You are on page 1of 24

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
Jacques Malghem, MDc, Alexander So, FRCP, PhDb

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

 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.


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.
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:

Rheum Dis Clin N Am 42 (2016) 621–644
0889-857X/16/ª 2016 Elsevier Inc. All rights reserved.
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.


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
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
Table 2
Imaging features differentiating monosodium urate, calcium pyrophosphate dihydrate, and basic calcium phosphate crystals deposition diseases


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

(continued on next page)

Omoumi et al
Table 2
(continued )
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
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

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 <300 Hounsfield units [HU]), and articular/juxta-articular
bone erosions with overhanging margins (arrows). Three-dimensional reconstruction of
DECT (C) confirms the presence of MSU crystals in tophi, with the added value of showing
the distribution of tophi around the ankle and of volumetric analysis (total volume of tophi:
4.275 cm2). Note the presence of tophus inside the bone (arrows in [B]), causing bony
erosions with overhanging margins.

Calcium Pyrophosphate Dihydrate Deposition Disease

Radiographic features of chronic calcium pyrophosphate dihydrate deposition
disease arthropathy
CPPD can be found in all articular tissues, including hyaline cartilage and fibrocartilage
(deposits in the 2 types of cartilage being classically referred to as chondrocalcinosis),
synovium and ligaments, tendons, and other soft tissues (Fig. 4).17,18
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
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).


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

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
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


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
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


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 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.


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.


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
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).
640 Omoumi et al

4. Gentili A. Advanced imaging of gout. Semin Musculoskelet Radiol 2003;3(7):

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):
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;
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
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):
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;
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):
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):
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):
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)
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;
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
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
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
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
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):

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