Imaging in Gout and Other Crystal-Related Arthropathies

Page created by Kim Munoz
 
CONTINUE READING
Imaging in Gout and Other Crystal-Related Arthropathies
Im ag i n g i n G o u t an d
Other Crystal-Related
A r t h ro p a t h i e s
Patrick Omoumi, MD, MSc, PhDa,*, Pascal Zufferey,           MD
                                                                 b
                                                                     ,
Jacques Malghem, MDc, Alexander So, FRCP, PhDb

 KEYWORDS
  Gout  Crystal arthropathy  Calcification  Imaging  Radiography  Ultrasound
  Dual-energy CT  MRI

 KEY POINTS
  Crystal deposits in and around the joints are common and most often encountered as inci-
   dental imaging findings in asymptomatic patients.
  In the chronic setting, imaging features of crystal arthropathies are usually characteristic
   and allow the differentiation of the type of crystal arthropathy, whereas in the acute phase
   and in early stages, imaging signs are often nonspecific, and the final diagnosis still relies
   on the analysis of synovial fluid.
  Radiography remains the primary imaging tool in the workup of these conditions; ultra-
   sound has been playing an increasing role for superficially located crystal-induced ar-
   thropathies, and computerized tomography (CT) is a nice complement to radiography
   for deeper sites.
  When performed in the acute stage, MRI may show severe inflammatory changes that
   could be misleading; correlation to radiographs or CT should help to distinguish crystal
   arthropathies from infectious or tumoral conditions.
  Dual-energy CT is a promising tool for the characterization of crystal arthropathies, partic-
   ularly gout as it permits a quantitative assessment of deposits, and may help in the follow-up
   of patients.

INTRODUCTION

The deposition of microcrystals within and around the joint is a common phenomenon.
Intra-articular microcrystals are the most frequent cause of joint inflammation in adults.
The most common types are monosodium urate (MSU), the cause of gouty arthropathy;

 Disclosures: none.
 a
   Department of Diagnostic and Interventional Radiology, Lausanne University Hospital, Rue du
 Bugnon 46, Lausanne 1011, Switzerland; b Department of Rheumatology, Lausanne University
 Hospital, Av Pierre Decker 5, Lausanne 1011, Switzerland; c Department of Radiology, Saint Luc
 University Hospital, UC Louvain, Av Hippocrate 10, Brussels 1200, Belgium
 * Corresponding author. Department of Diagnostic and Interventional Radiology, Lausanne
 University Hospital, Rue du Bugnon 46, Lausanne 1011, Switzerland.
 E-mail address: patrick.omoumi@chuv.ch

 Rheum Dis Clin N Am 42 (2016) 621–644
 http://dx.doi.org/10.1016/j.rdc.2016.07.005                              rheumatic.theclinics.com
 0889-857X/16/ª 2016 Elsevier Inc. All rights reserved.
Imaging in Gout and Other Crystal-Related Arthropathies
622   Omoumi et al

      calcium pyrophosphate dihydrate (CPP), causing CPP deposition disease (CPPD); and
      basic calcium phosphate (BCP), causing BCP deposition disease (Table 1). In this article,
      the authors consider the manifestations of intra-articular as well as periarticular crystal
      deposits. Most cases of crystal deposits are asymptomatic and represent incidental find-
      ings at imaging. In case of symptomatic arthropathies, imaging can play an important
      role in the diagnosis and the assessment of disease progression as well as the extent
      of crystal deposits. Conventional radiography is the most common imaging modality
      and still remains essential to the workup. But ultrasound (US), conventional computer-
      ized tomography (CT), dual-energy CT (DECT), and MRI all play an increasing role. For
      example, the new 2015 American College of Rheumatology/European League Against
      Rheumatism’s classification criteria for gout take into account the radiological signs
      obtained by standard radiology as well as by DECT and US.1
         The authors review typical radiographic features of each of these crystal-induced
      arthropathies as well as findings that help to differentiate them. The increasing role
      of complementary imaging techniques will also be emphasized.

      CONVENTIONAL RADIOGRAPHY

      Radiography remains the primary imaging technique in the diagnosis of crystal ar-
      thropathies. Table 2 gives an overview of the imaging features, underlying the main
      differences to help in diagnosis.
      Monosodium Urate (Gout)
      Radiographic features of chronic gouty arthropathy
      Deposits of MSU crystals are found in extra-articular as well as intraarticular sites,
      including cartilage.2 Gouty arthropathy may affect any joint in the body, including
      the axial skeleton.3 In the acute setting, gout most often affects the first joints of the
      lower limbs, most typically the first metatarsophalangeal joints.2,4

       Table 1
       Composition and structure of the common pathogenic crystals in rheumatic diseases

       Type of Crystal
       Deposit and
       Chemical          Size and Shape of        Detection of Crystals in Common Associated
       Composition       Crystals                 Synovial Fluid/Biopsy    Clinical Conditions
       Monosodium        2–30 mm, typically       By polarizing light        Acute gout
         urate (MSU)       needle shaped            microscopy:              Chronic gout
       C5H3N4O3.Na                                  negatively                (tophaceous gout)
                                                    birefringent crystals    Urate stones (contain
                                                                              uric acid crystals)
       Calcium           1–20 mm, rhomboidal      By polarizing light       Acute CPPD
         phosphate         shaped                   microscopy: positively   arthropathy (formerly
         dihydrate (CPP)                            birefringent crystals    referred to as
       Ca2P2O7                                                               pseudogout)
                                                                            Chronic CPPD
                                                                             arthropathy
       Basic phosphate   1 nm, 5–20 mm in clumps  Difficult to detect by    BCP deposition
         calcium (BCP)                             light microscopy           disease including
       Ca5(PO4)3(OH)                              Fluorescence                Calcific tendinitis
                                                   microscopy                  Calcific bursitis
                                                  Aspecific alizarin
                                                   staining on tissue
                                                   samples
Imaging in Gout and Other Crystal-Related Arthropathies
Table 2
Imaging features differentiating monosodium urate, calcium pyrophosphate dihydrate, and basic calcium phosphate crystals deposition diseases

                   MSU                                             CPPD                                           BCP
Distribution       Mostly para-articular structures (tendons,      Mostly articular tissues (hyaline cartilage,   Mostly para-articular structures, in
  (in the joints      ligaments, bursae)                             fibrocartilage, synovium, capsule,             periarticular locations (tendons111,
  /in the body)    Intraarticular deposits less prominent            ligament)                                      bursae, ligaments)
                   May be mono-articular or polyarticular          Usually polyarticular                          Usually monoarticular

                                                                                                                                                                  Imaging in Gout and Other Crystal-Related Arthropathies
                   First metatarsophalangeal joints in acute       Knees, pubic symphysis, wrist                  Any joint can be affected, but in decreasing
                      phase, but any joint can be affected,                                                         order of frequency: shoulder, hips, elbows,
                      especially in chronic phase                                                                   wrists and knees
Radiographic       Soft tissue swelling, joint effusion (acute     Dense                                          Dense if quiescent, can lose density when
  aspect             phase)                                        Fine, linear, punctate                          resorption occurs Homogeneous cloudlike,
                   Asymmetric soft tissue nodules that may be                                                      amorphous
                     faintly hyperdense (tophaceous gout)
                   Well-defined, punched-out erosion with
                     overhanging edges, with preservation of
                     joint space
                   Expansive intraosseous erosions
CT                 Denser than soft tissues but lower density      Dense (450 HU or more)                         Dense (450 HU or more)
                     than calcified crystals (160–170 HU, with a   Fine, linear, punctate                         Homogeneous cloudlike, amorphous
                     maximum of 300 HU)
                   Nodular extra-articular and intraarticular
                     deposits

