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MRI of ArthritisAshley G. Grindol1, Edward Derrick, Kurt F. Scherer, Christopher Wasyliw, Laura W. Bancroft

The shoulders, hips, spine, and sacroiliac joints are often in-cluded in the imaging fields of chest, abdominal, and pelvic MRI examinations interpreted by body imagers. Therefore, body im-agers should be familiar with the MRI features of the common arthritides and be comfortable proposing a limited differential di-agnosis when encountered in the axial joints and spine. Although several arthritides have relatively specific characteristics, others have nonspecific, overlapping imaging features. In this chapter, the imaging findings of osteoarthritis (OA), inflammatory arthri-tis (rheumatoid arthritis [RA] and juvenile idiopathic arthritis [JIA]), seronegative spondyloarthropathies (axial spondyloar-thritis [AS], enteropathic arthropathies, and psoriatic arthritis), septic arthritis, crystal-deposition and other deposition-induced arthropathies, and synovium-based processes will be discussed.

OsteoarthritisOA, or osteoarthrosis, is the most prevalent arthritis and is the

most common chronic musculoskeletal cause of morbidity and disability in the elderly population [1]. It is characterized by ar-ticular cartilage wear and joint failure secondary to dysfunctional compensatory changes. Although conventional radiography is commonly used as the initial assessment for OA to assess for joint space narrowing and osteophytes, MRI is better able to depict the osseous and soft-tissue structures of the joint, including the articu-lar cartilage and bone marrow. Common findings of OA on MRI include articular cartilage loss, osteophyte formation, bone mar-row edema (BME), synovitis, joint effusions, and meniscal or ac-etabular labral and glenoid labral abnormalities [1] (Fig. 1). MRI also allows evaluation of surrounding soft-tissue components such as the joint capsule, extraarticular ligaments, tendons, and muscle.

Several grading systems have been developed to assess the sever-ity of OA using arthroscopic or imaging criteria. One of the more commonly used classification systems for the assessment of articular cartilage damage is the system proposed by the International Carti-lage Repair Society [2]. This grading system can be applied when interpreting MRI: Grade 0 is assigned for normal, grade 1 for super-ficial cartilage cracks and fissures, grade 2 for lesions involving less than 50% of the cartilage depth, grade 3 for lesions involving greater than 50% of the cartilage depth but not extending to bone, and grade 4 for cartilage lesions extending to the subchondral bone [2]. BME

can occur subjacent to areas of articular cartilage loss and is hypoin-tense on T1-weighted images and hyperintense on T2-weighted se-quences because of the increased water content of bone marrow. In-traarticular osteochondral bodies may also occur with more advanced OA, sometimes because of fractured osteophytes. Intraarticular bod-ies, subchondral BME, and cysts in conjunction with osteophytes and cartilage destruction are nearly pathognomonic for OA and are frequently encountered in the elderly population.

The spine is another common location for degenerative change, and Modic and colleagues [3] described a spectrum of degenerative disk disease (DDD) characterized by bandlike signal-intensity abnor-malities in the vertebral body endplates and associated changes in the adjacent intervertebral disks. Type 1 Modic changes reflect acute reaction of the vertebral endplates to disk degeneration, with T1-hy-pointense and T2-hyperintense endplate signal changes [3, 4] (Fig. 1). Occasionally, type 1 Modic changes can be potentially confused with osteomyelitis; however, there are important imaging features that can be used to differentiate between the two causes. The intervertebral disk is usually T2-hypointense due to disk desiccation in DDD unlike the T2-hyperintense disk signal seen in infectious discitis [4]. Erosive endplate changes develop with osteomyelitis, whereas no endplate destruction is seen in Modic changes [4]. Type 2 Modic changes oc-cur with progression of DDD, which is characterized by fatty marrow at the endplates causing hyperintense signal on T1- and T2-weighted images [3]. In type 3 Modic change, there is hypointense signal on all sequences secondary to endplate sclerosis [3]. Vacuum phenomenon of the intervertebral disks is another common finding associated with degenerative change and occurs when nitrogen gas enters the disks because of negative pressure generated by loss of disk fluid [4]. The vacuum phenomenon is characterized by hypointense signal on all MRI sequences. Unlike gas in other soft tissues, gas is rare in infec-tious discitis and its presence is almost always seen in DDD and ef-fectively excludes infection [4].

