Juvenile idiopathic arthritis: what is the utility of

ultrasound?

Abstract
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INTRODUCTION
Juvenile idiopathic arthritis (JIA) is an umbrella term encompassing a group of disorders
characterized by synovial inflammation. JIA is a diagnosis of exclusion and is the most
common rheumatic disorder of childhood, with a prevalence of 0.6–1.9 per 1000.1 It is
defined as arthritis of unknown cause lasting over 6-week duration in a child less than 16
years of age.
Disorders classified as JIA have been grouped according to clinical and biochemical markers
to aid detection, treatment and research. A widely used classification is the International
League of Associations for Rheumatology,2 where presentation may be with arthritis in a
single joint, <4 joints—oligoarticular disease [oligoarticular juvenile idiopathic arthritis
(OJIA)], multiple joints—polyarticular [polyarticular juvenile idiopathic arthritis (PJIA)] or
with systemic features (systemic juvenile idiopathic arthritis). Further subtypes are also
described (Table 1).
Table 1.
Classification of juvenile idiopathic arthritis (JIA) according to frequency, age of onset and
gender distribution3

JIA subtype Percentage of all Onset age Sex

JIA ratio

Systemic arthritis 4–17% Throughout childhood F = M

Oligoarthritis 27–56% Early childhood; peak at 2–4 years F >>> M

R+veJIA 2–7% Late childhood or adolescence F >> M

JIA subtype Percentage of all Onset age Sex
JIA ratio

R−veJIA 11–28% Biphasic distribution; early peak at 2–4 years and later F >> M
peak at 6–12 years

Enthesitis-related 3–11% Late childhood or adolescence F >> M

arthritis

Psoriatic arthritis 2–11% Biphasic distribution; early peak at 2–4 years and later F > M
peak at 9–11 years

Undifferentiated 11–21%
arthritis

F, female; M, male; R+veJIA, rheumatoid factor-positive polyarthritis; R−veJIA, rheumatoid factor-negative

polyarthritis.

Other classification systems include those provided by the American College of

Rheumatology and European League Against Rheumatism. None of the classification systems
are perfect, and it is noteworthy that none take tendon sheath inflammation, which is a
classical feature of JIA, into account. Patients can meet criteria for >1 subtype, as seen in
rheumatoid factor-negative polyarthritis, PJIA and subtypes of OJIA (Figure 1). The
implication is that this inter group heterogeneity can cause difficulty in measuring effects of
treatment and follow-up, by either clinical or radiological means. As understanding of the
genetic, clinical and biochemical make-up of these diseases advances, we may find future
reorganization of the classifications.4,5
Figure 1.
Heterogeneity within juvenile idiopathic arthritis (JIA) classifications: features of some of the disease
subtypes can overlap with others, causing difficulties in accurate classification. This has implications
on diagnosis, treatment and follow-up. F, female; M, male.

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AETIOLOGY
Although the precise aetiology of JIA is unknown, there are suggestions that infections and
vaccinations may be triggers in children with genetic susceptibility. There is no confirmed
evidence of an environmental trigger, but support for genetic predisposition comes from
scrutiny of the Utah Genealogical Database. Extended families of patients with JIA were
identified, and an estimate of sibling recurrence risk was found to be approximately 30 times
that of the general population.6
Consistent genetic associations with certain human leukocyte antigen (HLA) alleles are
recognized (Table 2) with a striking association with HLA-A2, which is seen across different
JIA categories.6,7
Table 2.
Self-tissue antigen and environmental risk factors associated with the development of juvenile
idiopathic arthritis (JIA)5,8

JIA category HLA association Protective alleles Suspected infective

triggers

Oligoarthritis A2, DRB1*01, DRB1*08, DRB1*11, (Protective HLA Parvovirus B19

DRB1*13, DPB1*02, DQA1*04, DRB1*04, DRB1*07) Epstein–Barr virus
JIA category HLA association Protective alleles Suspected infective
triggers

DQB1*04

R−veJIA A2, DRB1*08, DQA1*04, DPB1*03

R+veJIA DRB1*04, DQA1*03, DQB1*03 DQA1*02

Enthesitis related B27, DRB1*01, DQA1*0101, DQB1*05 Enteric bacteria

Arthritis

Psoriatic arthritis DRB1*01, DQA1*0101 DRB1*04, DQA1*03 Enteric bacteria

Systemic arthritis Bartonella Henselae

n = 1

JIA not specified Mycoplasma

pneumonia
Streptococcus
pyogene
Chlamydia
pneumonia
Chlamydia
trachomatis
Chlamydophila
pneumoniae

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HLA, human leukocyte antigen.