                                                                                                                                     (continued on next page)

                                                                                                                                                                  623
624
                                                                                                                                                                   Omoumi et al
 Table 2
 (continued )
                  MSU                                            CPPD                                              BCP
 US               Double contour sign (hyperechoic on            Hyperechoic deposits in middle layer of           Hyperechoic foci with or without acoustic
                    cartilage surface)                             cartilage, in fibrocartilage, and in tendons      shadowing, variable shape depending on
                  Tophus                                           (linear, along the fibrillar tendo echo           stage
                  Aggregates                                       structure)                                      In acute phase: more fragmented
                  Erosions                                       In acute phase: synovitis and hyperemia             calcifications with surrounding hyperemia
                  In acute phase: synovitis and hyperemia in
                    tophi
 MRI              Intermediate or low signal intensity on        Usually punctate, linear low signal intensities   Signal depends on stage
                    T1-weighted sequences, variable and            on all sequences                                Nodular cloudlike low signal intensity on all
                    heterogeneous signal intensity on            Inflammatory signal changes in acute phase          sequences in case of mature quiescent
                    T2-weighted, and gadolinium-enhanced                                                             calcifications
                    T1-weighted sequences                                                                          Heterogeneous signal intensity in acute
                  Suggestive areas of concomitant low signal                                                         resorptive phase with potential migration
                    intensity on both enhanced T1- and                                                               and intense inflammatory signal changes
                    T2-weighed sequences                                                                             in surrounding tissues
                  No susceptibility artifacts on gradient echo
                    sequences

Abbreviation: HU, Hounsfield unit.
Imaging in Gout and Other Crystal-Related Arthropathies            625

Radiographic signs of chronic gout (also called tophaceous gout) include asymmetric
articular, juxta-articular, or periarticular soft tissue nodules, corresponding to tophi.5
These nodules may be as dense or slightly denser than the adjacent soft tissues but
are usually fainter than CPP or BCP deposits (Fig. 1D).6,7 MSU deposits can also occur
in cartilage, but usually in advanced stages; joint space narrowing occurs late in the
evolution of the disease, which is a characteristic feature of this condition (Fig. 2).
   Bone erosions are characteristic and present as well-defined intraarticular or juxta-
articular lesions with overhanging margins (Fig. 3).8 They can be expansive, some-
times progressing to a punched-out amputated aspect of bone.9 Bone erosions are

Fig. 1. 61-year old man with incidental signal abnormalities of the first metatarsophalangeal
joint detected on an MRI of the hindfoot for peroneal tendon rupture under fluoroquinolone
therapy. These signal abnormalities yielded to complete the study with an MRI of the fore-
foot, showing incidental asymptomatic chronic gouty arthropathy. Axial T1- (A), axial fat-
suppressed enhanced T1- (B) and coronal fat-suppressed T2-weighted (C) sequences show
arthropathy of first metatarsophalangeal joint with soft tissue swelling presenting interme-
diate to low signal intensity on T1-, heterogeneous signal intensity on fat-suppressed T2-,
and enhanced T1-weighted images. Note the presence of characteristic areas of low signal in-
tensity on all sequences (arrows), corresponding to crystal deposits and chronic fibrous reac-
tions. Radiograph of the foot (D) shows soft tissue swelling on medial aspect of first
metatarsophalangeal joint (asterisk), of similar density than surrounding soft tissues as well
as juxta-articular bone erosion (short arrow in [D]).
626   Omoumi et al

      Fig. 2. An 85-year-old man with gouty arthropathy. Radiograph (A) of the forefoot shows
      soft tissue swelling on medial aspect of first metatarsophalangeal joint, with calcic density,
      atypical for gout (arrow). Articular erosions of second and third metatarsophalangeal joints
      are also seen (short arrows). CT (B) confirms presence of calcic densities around metatarso-
      phalangeal joints, with unusually high densities for tophi (typical average of 150–170
      Hounsfield [HU], with maximum intensities of 300 HU). DECT with calcium (C) and MSU
      (D) images confirms the presence of calcified tophus (intense on both calcium and MSU
      images (arrows in [C] and [D]). Noncalcified tophi are also present on contralateral foot
      (short arrows in [B–D]). Note the relative preservation of the joint space (in [A]) despite
      advanced erosions due to the penetration of the tophi into the bone (long arrow in [C]).

      usually found in the vicinity of tophi, being a direct consequence of their growth into
      the bone.4,9 There is usually no periarticular osteopenia in gout. Bone proliferation is
      sometimes present, mostly in the form of irregular spicules, best seen on the medial
      aspect of the first MTP or tarsal joints.9 This aspect of bone proliferation is probably
      also due to the cortical growth of tophi, to be differentiated from the chronic periosteal
      reactions seen in psoriatic arthritis.
        Intraosseous calcifications due to the penetration of calcified MSU deposits in the
      bone have been described in severe cases of gout and should not be mistaken with
      enchondromas or bone infarcts.10
        The differential diagnosis of tophaceous gout is wide and includes rheumatoid arthritis
      and amyloid arthropathy.11 Tophi in some locations, particularly in the axial skeletaon,
      may mimic other inflammatory disorders, such as infectious spondylodiscitis or
      sacroiliits.3,12,13 For those cases, CT examination is invaluable (see later discussion).

      Radiographic features of acute gouty arthropathy
      In the acute phase, radiographs are normal or they only show soft tissue swelling and
      joint effusion, which are completely nonspecific findings.4 US or CT may be more sen-
      sitive in detecting signs of MSU deposits.14–16
Imaging in Gout and Other Crystal-Related Arthropathies            627

Fig. 3. A 68-year-old woman with gouty arthropathy of the foot. Radiography (A) shows
soft tissue swelling (asterisk) on medial aspect of first metatarsophalangeal joint, slightly
denser than surrounding soft tissues, typical for a tophus. CT (B) confirms gouty arthropathy
of first metatarsophalangeal joint combining the presence of a tophus with typical densities
(circle) (maximum densities usually
628   Omoumi et al

      Fig. 4. An 86-year-old woman with asymptomatic CPPD on radiographs of the knee,
      showing typical pattern and intraarticular distribution of CPP crystals. Note fine punctate
      triangular pattern of calcifications in menisci (long arrow in [A]); linear pattern in quadrici-
      pital tendon (short arrows in [B]), oriented along the long axis of tendon fibers; and linear
      pattern of deposits in hyaline cartilage, parallel to the subchondral bone (long arrows in
      [B]). Deposits can occur in all intraarticular tissues, including hyaline cartilage, meniscal fi-
      brocartilage, tendons (popliteal tendon (short arrows in [A]) and gastrocnemius tendon
      (asterisk in [B])), ligaments, and synovium.