Inflammatory ArthritidesRA is a chronic autoimmune disorder that most commonly af-

fects women older than 65 years old [5, 6]. It is characterized mainly by systemic inflammation, autoantibodies, and persistent polyarticular synovitis [5]. Early diagnosis and treatment of RA are paramount to the prevention of disease progression, and early treat-

1All authors: Department of Radiology, Florida Hospital, 601 E Rollins St, Orlando, FL 32803. Address correspondence to L. W. Bancroft (Laura.Bancroft.MD@flhosp.org).

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ment has been associated with improved clinical outcomes. MRI is not only benefi-cial in aiding in the diagnosis of early RA inflammation, but also helpful in tracking treatment response and verifying disease re-mission [7]. Similar to other inflammatory arthritides, the earliest imaging finding in RA is often synovitis. Synovitis manifests as increased synovial thickness, synovial volume, and synovial enhancement on con-trast-enhanced sequences [8]. Synovial vol-ume correlates with joint swelling and ten-derness and is predictive of clinical disease activity [9]. The rate and magnitude of sy-novial enhancement have been shown to be related to the severity of inflammation [10]. Rice bodies are small intraarticular loose bodies the size of rice that may develop in

patients with RA. Rice bodies are thought to be dissociated, infarcted synovium and will be low signal intensity on T1-weighted, T2-weighted, and intermediate-weighted sequences (Fig. 2). BME is another com-mon finding in RA that occurs in response to synovitis. BME is seen on fluid-sensitive sequences as ill-defined areas of hyperin-tense signal and will have corresponding ill-defined hypointense signal on T1-weighted images [11, 12].

The natural progression of RA after early synovitis and simple synovial prolif-eration is pannus formation [5]. A pannus is essentially hypervascular, hypertrophied synovium and displays intermediate to hy-pointense signal on T1-weighted and T2-weighted sequences (Fig. 2). As the disease

progresses, periarticular bone demineraliza-tion, cartilage destruction, and eventually subchondral bone erosions will follow [5]. Erosions appear as sharply demarcated jux-taarticular bone lesions and will be visible in at least two planes [11] (Fig. 2).

JIA shares many imaging findings with RA and is the leading cause of childhood rheumatic disease [13]. JIA occurs in chil-dren younger than 16 years old and persists for more than 6 weeks without an underly-ing identifiable cause [14]. JIA is character-ized by chronic inflammation and synovitis, which can lead to devastating structural dam-age and growth abnormalities. In 55–75% of patients, JIA presents as monoarticular or oligoarticular arthritis [15]. The most com-monly involved joint at onset is the knee

A

Fig. 1—Degenerative change on MRI. A, Axial T2-weighted fat-suppressed image of left shoulder in 46-year-old man with osteoarthritis (OA) shows full-thickness glenohumeral articular cartilage loss (arrowheads) with joint space narrowing, osteophyte formation (arrows), and joint effusion with debris. B, Sagittal T2-weighted image of 55-year-old man shows diffuse degenerative disk disease with multifocal disk desiccation, disk bulges and protrusions, hypointense vacuum disk phenomenon (arrowhead), and Modic type 1 changes in L4–L5 (arrow).

B

A

Fig. 2—Rheumatoid arthritis (RA) of shoulder.A, Sagittal intermediate-weighted MR image of 48-year-old woman with RA shows large glenohumeral joint effusion with synovial proliferation with rice bodies (asterisks) and humeral head erosions (arrows).B, Axial T1-weighted image of left shoulder in 57-year-old woman with long-standing inactive RA shows large erosions of anteromedial and posterolateral humeral head (asterisks).

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A

Fig. 3—Sequela of juvenile idiopathic arthritis in 33-year-old woman.A and B, Sagittal T1-weighted images through cervical spine show diminutive cervical vertebrae (arrow, A) relative to normal-sized thoracic vertebrae (arrowhead, A), ankylosed cervicothoracic junction (white asterisks), and facet joints (black asterisks, B).

