3-6 months of synovitis onset to prevent irreversible structural damage (erosions, cartilage damage, and tendon rupture) [9,30,34]. Because early initiation of treatment with DMARDs or biologic agents [5,17,26] is important to mitigate irreversible joint destruction and attain clinical remission, there has been increased use of both high-resolution US and MRI for the detection of early disease [7,10]. MRI may detect bone erosions at least 1 year earlier than radiographs [36]. Conaghan et al. showed that MRI assessment of structural damages at months 1 and 3 of treatment for RA was better at predicting response to treatment than clinical evaluation of response to treatment in those 3 months [37]. MRI can also be used to differentiate active from treated disease. Disease activity should be assessed frequently to ensure proper treatment regiments. Despite clinical remission with normal clinical examination and laboratory studies, subclinical active inflammatory disease can persist and result in progressive bone destruction [4,17,38-41]. MRI is useful in detecting this subclinical synovitis in patients with clinical remission, and it can more accurately evaluate the disease status.

For screening of suspected early RA, contrast-enhanced MRI of the hands is useful in detecting active synovitis, and it will frequently show bilateral enhancement of the wrist, MCP, and PIP joints [33]. On MRI, BMO and enhancement, joint effusions, synovitis, and tenosynovitis are the first signs of RA. BMO is a known precursor to erosions [3,14,35,41,42]. In the hand and wrist, BMO is a predictor of future negative outcomes [1,30,35,43-46]. As the disease progresses, the erosions that initially occur at the bare areas will extend centrally leading to progressive cartilage and bone destruction [11]. Destructive cartilage and bone changes may result in intra-articular bodies [11]. Rice bodies, which are small particles of varying substances, are a form of intraarticular body that may form in RA. In the wrist, the dorsal extensor compartments and the extensor carpi ulnaris tendon are frequently involved in early RA to varying extents ranging from tendinosis and tenosynovitis to partial-thickness tears and tendon ruptures [9,31,47]. The flexor tendons of the hand are also often affected, and tenosynovitis of these tendons is more specific for the diagnosis of early RA than for other arthropathies. However, flexor tenosynovitis decreases in frequency as the disease progresses [1,7,41].

Crystalline arthropathies: gouty and calcium pyrophosphate deposition arthropathies

Psoriatic arthritis and reactive arthritis

PsA and reactive arthritis are seronegative spondyloarthropathies with a high association with HLA-B27 [67]. The hallmarks of PsA and reactive arthritis include joint inflammation and erosions, bone proliferation, periostitis, and enthesitis [22,23,68]. PsA and reactive arthritis have similar imaging findings, and the diagnosis is often made clinically and with laboratory data.

Ankylosing spondylitis (AS)

AS is the most common seronegative spondyloarthropathy [4,85,86]. This is an inflammatory arthritis with up to 96% of patients HLA-B27 positive [22,87]. Age of onset of AS is between 20 and 40 years, and men are 3 times more likely to be affected than women [22,87]. Early clinical symptoms include back pain and stiffness as well as peripheral joint pain.

The hallmark of AS is inflammation at entheses, most commonly involving the sacroiliac joints and spine, with eventual ankylosis [87]. Involvement of the axial skeleton is more common than peripheral joint involvement, and it usually occurs earlier and more severely than peripheral joint involvement [87].

Sacroiliac joint disease in AS usually precedes spinal involvement [22]. In early AS radiographs of the sacroiliac joints are often normal and may remain normal for many years. Therefore, MRI is useful in detecting early changes of sacroiliitis before radiographic changes are apparent [88]. MRI demonstrates both active and chronic inflammatory changes in the sacroiliac joints [89] (Figures 15-17). In active sacroiliitis, there is periarticular BMO, often with joint effusion or synovitis, and erosions of the subchondral bone plate, with absence of periarticular muscle oedema (Figures 15, 16). With chronic sacroiliitis, the periarticular bone marrow signal may be diffusely low on both T1W and fluid-sensitive sequences, secondary to sclerotic changes, with eventual ankylosis (Figure 17). Although sacroiliitis in AS is typically bilateral, it is less often symmetric on MRI than on radiography; only 60% of cases on MRI demonstrate bilaterally symmetric involvement, while 86% of cases show bilaterally symmetric involvement on radiographs [4,90]. Wick et al. found that BMO and enhancement did not predict eventual formation of erosions of the sacroiliac joints. DWI and DCE MRI can be used to differentiate active from inactive sacroiliitis in patients with AS [91-95].