         The sites most often affected are the knee, pubic symphysis, and the wrist. Using
      radiographs of these joints as a screening test for CPPD, the sensitivity obtained
      was 100%.18 However, CPPD can occur in other locations, including the spine
      (the crowned dens syndrome) (Fig. 5).19,20
         Typically, CPP deposits present a fine, linear, or punctate pattern, somehow
      following the fibrillar architecture of the affected tissues, particularly in tendons where
      CPP crystals deposit between fibers (see Fig. 4). In cartilage, crystals tend to deposit
      in the middle layer of cartilage, organized in a linear pattern, parallel to the subchondral
      bone (Fig. 6).17

      Fig. 5. A 62-year-old man with history of CPPD with chronic neck pain. MRI (A–D) shows
      destructive arthropathy of the atlanto-axial joint, associated with area of low signal inten-
      sity on all sequences (T1- [A], fat-suppressed enhanced T1- [B], and T2-weighted sequences
      [C]), compatible with chronic reactional changes. The correlation with CT (D) confirms the
      arthropathy with erosions of the dens (black arrow in [D]), associated with calcifications
      that are compatible with CPP (white arrow in [D]), not visible on MRI (or radiographs, not
      shown). These features are typical of crowned dens syndrome.
Imaging in Gout and Other Crystal-Related Arthropathies              629

Fig. 6. Comparison of US aspect of CPP (A) and MSU (C) crystals in cartilage (different patients).
CPP crystal typically deposit within the layer of cartilage (A), forming hyperechoic foci (long
arrows in [A]) (see radiograph of same patient in [B] for comparison), whereas MSU crystals de-
posit on the surface of cartilage, forming the so-called double contour sign (superficial hyper-
echoic line due to MSU deposits on surface of cartilage and deep fainter hyperechoic line due to
subchondral bone) (short arrows in [C]) (MSU deposits in cartilage are not visible on radio-
graphs). Note that on the control US examination performed under appropriate hypouricemic
treatment, the double contour sign has disappeared with only one hyperechoic line visible due
to subchondral bone, which is now brighter (D).

  Most cases of CPPD are asymptomatic and are discovered incidentally. The prev-
alence of CPPD is high and increases with age (prevalence of up to 25% in subjects
older than 85 years).21–23 Below 50 years of age, however, idiopathic CPPD is rare; if
present, predisposing metabolic disorders should be excluded.1
  CPPD may sometimes progress to a destructive arthropathy resembling osteoar-
thritis (OA). Radiographic features may help to differentiate primary OA and CPPD
arthropathy.1,18,24 In case of CPPD, arthropathic changes tend to be more severe
and progressive, with extensive fragmentation of bone causing formation of intraartic-
ular osseous bodies as well as prominent subchondral cystic changes. Also very sug-
gestive of CPPD chronic arthropathy is the distribution: non–weight-bearing joints
(shoulder, elbow, wrist) can be affected as much as weight-bearing joints (Fig. 7).18
Some sites are particularly suggestive of CPPD, such as the radiocarpal compartment
of the wrist, the patellofemoral compartment of the knee (see Fig. 7), the hindfoot, or
midfoot.
  CPPD can also be associated with other conditions, such as hemochromatosis, hy-
perparathyroidism, and gout; radiographic features of both CPPD and the associated
condition can, therefore, be present simultaneously.25–27 In hemochromatosis, there is
more extensive destruction of the MCP joints (including the fourth and the fifth digits),
hooklike osteophytes but deposits in the first carpometacarpal joint and scapholunate
dissociation are less frequent.27
  Finally, it is of note that a potential causative relationship between CPP and BCP de-
posits and OA is under investigation.1,28,29
630   Omoumi et al

      Fig. 7. A 79-year-old woman with bilateral shoulder arthropathy (radiographs on [A] and
      [B]), resembling severe OA, uncommon at non–weight-bearing joints. This aspect is compat-
      ible with a crystal-induced chronic arthropathy. Previous examinations from the patient
      confirmed the presence of typical CPPD arthropathy at other sites (isolated severe femoro-
      patellar arthropathy seen on lateral radiographic view of the knee [arrow in (C)]) with
      calcifications in the suprapatellar recess that are typical for CPP [arrowhead in (C)], symphy-
      sis pubis seen on axial CT image (arrow in D), multiple discovertebral destructive arthropathy
      seen on sagittal CT reformat (arrow in E) associated with CPPD in some discs (not shown).

      Radiographic features of calcium pyrophosphate dihydrate deposition disease
      calcifications in the acute setting
      In the acute setting, the diagnosis of CPP is suggested by the presence of the char-
      acteristic features for CPPD described earlier. However, the diagnosis can only be
      proven by crystal identification.1 The sensitivity of radiography to detect CPPD in
      crystal-proven cases is weak: only 35.3% of histologically proven meniscal deposits
      were positive by radiograph in a cohort of 3228 patients.30 The reported sensitivities
      vary depending on the joint studied (from 29% to 93%).1

      Basic Calcium Phosphate
      Radiographic features of stable basic calcium phosphate calcifications
      BCP calcifications    are usually encountered in tendons, bursae, and other peritendi-
      nous structures.17    In descending order of frequency, the shoulder, hips, elbows,
      wrists, and knees     are the most affected sites.31,32 However, any location can be
      affected, including   unusual ones that often lead to diagnostic difficulties.33–35
Imaging in Gout and Other Crystal-Related Arthropathies         631

  Typically, BCP calcification in the quiescent phase presents a dense, homoge-
neous, amorphous, cloudlike appearance (Fig. 8E, F).32 This aspect might be related
to the pathophysiology of the disease: one of the prevailing theories is that dystrophic
calcifications form in areas of necrotic changes due to repetitive microtrauma and
vascular changes.9,17,32
  This pattern allows them to be differentiated from the linear and punctate aspects of
CPP deposits. BCP calcifications lack a cortical or trabecular structure, unlike hetero-
topic ossifications and accessory ossicles (see Fig. 8E, F).36

Acute manifestations of basic calcium phosphate calcifications
Acute symptoms provoked by BCP deposits occur typically during the resportion of
calcifications. They lose the typical features described earlier and may become faint
and irregular (Figs. 9–11). Migration to bursae and adjacent soft tissues can occur
(see Figs. 9–11).36 As the calcification diminishes and disappears, the acute symp-
toms improve, typically over the course of a few days or weeks (see Fig. 10).36 Repeat

Fig. 8. A 33-year-old man with pain at the first metacarpophalangeal joint of the right
hand. MRI (A–C) shows area of hyposignal intensity (arrows) on all sequences (T1 [A], fat-
suppressed T2 [B], and fat-suppressed enhanced T1-weighted [C]), located in articular
soft-tissues of the first metacarpophalangeal joint. CT (D) and orthogonal radiographic
views (E, F) were ordered to confirm the presence of BCP calcification (long arrow in [D])
with erosion of the adjacent bone (short arrow in [D]), not visible on radiographs (E, F).
Note amorphous aspect of calcification on radiographs (arrow in [E]), not to be confused
with sesamoid bones (circle in [F]), which present a typical cortico-trabecular pattern of
bone, contrary to calcifications.
632   Omoumi et al

      Fig. 9. Three cases of rotator cuff BCP calcifications, with correlations between radiographs
      and US. (A, B) BCP calcification in resorptive phase. Radiograph (A) shows slightly blurry con-
      tours. US (B) shows multiple hyperechoic fragments visible (arrows). Parts of the fragments
      are in the subacromial bursa (short arrows). (C, D) BCP calcification that has migrated into
      the subacromial bursa (arrows). Radiograph (C) shows faint calcification, whereas US (D)
      shows hyperechoic nodule. (E, F) BCP calcification that is migrating into the bone. Radio-
      graph (E) shows calcification with blurry margins (arrow in E), especially on the inferior
      aspect. At US (F), a hyperechoic nodule is seen (arrow in F). The continuity of the calcifica-
      tion with bone erosion is clearly depicted. Hyperemic reaction at Doppler imaging is seen.
      Note that no shadowing is present in any of the cases of resorptive calcifications.
Imaging in Gout and Other Crystal-Related Arthropathies            633