B

D

A

Fig. 4—Active versus inactive sacroiliitis.A and B, Coronal oblique T1-weighted (A) and axial T2-weighted fat-suppressed (B) images of sacroiliac joints in 56-year-old man with active sacroiliitis show bilateral, asymmetric T1-hypointense and T2-hyperintense signal (arrows) paralleling indistinct sacroiliac joints.C and D, Coronal oblique T1-weighted (C) and T2-weighted fat-suppressed (D) images through sacroiliac joints in 17-year-old man with AS show bandlike iliac (arrows) and patchy sacral T1-hyperintense signal (asterisks, C) and T2-hypointense signal (asterisks, D) from fatty marrow replacement surrounding irregular sacroiliac joints.

C

B

followed by the hands and wrist joints, hips, ankles, and tarsal joints [15]. Hip involve-ment is a major source of morbidity, with total hip replacement needed in 26–44% of children within the first 10 years from onset [16]. MRI assessment of a patient with ac-tive JIA will yield findings similar to those seen in a patient with RA, such as synovitis, increased synovial volume, and pannus for-

mation with enhancement. Chronic fibrotic disease is characterized by a lack of pannus enhancement, subchondral bone changes, erosions, and eventual deformations of joint surfaces [16, 17]. In the spine, these areas of inflammation can lead to spondylodiscitis and other complications such as spinal ste-nosis and subluxations. Ankylosis resulting from chronic JIA is more common than in

adult RA and can cause loss of motion and significant growth disturbances [16] (Fig. 3).

SpondyloarthropathiesThe seronegative spondyloarthropathies

are a group of disorders with common clinical, laboratory, and genetic features, with the most important being human leu-kocyte antigen (HLA)-B27 positivity [18].

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The most common spondyloarthropathies include AS (previously known as ankylos-ing spondylitis), psoriatic arthritis, reactive arthritis, and enteropathic arthritis. The As-

sessment of Spondyloarthritis International Society characterizes disease on the basis of sacroiliitis detected on imaging, HLA-B27 positivity, and the presence of defining clin-

ical features (including, but not limited to, inflammatory back pain, arthritis, enthesitis, psoriasis, Crohn disease, and a positive fam-ily history of spondyloarthropathy) [18].

A CB

ED

Fig. 5—Classic imaging features of axial spondylitis (AS).A, Sagittal T2-weighted image of 42-year-old man with AS shows multiple edematous foci of endplate corner enthesis (arrowheads) and anterior Romanus lesions.B, Sagittal T1-weighted image of thoracic spine in 62-year-old man with advanced AS shows bamboo spine with thick ossification of anterior longitudinal ligament (arrowheads), partial ankylosis across posterior disk space (arrow), and heterogeneously high signal intensity in remaining disks.C, Sagittal T2-weighted image of 35-year-old man with AS shows extensive reactive edema (asterisks) and early Andersson lesion (arrowheads) caused by noninfectious spondylodiscitis.D and E, Sagittal T1-weighted image (D) and 2D reconstruction from CT (E) of paraplegic 62-year-old man with advanced AS shows pathologic fracture (arrows) through mid thoracic spine.

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be responsible for clinical symptoms such as inflammatory back pain and morning stiff-ness [18]. The earliest presenting symptoms of patients with AS are inflammatory back pain with alternating gluteal pain secondary to sacroiliitis [19]. Sacroiliitis is well evalu-ated on fluid-sensitive sequences, such as

T2-weighted fat-suppressed sequences and STIR sequences. Findings suggestive of ac-tive sacroiliitis include loss of the normal thin band of cartilage on T1-weighted im-ages, T2-hyperintense synovial signal, sub-chondral BME, erosions, and synovial and subchondral bone marrow enhancement [19]

AS is the prototypical spondyloarthropa-thy, is more common in men than women, and usually affects the axial skeleton [18]. AS is characterized by inflammatory lesions of the entheses or the junctional areas be-tween the bones and the tendons, ligaments, fascia, or capsules. Enthesitis is thought to

Fig. 7—24-year-old woman with pigmented villonodular synovitis of left hip.A and B, Coronal intermediate-weighted fat-suppressed (A) and sagittal T2-weighted (B) images of left hip show extensive low-signal-intensity synovial proliferation (asterisks), joint effusion, and acetabular erosions (arrowheads). In B, A = anterior, P = posterior.