Spine involvement in AS includes osteitis, syndesmophyte formation, and facet joint inflammation, with eventual facet joint and vertebral body ankylosis, typically occurring at the thoracolumbar or lumbosacral junctions [22,87,96] (Figure 18). Characteristic radiographic features of AS in the spine include vertebral body squaring, osteopaenia, syndesmophytes, joint capsule and ligament ossification, vertebral osteitis, and spondylodiscitis. Spine radiographs may also be normal in early AS [87].

Early inflammation, enthesitis, and erosions occur at the anterior and, to a lesser extent, posterior margins of the vertebral body at the discovertebral junction, at the attachments of the annulus fibrosus and longitudinal ligaments, known as the Romanus lesion [22,87]. On MRI, Romanus lesions show decreased signal intensity on T1W images and increased signal intensity on fluid-sensitive sequences, often with homogeneous enhancement, due to active inflammation and hypervascularity [87]. Eventual healing and resulting sclerosis in these regions of vertebral body corner inflammation, known as the “shiny corner” sign on radiographs, will result in low MRI signal on all pulse sequences [22,76,87] (Figures 19, 20). Vertebral body corner inflammation as well as vertebral body corner fat deposition, presumably from prior inflammation, have been shown to be precursors of syndesmophyte formation [96].

Inflammatory spondylodiscitis, known as the Andersson lesion, occurs in AS (Figures 19, 21). On MRI, there is usually hyperintense signal intensity within the disc space and surrounding vertebral bodies on fluid-sensitive images, due to increased inflammation, BMO, and vascularization, which is surrounded by a hypointense rim due to sclerosis [76,87].

Ossification of the posterior longitudinal ligament occurs in AS and is seen as a linear band of low signal intensity on all pulse sequences, posterior to the vertebral bodies, which may narrow the spinal canal [87].

Bilateral hip involvement can be seen with AS, with uniform joint space narrowing, acetabular protrusion, subchondral cyst-like changes, and femoral neck rim osteophytes [22]. Involvement of the glenohumeral joint can also occur with AS.

Osteoarthritis (OA)

OA is the most common arthropathy, most often resulting from repetitive microtrauma to articular cartilage as a result of overuse and aging [10,66,97]. It is also thought that the subchondral trabecular bone can undergo changes prior to cartilage damage, with resulting BMO-like lesions that are associated with pain and eventual cartilage loss [98] (Figure 22). Synovitis is also often present in OA, due to low-grade inflammation caused by trauma and inflammatory factors [8]. OA can also occur secondary to inflammatory arthritis, acute trauma, and prior infection [97]. This disease commonly involves the acromioclavicular joint, the small joints of the hands and feet, the knee, the hip, the shoulder, and the spine.

Erosive OA is a subtype of OA that occurs most commonly in the hands of postmenopausal females [99]. Erosive OA typically involves the DIP joints, followed by the PIP joints, and has a characteristic pattern of central erosions, which produces a “gullwing” deformity at the joint (Figure 23).

MRI shows various degrees of cartilage loss in the affected joint, which may be focal or diffuse with cartilage denudation in end-stage disease (Figure 22). The modified Outerbridge grading system is often used to describe cartilage loss (Table 1) [100-105]. Osseous findings include marginal osteophyte formation, subchondral/subcortical bone sclerosis, and subchondral bone marrow oedema and cyst-like changes. Joint effusions and synovitis may also be present [10].