Fig. 10. A 60-year-old man with acute neck pain. MRI of the spine (A, B) shows inflammatory
changes in longus colli muscle (arrows). There is intermediate signal intensity on T1- (A) and
high signal intensity on fat-suppressed T2-weighted sequence (B). Aspecific arthropathy of
atlanto-axial is also depicted (short arrow in [B]). Radiograph of the cervical spine per-
formed on the same day shows well-defined calcification projecting at the anterior aspect
of odontoid (arrow in [C]). Short-term follow-up radiograph at 10 days (D) shows a change
in aspect of the calcification, being more elongated and fainter (arrows). This rapid change
in density and shape is typical of BCP calcifications in the resorptive phase. A follow-up
radiograph at 3 months (E) shows complete disappearance of calcification.

radiographs can show a change in calcification and help to confirm the diagnosis (see
Fig. 10). When the diagnosis is unclear, CT (especially for the spine [see Fig. 11]) or US
(for superficial locations) may be useful (see later discussion).

ULTRASOUND

In recent years, major technical advances have led to improved image quality and per-
formance of US. It is particularly useful for the diagnosis of crystal arthropathies and
has become, along with radiography, one of the main imaging techniques used.

Monosodium Urate Crystals
Ultrasound features of chronic tophaceous gout
The US features of MSU deposits are the double contour (DC) sign, tophi, aggregates,
and erosions.37 The DC sign is defined as an “abnormal hyperechoic band over the
superficial layer of the cartilage, independent of the angle of probe and may be either
634   Omoumi et al

      Fig. 11. A 56-year-old man with esophageal carcinoma. The PET-CT performed for the stag-
      ing showed high uptake in the thoracic spine, interpreted as a metastasis (arrow in A). MRI
      (B–D), performed 10 days after the PET-CT shows inflammatory signal intensity on either side
      of an intervertebral disc (low signal intensity on T1- [B], heterogeneous signal intensity on
      T2- [C], high signal intensity on fat-suppressed enhanced T1-weighted sequences [D]
      (dashed circles)). The pattern (both sides of a disc) and signal abnormality are not compat-
      ible with a bone marrow replacement lesion that would be typical of a metastasis. The disc
      itself does not show significant abnormality except for mild heterogeneous signal. Analysis
      of the CT examination (F) performed during the PET-CT shows heterogeneous dense calcifi-
      cation in the intervertebral disc (arrow). The calcification has clearly changed aspect when
      compared with a CT examination (arrow in E) performed 2 weeks prior, on which it ap-
      peared more homogeneous. These features are characteristic of a BCP calcification in the
      resorptive phase, leading to inflammatory reactions. On a follow-up CT performed 5 months
      later (G), the calcification is less dense at the center and bone erosions (arrowheads) are
      visible at both vertebral plates, confirming the intraosseous migration of the calcification.

      irregular or regular, continuous or intermittent and can be distinguished from the carti-
      lage interface sign” (see Fig. 6C, D).37,38 The specificity of this sign for gout has, how-
      ever, been questioned.39
         Tophi are defined as « circumscribed, inhomogeneous, hyperechoic and/or hypoe-
      choic aggregates, which may be surrounded by a small anechoic rim » (Fig. 12).37
         Aggregates are defined as « heterogeneous hyperechoic foci that have a high de-
      gree of reflectivity, even when the gain setting is minimized or the probe angle
      changed ».37 They can have intraarticular or intratendinous locations.
         Erosions are defined as an « intra- and/or extra-articular discontinuity of the bone
      surface (visible in two perpendicular planes)».37 Erosions have to be differentiated
      from normal variations of cortical contour, degenerative, and traumatic changes.40
         The inter-reader and intrareader agreement of these signs vary and are higher for
      the DC sign (kappa 5 0.69–96) and tophi (kappa 5 0.65–1) than for aggregates.37,41
         The diagnostic performance of US for gout depends on several factors, including
      the duration of the condition. The DC sign has been found in asymptomatic hyperur-
      icemic patients.40,42 When present, tophi and erosions seem to be depicted at US with
      high sensitivity compared with radiography, MRI, or DECT.41,43,44 Of note, US has
      been used to assess the efficacy of urate-lowering therapy and can show a reduction
      in size of tophi as well as the disappearance of the DC sign (see Fig. 6).44–46
Imaging in Gout and Other Crystal-Related Arthropathies           635

Fig. 12. A 77-year-old man with gout. US of the first metatarsophalangeal joint shows hy-
perechoic intraarticular mass with a slightly hypoechoic rim (arrow in A). The same patient
during an acute flare shows the same image as in (A), with accompanying hyperemia (B).

Ultrasound features of acute gout
In the acute phase, the aforementioned signs of gouty arthropathy can be visible.
As for all acute arthritic flares, joint effusion and synovitis may be detected on B
mode and Doppler but are nonspecific.47 Synovitis may be heterogeneous with
hyperechoic foci corresponding to MSU aggregates.40 Tophi can become
hyperemic during an acute flare (see Fig. 12). Current data do not support the
use of US as a replacement for joint fluid examination for the diagnosis of acute
gout.14

Calcium Pyrophosphate Dihydrate Crystals
Ultrasound features of chronic calcium pyrophosphate dihydrate deposition disease
US is now a well-accepted method for the diagnosis of CPPD, and several criteria
have been used to define CPP deposits.1 In hyaline cartilage, they are described
as « hyperechoic, placed within the layer of the cartilage, that can reach large dimen-
sions » (see Fig. 6); in fibrocartilage as « hyperechoic, rounded or amorphous-shaped
deposits »; and in tendon as « linear deposits with a the fibrillar texture (multiple or sin-
gle lines or thick solid band) ».48
  The sensitivity and specificity of US for the detection of CPP crystal deposits
depend on the diagnostic gold standard used: with radiograph as a gold standard,
pooled sensitivities/specificities were 0.58/0.84; with synovial fluid analysis, they
were 0.87/0.98.48 The performance also varied depending on the location of CPPD:
there was a good accuracy for hyaline and fibrous cartilage, but the performance
for tendon lesions was poor.48 The interobserver agreement varies from 0.55 to
0.81 for hyaline cartilage deposits.48
636   Omoumi et al

      Ultrasound of acute calcium pyrophosphate dihydrate deposition disease
      In the acute phase, the aforementioned signs of CPPD are usually accompanied by a
      variable degree of synovitis as well as hyperemia on Doppler examination.49
         The value of US as a diagnostic modality was assessed recently. In the absence of
      any signs of crystal deposit in the symptomatic joint, as well as in knees, ankles, and
      first metatarsophalangeal joints, CPPD can be ruled out with a negative predictive
      value of 87%, using synovial fluid analysis as the gold standard.14 In this study, there
      was no statistically significant difference between US, radiography, and synovial fluid
      analysis as a diagnostic tool; but other studies have reached different
      conclusions.48,50
      Basic Calcium Phosphate Calcifications
      Ultrasound features of basic calcium phosphate calcification
      The main signs are hyperechoic foci with variable acoustic shadowing.51,52 The pres-
      ence of shadowing depends on their structure, the degree of fragmentation of the
      deposit, and size.51 Four types of deposits have been described: arc-shaped
      (an echogenic arc with clear shadowing), fragmented or punctuate (at least 2 sepa-
      rated echogenic spots or plaques with or without shadowing), nodular (an echogenic
      nodule without shadowing), and cystic. This classification has however not been vali-
      dated (see Fig. 9).53
      Ultrasound features of acute basic calcium phosphate calcification
      The presence of hyperemia on Doppler and of the features described above seems to
      correlate with the evolutive stage of the calcification and symptoms. A fragmented
      appearance is associated with both worsening pain as well as the spontaneous reso-
      lution of symptoms.52,54 Doppler activity around the deposit and presence of effusion
      suggest inflammation and are correlated with pain.53,54
         Migration to surrounding structures (ie, bursae or bone), usually with accompanying
      hyperemia, can be detected by US (see Fig. 9).36 Correlation with radiography helps in
      providing the correct diagnosis.51