A B

A

Fig. 6—Septic arthritis.A, Coronal T2-weighted image of right hip in 45-year-old man with late-stage septic arthritis shows femoral and acetabular erosions (asterisks), synovitis, and extensive periarticular inflammatory change (arrows).B and C, Axial T1-weighted (B) and T2-weighted fat-suppressed (C) images of 44-year-old man with right sacroiliac joint septic arthritis shows periarticular T1-hypointense marrow signal (asterisks, B); mildly distended sacroiliac joint (arrow, C); and inflammatory changes involving iliopsoas (asterisk, C) and gluteal (arrowheads, C) muscles.

C

B

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(Fig. 4). Imaging of inactive sacroiliitis will transition to more distinct (yet irregular) joint margins and fatty metaplasia of the adjacent marrow, showing signal intensity equal to that of fat on all MRI sequences (Fig. 4).

Sacroiliitis is commonly bilateral and symmetric in later stages of AS but can be unilateral in the early stages of disease and in psoriatic arthritis, other spondyloarthropa-thies, and infectious sacroiliitis [20]. Kang and colleagues [20] reported that findings such as large bone erosions, thick capsu-litis, extracapsular fluid collections, and periarticular muscle edema favor infectious sacroiliitis, whereas iliac-dominant BME and joint space enhancement are suggestive of sacroiliitis associated with spondyloar-thropathy. In fact, they found that periar-ticular muscle edema was the most pertinent predictor for infectious sacroiliitis [20]. Ero-sions will be hypointense on unenhanced sequences and, if confluent or large enough, can mimic joint space widening [18]. Sub-chondral sclerosis can develop on both sides of the sacroiliac joint and is characterized by T2-hypointense nonenhancing foci.

Spinal involvement is also common in AS with acute inflammation presenting as spondylitis, spondylodiscitis, facet joint ar-thritis, costovertebral arthritis, and enthesi-tis of the spinal ligaments [18]. Spondylitis will result in hyperintense bone marrow signal involving the anterior or posterior vertebral corners on fluid-sensitive and en-hanced sequences [18] (Fig. 5). Up to 67% of patients with spondyloarthropathy will have anterior spondylitis, also known as a Romanus lesion, and when three or more corners are involved without the presence of osteophytes or Schmorl nodes, this finding is 81% specific or 97% specific in patients younger than 40 years old [6, 21]. Spondy-lodiscitis or Andersson lesions are seen in 33% of spondyloarthropathy patients, and Andersson lesions have a specificity of 59% for spondyloarthropathy [21]. Anders-son lesions present as hyperintense signal at the cortical endplates adjacent to the inter-vertebral disks with variable hyperintense signal in the center or throughout the inter-vertebral space on STIR and fat-suppressed contrast-enhanced T1-weighted sequences [18] (Fig. 5). Additional spinal findings in-clude facet joint and costovertebral arthritis characterized by BME involving the poste-

rior elements, posterior aspects of the verte-bral bodies and adjacent ribs, enthesitis of the spinal ligaments, and syndesmophytes [18, 21]. Enthesitis of the spinal ligaments will present with hyperintense signal at the osseous insertions on fluid-sensitive and enhanced sequences and has a specificity of 87% for spondyloarthropathy [18, 21].

Chronic inflammatory lesions of the spine in AS include syndesmophytes, ankylosis, and fat metaplasia. Syndesmophytes are ver-tically oriented new bone that forms along the periphery of the disks, resulting in a bam-boo spine appearance [18] (Fig. 5). Disks can become heterogeneous and hyperintense in signal, and ankylosis can develop partially or completely across the intervertebral disks [18] (Fig. 5). Chronic postinflammatory fatty bone marrow metaplasia is common in the corners of the vertebral bodies, evidenced by hyperintense signal on T1-weighted imaging and hypointense signal on T2-weighted im-aging. Finally, long-standing AS can result in erosions of the posterior spinal elements and arachnoid diverticula [22]. This process begins with atrophy of the peridural tissues and adherence of the dura to adjacent struc-tures, which causes reduced compliance and elasticity of the caudal thecal sac. In turn, de-creased compliance leads to reduced ability to diminish fluctuations in CSF pressure and eventually causes enlarging diverticula and scalloped erosions of the laminae, pedicles, and posterior vertebral body [22].

The enteropathic arthropathies are in-cluded in the seronegative spondyloar-thropathies and often have manifestations indistinguishable from AS [23]. Entero-pathic arthropathies are associated with the inflammatory bowel diseases (IBDs) such as Crohn disease and ulcerative colitis and with enteropathic infections such as Sal-monella, Shigella, and Yersinia infections and can occur after gastric bypass surgery. Between 10% and 30% of patients with IBD have symptomatic sacroiliitis [24]. Enteropathic-associated arthritis of the ax-ial joints resembles AS with inflammatory lesions such as bilateral sacroiliitis, anky-losis or vertebral fusion, syndesmophytes, and bony sclerosis [25].

Septic ArthritisSeptic arthritis is most commonly

monoarticular and can be caused by he-

matogenous spread, direct inoculation, or contiguous spread of infection [26]. Early diagnosis of septic arthritis is paramount for optimal outcome because delayed di-agnosis can lead to cartilage and joint de-struction. The most sensitive findings for acute septic arthritis in a study conducted by Karchevsky and colleagues [27] was synovial enhancement (98% sensitive), which likely indicates increasing vascu-larity. Joint effusions were also common (especially in large axial joints), and peri-articular edema (likely due to increased capillary permeability) was 84% specific for septic arthritis [27]. Kang and col-leagues [20] determined that periarticular muscle edema was the strongest predictor of infectious sacroiliitis when differentiat-ing septic arthritis and spondyloarthropa-thies. Late inflammatory changes include inflammatory pannus formation, destruc-tion of articular cartilage with joint space narrowing, marginal and central erosions that can cause apparent joint space widen-ing (Fig. 6), fibrosis, and bony ankylosis.

Pyogenic spondylitis is most often caused by Staphylococcus aureus and has a predilection for the lumbar spine [4]. Most cases of pyogenic spondylitis involve two adjacent vertebral bodies and the interven-ing disk and have the following MRI char-acteristics: T1-hypointense and T2-hyper-intense vertebral body marrow, erosion of vertebral endplates, disk T2 hyperintensity and enhancement, paraspinous inflammato-ry tissue, and a soft-tissue mass or fluid col-lection [4]. When a Mycobacterium species is the responsible organism, the infection may be more indolent and will differ in its progression as it spreads beneath the spinal longitudinal ligaments [4]. This mechanism of dissemination allows the involvement of adjacent vertebral bodies and sparing of the intervertebral disks, often resulting in ante-rior gouge defects. Mycobacterium infec-tious spondylitis can also present with skip lesions and may involve only a portion of the vertebral body, potentially mimicking lymphoma or metastatic disease [4].

Pyogenic sacroiliitis is most often unilat-eral, and S. aureus is the most common in-oculated pathogen [4]. MRI characteristics include sacroiliac joint effusion, synovial outpouching, surrounding reactive BME with enhancement of the sacrum and ilium,

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loss of normal cortical margins, and rim-en-hancing abscess formation in the iliopsoas or paraspinal soft tissues (Fig. 6) [4].

Crystal and Deposition-Induced Arthritides

Gout is the most common crystalline arthropathy and the most common inflam-matory arthropathy in men. The hallmark of gout is hyperuricemia with deposition of monosodium urate crystals in joints, tendons, and soft tissues, which leads to inflammation and symptomatic disease. There is a strong association of gout with metabolic syndrome, myocardial infarc-tion, diabetes mellitus, and premature death [28]. Gout is generally polyarticular and asymmetric in distribution, with an affinity for the lower extremities (particu-larly the first metatarsophalangeal joint); involvement of the spine is rare. Early gout has imaging features similar to other inflammatory arthropathies, such as syno-vitis and joint effusions. Marginal erosions with a so-called “overhanging edge” and BME can develop; gouty tophi (nodular masses of accumulated monosodium urate crystals) can form along tendons, liga-ments, cartilage, and other soft tissues as well as within bones. Tophi typically have intermediate to hypointense signal on T1-weighted images, are heterogeneous sig-nal intensity on T2-weighted images, and may enhance homogeneously or heteroge-neously [28, 29].

Calcium pyrophosphate deposition dis-ease (CPPD) is a metabolic disorder char-acterized by intraarticular and periarticular accumulation of calcium pyrophosphate dihydrate crystals. This disease often has alternating phases of modest chronic in-flammation with superimposed episodes of intense inflammation [30]. Pseudogout is the most common manifestation of CPPD and refers to the presence of goutlike ar-thritis and chondrocalcinosis or calcifica-tion within fibrous or hyaline cartilage structures [30]. CPPD is more common in women than men and is usually secondary to a familial cause or metabolic disorder such as hyperparathyroidism, hemochro-matosis, or hypothyroidism [30].