      CONVENTIONAL COMPUTERIZED TOMOGRAPHY

      Thanks to its excellent resolution and high contrast, CT is the technique of choice for
      the assessment and characterization of crystal arthropathies. Crystal deposits are
      usually hyperdense compared with the adjacent soft tissues. Their density usually
      helps in differentiating them. Typically, MSU deposits have average densities of
      160 to 170 Hounsfield units (HU), with the densest areas around 300 HU. Calcium hy-
      droxyapatite and calcium pyrophosphate deposits typically present densities of 450
      HU or more.55–57 The latter two types of calcifications are easily differentiated by
      applying the same semiology as that described for radiography (fine, punctate, linear,
      oriented along the long axis of fibrillar structures for CPPD vs amorphous, cloudlike for
      BCP).
        CT’s main limitation is radiation exposure.58,59 In current clinical practice, CT is an
      adjunct diagnostic tool to confirm the presence and nature of crystals in difficult cases,
      especially in locations that are difficult to visualize by radiography.19,36,57,60 In cases
      of crystal arthropathies affecting the axial skeleton, CT is particularly useful
      (see Fig. 11).3,61 A typical example of spinal deposit is the crowned dens syndrome,
      usually due to CPPD but rarely also a manifestation of BCP deposits (see Fig. 5).19,20
        The incidental positivity of crystal arthropathies on PET and single-photon emission
      CT scans has been reported, and careful analysis of the CT examination should avoid
      erroneous diagnoses of tumoral or infectious disorders (see Fig. 11).3,61–63
Imaging in Gout and Other Crystal-Related Arthropathies          637

  Finally, CT has also been suggested as a quantitative tool to score bone erosions as
an outcome measure for chronic gout studies.64

DUAL-ENERGY COMPUTERIZED TOMOGRAPHY

More recently, the advent of DECT has opened new perspectives. This technique al-
lows differentiating deposits by their different x-ray spectra, using the principle that the
attenuation of tissues depends not only on their density but also on their atomic num-
ber Z as well as the energy of the photon beam.65
   Along with the characterization of urinary stones, one of the main applications of
DECT over the past decade has been the assessment of crystal arthropathies
(see Figs. 2 and 3).
   DECT shows a high diagnostic performance for the assessment of MSU deposition.
Reported sensitivities and specificities vary from 75% to 100% depending on the
studies, and there is high interobserver agreement (kappa 5 0.87–1).66–70 Compared
with US, DECT has shown comparable or higher specificity but lower sensitivity in
detecting smaller urate crystal deposits in joints.43,71
   Numerous causes of false negatives exist. These causes can be due to less dense
tophi with lower crystal concentrations, small size of tophi/crystals (usually not visible
at less than 2 mm), or even technical parameters.69,72,73
   There are also many causes of false-positive results. Postprocessed color-coded
images can falsely mimic the presence of MSU deposits when tissues present similar
index values, such as keratin. These false-positive results can be found around nail
beds and in the skin but also in regions of beam hardening and metal artifacts or
they can take the shape of single pixels scattered around the image, probably related
to image noise.68,74 False-positive cases have also been described in cases of severe
OA.69 A recent study has found abnormal intensities compatible with extensive depo-
sition of MSU in costal cartilages and intervertebral discs of patients with gout and
age-matched controls, suggesting that this finding might represent an artifact,
although this would need to be confirmed.75
   More work is needed to standardize postprocessing parameters in order to
improve the performance of DECT.73 Furthermore, several spectral imaging tech-
niques are used by different manufacturers to obtain DECT.65 Most of the data in
the literature were obtained with dual-source scanners, which seem to represent
the most robust technique. Results still need to be confirmed using other spectral im-
aging methods.
   One of the main advantages of DECT is to offer automatic volume measurement of
MSU deposits, with potential applications not only in clinical practice but also in
research.66,67,76,77 Therefore, DECT could serve as a tool to monitor tophus burden
as an outcome measure for gout.78 However, the sensitivity of DECT to change in
crystal deposit volume still needs to be determined, and measurement errors remain
a problem.79,80

MRI

MRI is not the modality of choice in the assessment of crystal arthropathies because of
its poor performance for the detection and characterization of crystals. In practice,
MRI of crystal deposits can be encountered in 2 settings: first, in asymptomatic pa-
tients presenting with crystal deposits as incidental findings (see Fig. 1) and, second,
in acute crystal arthropathies presenting as inflammation in unusual locations when
MRI is requested for diagnostic purposes (see Figs. 5 and 10). In this setting,
MR typically shows an intense inflammation in soft tissues and bones, which can be
638   Omoumi et al

      mistaken for infectious or tumoral conditions. A correlation with radiographs, CT, and
      US is, therefore, essential to prove the presence of crystals in the inflamed area (see
      Figs. 5 and 10).36

      MRI Features of Monosodium Urate Crystal Deposits
      MRI features of gouty arthropathy are variable and nonspecific. Tophi usually present
      intermediate or low signal intensity on T1-weighted sequences. On T2-weighted and
      gadolinium-enhanced T1-weighted sequences, the signal intensity is heterogeneous
      (see Fig. 1).40,81 The more inflammatory the tophus is, the higher the signal on these
      sequences. However, areas of concomitant low signal intensity on both enhanced
      T1- and T2-weighed sequences, corresponding to crystal deposits and chronic
      fibrous reactions, are often visible even at the inflammatory stage and can be sugges-
      tive of gouty arthropathy (see Fig. 1).5,7
         The presence of synovial thickening with low signal intensity on T2-weighted se-
      quences can also be seen in pigmented villonodular synovitis; but in case of MSU de-
      posits, there is no signal attenuation on gradient echo sequences.7,11

      MRI Features of Calcified Crystal Deposits (Calcium Pyrophosphate Dihydrate
      Deposition Disease, Basic Calcium Phosphate)
      The detectability of calcifications by MRI depends on multiple factors, such as their
      size, type and level of maturation, as well as the technical parameters that will define
      contrast, spatial resolution, and potential artifacts, such as magnetic susceptibil-
      ity.82,83 Signal characteristics of calcifications in the musculoskeletal system are not
      completely understood. Because of their low proton density and short T2 value, cal-
      cifications are often hypointense on most sequences, especially larger ones. Howev-
      er, meniscal calcifications may appear hyperintense on some MRI sequences and be
      mistaken for meniscal tears.84–86 The cause of this high signal intensity is still contro-
      versial. A likely hypothesis is the presence of degenerative tissue around the calcifica-
      tion (Fig. 13).85,86
         High T1 signal intensity calcifications have also been described in the intervertebral
      discs,87 although, in most cases, the high signal intensities are due to the presence of
      fatty bone marrow following disc ossification.88

      Fig. 13. CT (A) and MRI (B) of a 52-year-old man with tibial plateau fracture showing inci-
      dental CPPD. Fine, punctate (arrowhead) or linear (short arrows) calcifications are present
      in hyaline cartilage and meniscal fibrocartilage. MRI (fat-suppressed proton-density-
      weighted sequence) (B) shows areas of low signal intensity in cartilage corresponding to cal-
      cium deposits (long arrows in [A] and [B]). Calcifications in meniscus are usually not visible
      (dashed circle in [A] and [B]), but when associated with degenerative tissue changes, areas
      of high signal intensity can be visible (full circles in [A] and [B]).
Imaging in Gout and Other Crystal-Related Arthropathies           639

   One of the key factors influencing the signal characteristics of calcification is their
stage of maturation.82 The signal intensity of BCP deposits in tendons is usually low
on all sequences during their quiescent, mature phase (see Fig. 8).89 Most frequent
differential diagnoses for this pattern include the presence of gas related to a vacuum
phenomenon, postsurgical magnetic artifact due to intraarticular metallic debris, and
pigmented villonodular synovitis.17,86
   During the resolution phase of calcific tendinitis, the calcification is no longer
compact and the signal intensity of neighboring inflammatory tissues becomes het-
erogeneous, with areas of intermediate signal on T1- and T2-weighted sequences.83
During this phase, extensive regional high signal intensities on T2- and fat-suppressed
enhanced T1-weighted sequences, due to inflammation, usually prevail. These signal
changes are located in the tendon itself and in adjacent tissues where migration of the
calcification may occur and should not be mistaken for infectious or tumoral condi-
tions (see Fig. 10).32,36
   The detectability of calcifications by MRI also depends on the background tissue.82,83
Calcifications in the knee are usually easier to detect when located in hyaline cartilage
compared with menisci, which have relatively lower background signal intensity
(therefore, creating less contrast with the low intensity calcifications) (see Fig. 13).86,90
   Of note, novel MRI techniques are being developed, which have the potential to
allow morphologic as well as quantitative assessment of calcifications.82 More work
is needed, however, to shorten their acquisition times for routine clinical use.

SUMMARY

Crystal deposits in and around the joints are common and most often encountered as
incidental imaging findings in asymptomatic patients. However, they can also cause
chronic or acute arthropathy, generating symptoms.
   In the chronic setting, imaging features are usually characteristic and allow the
differentiation of the type of crystal arthropathy. In the acute phase and in the early
stages of the crystal deposition, imaging signs are often nonspecific and the final diag-
nosis still relies on the analysis of synovial fluid.
   Radiography is the main imaging modality for the workup of these conditions. It can
confirm the diagnosis and often characterizes the type of crystal arthropathy. In recent
years, US has played an increasingly important role in this setting and is a useful tool in
superficially located crystal-induced arthropathies. CT nicely complements radiog-
raphy for deeper sites, especially the axial skeleton. DECT is a promising tool for
the characterization of crystal arthropathies, in particular gout as it permits a quanti-
tative assessment of deposits, and may help in the follow-up of patients.
   When performed in the acute stage, MRI may show severe inflammatory changes
that could be misleading, and correlation to radiographs or CT should help to distin-
guish crystal arthropathies from infectious or tumoral conditions.

REFERENCES

 1. Zhang W, Doherty M, Bardin T, et al. European League Against Rheumatism rec-
    ommendations for calcium pyrophosphate deposition. Part I: terminology and
    diagnosis. Ann Rheum Dis 2011;4(70):563–70.
 2. Monu JUV, Pope TL. Gout: a clinical and radiologic review. Radiol Clin North Am
    2004;1(42):169–84.
 3. Cardoso FN, Omoumi P, Wieers G, et al. Spinal and sacroiliac gouty arthritis:
    report of a case and review of the literature. Acta Radiol Short Rep 2014;8(3).
    2047981614549269.
640   Omoumi et al

       4. Gentili A. Advanced imaging of gout. Semin Musculoskelet Radiol 2003;3(7):
          165–74.
       5. Dalbeth N, Pool B, Gamble GD, et al. Cellular characterization of the gouty
          tophus: a quantitative analysis. Arthritis Rheum 2010;5(62):1549–56.
       6. Bloch C, Hermann G, Yu TF. A radiologic reevaluation of gout: a study of 2,000
          patients. AJR Am J Roentgenol 1980;4(134):781–7.
       7. Malghem J, Vande Berg B, Lecouvet F, et al. Goutte d’hier et d’aujourd’hui. In:
          Imagerie de l’appareil musculo-squlettique: Textes choisis. Montpellier (France):
          Sauramps Medical; 2011. p. 35–44.
       8. Martel W. The overhanging margin of bone: a roentgenologic manifestation of
          gout. Radiology 1968;4(91):755–6.
       9. Choi MH, MacKenzie JD, Dalinka MK. Imaging features of crystal-induced
          arthropathy. Rheum Dis Clin North Am 2006;2(32):427–46, viii.
      10. Resnick D, Broderick TW. Intraosseous calcifications in tophaceous gout. AJR
          Am J Roentgenol 1981;6(137):1157–61.
      11. Sheldon PJ, Forrester DM, Learch TJ. Imaging of intraarticular masses. Radio-
          graphics 2005;1(25):105–19.
      12. Barrett K, Miller ML, Wilson JT. Tophaceous gout of the spine mimicking epidural
          infection: case report and review of the literature. Neurosurgery 2001;5(48):
          1170–2 [discussion: 1172–3].
      13. Bastani B, Vemuri R, Gennis M. Acute gouty sacroiliitis: a case report and review
          of the literature. Mt Sinai J Med 1997;6(64):383–5.
      14. Zufferey P, Valcov R, Fabreguet I, et al. A prospective evaluation of ultrasound as
          a diagnostic tool in acute microcrystalline arthritis. Arthritis Res Ther 2015;17:188.
      15. Carter JD, Kedar RP, Anderson SR, et al. An analysis of MRI and ultrasound
          imaging in patients with gout who have normal plain radiographs. Rheumatology
          (Oxford) 2009;11(48):1442–6.
      16. Rettenbacher T, Ennemoser S, Weirich H, et al. Diagnostic imaging of gout: com-
          parison of high-resolution US versus conventional x-ray. Eur Radiol 2008;3(18):
          621–30.
      17. Steinbach LS. Calcium pyrophosphate dihydrate and calcium hydroxyapatite
          crystal deposition diseases: imaging perspectives. Radiol Clin North Am 2004;
          1(42):185–205, vii.
      18. Resnick D, Niwayama G, Goergen TG, et al. Clinical, radiographic and patho-
          logic abnormalities in calcium pyrophosphate dihydrate deposition disease
          (CPPD): pseudogout. Radiology 1977;1(122):1–15.
      19. Scutellari PN, Galeotti R, Leprotti S, et al. The crowned dens syndrome. Evalua-
          tion with CT imaging. Radiol Med 2007;2(112):195–207.
      20. Baysal T, Baysal O, Kutlu R, et al. The crowned dens syndrome: a rare form of
          calcium pyrophosphate deposition disease. Eur Radiol 2000;6(10):1003–5.
      21. Ellman MH, Brown NL, Levin B. Prevalence of knee chondrocalcinosis in hospital
          and clinic patients aged 50 or older. J Am Geriatr Soc 1981;4(29):189–92.
      22. Felson DT, Anderson JJ, Naimark A, et al. The prevalence of chondrocalcinosis in
          the elderly and its association with knee osteoarthritis: The Framingham study.
          J Rheumatol 1989;9(16):1241–5.
      23. Stensby JD, Lawrence DA, Patrie JT, et al. Prevalence of asymptomatic chondro-
          calcinosis in the pelvis. Skeletal Radiol 2016;7(45):949–54.
      24. Martel W, McCarter DK, Solsky MA, et al. Further observations on the arthrop-
          athy of calcium pyrophosphate crystal deposition disease. Radiology 1981;
          1(141):1–15.
Imaging in Gout and Other Crystal-Related Arthropathies         641