Pseudogout tends to be symmetric in dis-tribution and affects hyaline cartilage and fibrocartilage of non–weight-bearing joints

such as the shoulder, elbow, wrist, patel-lofemoral, and metacarpophalangeal joints [30]. It can also involve the pubic symphy-sis, acetabular labra, and annulus fibrosis. Deposition will be evident on MRI as lin-ear or punctate areas of hypointense signal within hyaline cartilage or intervertebral disks on all sequences, and the mineraliza-tion may be more prominent on gradient-echo sequences or 3-T imaging. At the time of acute attacks, joint effusion and soft-tis-sue edema will often be seen. Later stages of disease can have an OA-like appearance or even neuropathic joint–like appearance with osseous fragmentation and collapse and intraarticular bodies [30].

Hydroxyapatite deposition tends to be asymptomatic but can be associated with acute inflammation, soft-tissue deposition, and chronic inflammation [31]. The hy-droxyapatite deposits occur in fibrous con-nective tissues and are usually amorphous, milky, or cheesy in quality. Deposition is most common in the shoulder—specifical-ly, in the rotator cuff tendons [31]. The sur-rounding inflammatory changes induced by the crystal disease in the shoulder can be detected as hyperintense signal changes and fluid in the subacromial or subdeltoid bursa and are best seen on fluid-sensitive sequences. “Milwaukee shoulder” is an eponym for the extreme, destructive shoul-der arthropathy caused by hydroxyapatite deposition, which was originally identified in elderly women and is accompanied by rotator cuff tears [31].

Synovial-Based ProcessesSynovial chondromatosis is a monoar-

ticular, benign neoplastic, synovial-based process that results in synovial generation of multiple cartilaginous nodules. It is most prevalent in the third to fifth decades and af-fects men 2–4 times more than women [32]. Patients typically present with joint pain, swelling, and limitation of motion. The knee, hip, and elbow are the most common-ly involved joints. Cartilaginous nodules can detach and become intraarticular bodies and can also become ossified (osteochon-dromatosis). Unmineralized cartilaginous nodules are fairly isointense to hyaline car-tilage on all sequences, and ossified bodies will parallel medullary and cortical signal intensity on all sequences. Marginal ero-

sions secondary to increased intraarticular pressure can also occur, especially in tight joints such as the hip.

Pigmented villonodular synovitis (PVNS) is another synovial-based pro-cess characterized by hyperplasia of the synovium with hypervascularity and ac-cumulation of histiocytes [33]. Masslike synovial and soft-tissue proliferation is usually monoarticular and most commonly affects the knees, hips, ankles, and shoul-ders [33]. Patients are typically young to middle-aged adults who present with joint pain, swelling, and limitation of motion. PVNS lesions have a propensity to bleed and cause accumulation of intra- and ex-tracellular hemosiderin [32]. The paramag-netic effect from the hemosiderin deposits causes the nodular intraarticular masses to be hypointense on all sequences (Fig. 7), with blooming effect on gradient-echo sequences. Joint space and bone mineral density tend to be preserved until late in the disease process in PVNS. Erosions are less common compared with osteochon-dromatosis but can occur, especially in the hip [32].

ConclusionArthritic shoulders, hips, spine, and sac-

roiliac joints are often included in chest, abdominal, and pelvic MRI examinations interpreted by body imagers. Common MRI findings of OA include articular cartilage loss, osteophyte formation, BME, synovi-tis, joint effusions, meniscal abnormalities, and acetabular and glenoid labral abnor-malities. RA is characterized by synovitis, pannus formation, BME, and erosions. The seronegative spondyloarthropathies have a strong association with HLA-B27 positiv-ity, sacroiliitis, enthesitis, and inflammatory back pain. Septic arthritis can be rapidly destructive and should be suspected in pa-tients with bacteremia, leukocytosis, joint effusion, synovial enhancement, and peri-articular edema. Gout rarely involves the spine or axial joints but can show marginal erosions with an overhanging edge, BME, and tophi. Finally, PVNS has a characteris-tic “blooming” synovial proliferation due to hemosiderin deposition, and synovial chon-dromatosis should be considered in patients with joint pain, limited joint motion, and synovial-based or intraarticular bodies.

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