25. Dodds WJ, Steinbach HL. Gout associated with calcification of cartilage. N Engl J
    Med 1966;14(275):745–9.
26. Hamilton EB. Diseases associated with CPPD deposition disease. Arthritis
    Rheum 1976;19(Suppl 3):353–7.
27. Adamson TC, Resnik CS, Guerra J, et al. Hand and wrist arthropathies of hemo-
    chromatosis and calcium pyrophosphate deposition disease: distinct radio-
    graphic features. Radiology 1983;2(147):377–81.
28. Ea H-K, Nguyen C, Bazin D, et al. Articular cartilage calcification in osteoarthritis:
    insights into crystal-induced stress. Arthritis Rheum 2011;1(63):10–8.
29. Ea H-K, Lioté F. Diagnosis and clinical manifestations of calcium pyrophosphate
    and basic calcium phosphate crystal deposition diseases. Rheum Dis Clin North
    Am 2014;2(40):207–29.
30. Fisseler-Eckhoff A, Müller KM. Arthroscopy and chondrocalcinosis. Arthroscopy
    1992;1(8):98–104.
31. Malghem J. Aspect radiologique des dépôts microcristallins. In: Imagerie de l’ap-
    pareil musculo-squlettique: Textes choisis. Montpellier (France): Sauramps Med-
    ical; 2011. p. 29–34.
32. Hayes CW, Conway WF. Calcium hydroxyapatite deposition disease. Radio-
    graphics 1990;6(10):1031–48.
33. Cox D, Paterson FW. Acute calcific tendinitis of peroneus longus. J Bone Joint
    Surg Br 1991;2(73):342.
34. Hammoudeh M. Calcific tendinitis mimicking acute sternoclavicular joint arthritis.
    Rheumatology (Oxford) 2001;11(40):1316–7.
35. Moon SG, Kim NR, Choi JW, et al. Acute coccydynia related to precoccygeal
    calcific tendinitis. Skeletal Radiol 2012;4(41):473–6.
36. Malghem J, Omoumi P, Lecouvet F, et al. Intraosseous migration of tendinous
    calcifications: cortical erosions, subcortical migration and extensive intramedul-
    lary diffusion, a SIMS Series. Skeletal Radiol 2015;44(10):1403–12.
37. Gutierrez M, Schmidt WA, Thiele RG, et al. International consensus for ultrasound
    lesions in gout: results of Delphi process and web-reliability exercise. Rheuma-
    tology (Oxford) 2015;10(54):1797–805.
38. Thiele RG, Schlesinger N. Diagnosis of gout by ultrasound. Rheumatology
    (Oxford) 2007;7(46):1116–21.
39. Löffler C, Sattler H, Peters L, et al. Distinguishing gouty arthritis from calcium
    pyrophosphate disease and other arthritides. J Rheumatol 2015;3(42):513–20.
40. Girish G, Glazebrook KN, Jacobson JA. Advanced imaging in gout. AJR Am J
    Roentgenol 2013;3(201):515–25.
41. Durcan L, Grainger R, Keen HI, et al. Imaging as a potential outcome measure in
    gout studies: a systematic literature review. Semin Arthritis Rheum 2016;5(45):
    570–9.
42. Pineda C, Amezcua-Guerra LM, Solano C, et al. Joint and tendon subclinical
    involvement suggestive of gouty arthritis in asymptomatic hyperuricemia: an ultra-
    sound controlled study. Arthritis Res Ther 2011;1(13):R4.
43. Huppertz A, Hermann K-GA, Diekhoff T, et al. Systemic staging for urate crystal
    deposits with dual-energy CT and ultrasound in patients with suspected gout.
    Rheumatol Int 2014;6(34):763–71.
44. Perez-Ruiz F, Martin I, Canteli B. Ultrasonographic measurement of tophi as an
    outcome measure for chronic gout. J Rheumatol 2007;9(34):1888–93.
45. Thiele RG, Schlesinger N. Ultrasonography shows disappearance of monoso-
    dium urate crystal deposition on hyaline cartilage after sustained normouricemia
    is achieved. Rheumatol Int 2010;4(30):495–503.
642   Omoumi et al

      46. Ottaviani S, Gill G, Aubrun A, et al. Ultrasound in gout: a useful tool for following
          urate-lowering therapy. Joint Bone Spine 2015;1(82):42–4.
      47. Mathieu S, Pereira B, Couderc M, et al. Usefulness of ultrasonography in the
          diagnosis of gout: a meta-analysis. Ann Rheum Dis 2013;10(72):e23.
      48. Filippou G, Adinolfi A, Iagnocco A, et al. Ultrasound in the diagnosis of calcium
          pyrophosphate dihydrate deposition disease. A systematic literature review and
          a meta-analysis. Osteoarthritis Cartilage 2016;6(24):973–81.
      49. Taljanovic MS, Melville DM, Gimber LH, et al. High-Resolution US of rheumato-
          logic diseases. Radiographics 2015;7(35):2026–48.
      50. Filippou G, Adinolfi A, Cimmino MA, et al. Diagnostic accuracy of ultrasound,
          conventional radiography and synovial fluid analysis in the diagnosis of calcium
          pyrophosphate dihydrate crystal deposition disease. Clin Exp Rheumatol 2016;
          2(34):254–60.
      51. Rutten MJCM, Jager GJ, Blickman JG. From the RSNA refresher courses: US of
          the rotator cuff: pitfalls, limitations, and artifacts. Radiographics 2006;2(26):
          589–604.
      52. Le Goff B, Berthelot J-M, Guillot P, et al. Assessment of calcific tendonitis of rota-
          tor cuff by ultrasonography: comparison between symptomatic and asymptom-
          atic shoulders. Joint Bone Spine 2010;3(77):258–63.
      53. Chiou H-J, Chou Y-H, Wu J-J, et al. Evaluation of calcific tendonitis of the rotator
          cuff: role of color Doppler ultrasonography. J Ultrasound Med 2002;3(21):289–95
          [quiz: 296–7].
      54. Zufferey P, So A. A pilot study of IL-1 inhibition in acute calcific periarthritis of the
          shoulder. Ann Rheum Dis 2013;3(72):465–7.
      55. Malghem J, Vande Berg B, Vanden Berghe M, et al. Aspect TDM des tophi gout-
          teux. J Radiol 1995;76:865.
      56. Gerster JC, Landry M, Duvoisin B, et al. Computed tomography of the knee joint
          as an indicator of intraarticular tophi in gout. Arthritis Rheum 1996;8(39):1406–9.
      57. Gerster JC. Imaging of tophaceous gout: computed tomography provides spe-
          cific images compared with magnetic resonance imaging and ultrasonography.
          Ann Rheum Dis 2002;1(61):52–4.
      58. Omoumi P, Becce F, Ott JG, et al. Optimization of radiation dose and image
          quality in musculoskeletal CT: emphasis on iterative reconstruction techniques
          (part 1). Semin Musculoskelet Radiol 2015;5(19):415–21.
      59. Omoumi P, Verdun FR, Becce F. Optimization of radiation dose and image quality
          in musculoskeletal CT: emphasis on iterative reconstruction techniques (part 2).
          Semin Musculoskelet Radiol 2015;5(19):422–30.
      60. McQueen FM, Doyle A, Dalbeth N. Imaging in the crystal arthropathies. Rheum
          Dis Clin North Am 2014;2(40):231–49.
      61. Bancroft LW, Peterson JJ, Kransdorf MJ. Cysts, geodes, and erosions. Radiol Clin
          North Am 2004;1(42):73–87.
      62. Duprez TP, Malghem J, Vande Berg BC, et al. Gout in the cervical spine: MR
          pattern mimicking diskovertebral infection. AJNR Am J Neuroradiol 1996;1(17):
          151–3.
      63. Pickhardt PJ, Shapiro B. Three-phase skeletal scintigraphy in gouty arthritis: an
          example of potential diagnostic pitfalls in radiopharmaceutical imaging of the ex-
          tremities for infection. Clin Nucl Med 1996;1(21):33–9.
      64. Dalbeth N, Doyle A, Boyer L, et al. Development of a computed tomography
          method of scoring bone erosion in patients with gout: validation and clinical im-
          plications. Rheumatology (Oxford) 2011;2(50):410–6.
Imaging in Gout and Other Crystal-Related Arthropathies       643

65. Omoumi P, Becce F, Racine D, et al. Dual-energy CT: basic principles, technical
    approaches, and applications in musculoskeletal imaging (part 1). Semin Muscu-
    loskelet Radiol 2015;5(19):431–7.
66. Choi HK, Burns LC, Shojania K, et al. Dual energy CT in gout: a prospective vali-
    dation study. Ann Rheum Dis 2012;9(71):1466–71.
67. Choi HK, Al-Arfaj AM, Eftekhari A, et al. Dual energy computed tomography in to-
    phaceous gout. Ann Rheum Dis 2009;10(68):1609–12.
68. Glazebrook KN, Guimaraes LS, Murthy NS, et al. Identification of intraarticular
    and periarticular uric acid crystals with dual-energy CT: initial evaluation. Radi-
    ology 2011;2(261):516–24.
69. Bongartz T, Glazebrook KN, Kavros SJ, et al. Dual-energy CT for the diagnosis of
    gout: an accuracy and diagnostic yield study. Ann Rheum Dis 2015;6(74):
    1072–7.
70. Finkenstaedt T, Manoliou A, Toniolo M, et al. Gouty arthritis: the diagnostic and
    therapeutic impact of dual-energy CT. Eur Radiol 2016;1–11.
71. Gruber M, Bodner G, Rath E, et al. Dual-energy computed tomography
    compared with ultrasound in the diagnosis of gout. Rheumatology (Oxford)
    2014;1(53):173–9.
72. Melzer R, Pauli C, Treumann T, et al. Gout tophus detection-a comparison of dual-
    energy CT (DECT) and histology. Semin Arthritis Rheum 2014;5(43):662–5.
73. McQueen FM, Doyle AJ, Reeves Q, et al. DECT urate deposits: now you see
    them, now you don’t. Ann Rheum Dis 2013;3(72):458–9.
74. Mallinson PI, Coupal T, Reisinger C, et al. Artifacts in dual-energy CT gout proto-
    col: a review of 50 suspected cases with an artifact identification guide. AJR Am J
    Roentgenol 2014;1(203):W103–9.
75. Carr A, Doyle AJ, Dalbeth N, et al. Dual-Energy CT of urate deposits in costal
    cartilage and intervertebral disks of patients with tophaceous gout and age-
    matched controls. AJR Am J Roentgenol 2016;206(5):1063–7.
76. Dalbeth N, Aati O, Gao A, et al. Assessment of tophus size: a comparison be-
    tween physical measurement methods and dual-energy computed tomography
    scanning. J Clin Rheumatol 2012;1(18):23–7.
77. Shi D, Xu J-X, Wu H-X, et al. Methods of assessment of tophus and bone erosions
    in gout using dual-energy CT: reproducibility analysis. Clin Rheumatol 2015;
    4(34):755–65.
78. Schumacher HR, Taylor W, Edwards L, et al. Outcome domains for studies of
    acute and chronic gout. J Rheumatol 2009;10(36):2342–5.
79. Bacani AK, McCollough CH, Glazebrook KN, et al. Dual energy computed
    tomography for quantification of tissue urate deposits in tophaceous gout: Help
    from modern physics in the management of an ancient disease. Rheumatol Int
    2012;1(32):235–9.
80. Rajan A, Aati O, Kalluru R, et al. Lack of change in urate deposition by dual-
    energy computed tomography among clinically stable patients with long-
    standing tophaceous gout: a prospective longitudinal study. Arthritis Res Ther
    2013;5(15):R160.
81. Chen CK, Yeh LR, Pan HB, et al. Intra-articular gouty tophi of the knee: CT and MR
    imaging in 12 patients. Skeletal Radiol 1999;2(28):75–80.
82. Omoumi P, Bae WC, Du J, et al. Meniscal calcifications: morphologic and
    quantitative evaluation by using 2D inversion-recovery ultrashort echo time and
    3D ultrashort echo time 3.0-T MR imaging techniques–feasibility study. Radiology
    2012;1(264):260–8.
644    Omoumi et al

       83. Vuillemin V, Guérini H, Omoumi P, et al. Le piège des calcifications en IRM. In:
           IRM musculo-squelettique de la clinique à la technique: techniques, pièges et as-
           tuces, ceintures scapulaire et pelvienne, rachis et pathologie tumorale, genou,
           IRM des extrémités. Montpellier (France): Sauramps médical; 2014. p. 91–111.
       84. Burke BJ, Escobedo EM, Wilson AJ, et al. Chondrocalcinosis mimicking a menis-
           cal tear on MR imaging. AJR Am J Roentgenol 1998;1(170):69–70.
       85. Kaushik S, Erickson JK, Palmer WE, et al. Effect of chondrocalcinosis on the
           MR imaging of knee menisci. AJR Am J Roentgenol 2001;4(177):905–9.
       86. Beltran J, Marty-Delfaut E, Bencardino J, et al. Chondrocalcinosis of the hyaline
           cartilage of the knee: MRI manifestations. Skeletal Radiol 1998;7(27):369–74.
       87. Major NM, Helms CA, Genant HK. Calcification demonstrated as high signal in-
           tensity on t1-weighted MR images of the disks of the lumbar spine. Radiology
           1993;2(189):494–6.
       88. Malghem J, Lecouvet FE, François R, et al. High signal intensity of intervertebral
           calcified disks on t1-weighted MR images resulting from fat content. Skeletal
           Radiol 2005;2(34):80–6.
       89. Loew M, Sabo D, Mau H, et al. Proton spin tomography imaging of the rotator cuff
           in calcific tendinitis of the shoulder. Z Orthop Ihre Grenzgeb 1996;4(134):354–9
           [in German].
       90. Zubler C, Mengiardi B, Schmid MR, et al. MR arthrography in calcific tendinitis of
           the shoulder: diagnostic performance and pitfalls. Eur Radiol 2007;6(17):
           1603–10.

      The author has requested enhancement of the downloaded file. All in-text references underlined in blue are l
You can also read