The genes controlling these alleles are thought to confer HLA-specific window of
susceptibility related to patient demographics during which the subject is most at risk of
developing an autoimmune process. This effect is seen to be strongest in OJIA in which
certain HLA alleles confer a variable risk according to age.7 At other ages, certain alleles are
likely to be neutral or even protective as in the case of HLA-DRB1*04, which is protective
for OJIA but is a risk factor for rheumatoid factor-positive polyarthritis.3,7
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PATHOGENESIS OF JOINT DAMAGE

Synovitis in JIA is characterized by infiltration by T-cells, B-cells and activated
macrophages.8 The release of proinflammatory cytokines stimulates arrival of further
inflammatory cells. This inflammatory soup contributes to the formation of pannus (Figure 2).
Synovial fibroblast, chondrocyte and osteoclast roles are modified such that joint damage
occurs via degradation of the cartilage and then eventually bone erosion.9,10 As the cartilage
and articular bone are damaged, classical features of joint space loss and erosions and in
advanced disease, ankylosis, growth disturbance and joint misalignment are seen.

Figure 2.
Pathogenesis of joint damage: an unknown inciting trigger activates T and B cells of the adaptive
immune system. These immune orchestrators promote joint infiltration by activating macrophages and
promoting osteoclastic activity. Over time, fibroblast and chondrocyte functions are altered, impairing
healing. The synovium becomes thickened and the cartilage is degraded, exposing the subchondral
bone to further erosive damage. Fluid can collect in the joint forming an effusion.

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ROLE OF IMAGING
It has been suggested that there is a “window of opportunity” in early disease during which
prompt treatment delays progression and induces higher rates of remission.11 Although JIA is
a clinical diagnosis, imaging plays an important role in support of the diagnosis, monitoring
of therapeutic response and detecting chronic changes. The mainstay of imaging remains plain
film, which is readily accessible, reproducible and suitably placed to longitudinally monitor
bone and joint changes over time.
Radiographs are, however, insensitive for inflammatory soft tissue changes which form a
significant part of the disease process.12,13 In the past 15 years, there has been a shift in the
management of JIA with early aggressive treatment.8,14,15 This requires detection of soft tissue
abnormalities prior to the development of established radiographic changes.
MRI is frequently utilized in JIA to assess joint, bone marrow and soft tissue changes, in
particular to evaluate bone marrow oedema and synovitis. Whilst MRI provides excellent soft
tissue and bone definition, there are certain disadvantages in children, namely long
examination times, the need for sedation or general anaesthesia in young children, relative
lack of access and the need to administer gadolinium to accurately diagnose synovitis.16 MRI
is also limited to evaluating predetermined joints or areas of interest, and it is time consuming
to examine multiple regions of the skeleton.
Ultrasound use has been recommended routinely in hands of experienced operators.17–19 It has
many advantages in children and is increasingly being utilized in JIA to confirm suspected
clinical findings, define affected anatomical compartments, guide arthrocentesis and perform
intra-articular therapy.20 Ultrasound is an ideal modality to use in children, being well
accepted, non-ionizing, dynamic, accessible and quick, and does not require sedation or
general anaesthesia. It can be used to compare symptomatic and asymptomatic sites and is
easily repeatable. There are, however, pitfalls and a learning curve when performing
musculoskeletal ultrasound (MSK-US) in children, and the technique is operator dependent.
In the following review, we interrogated the literature for the current evidence of ultrasound
in JIA by performing keyword searches in PubMed. The following terms were used: juvenile
idiopathic arthritis, inflammatory arthritis, musculoskeletal ultrasound, cartilage and normal
variants.
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TECHNICAL CONSIDERATIONS FOR ULTRASOUND IN JUVENILE

IDIOPATHIC ARTHRITIS
In common with other ultrasound examinations in children, establishing a good rapport with
the child and parents is a primary consideration, with a child-friendly ultrasound environment
being an important component in this.
MSK-US imaging requires a high-resolution image, and therefore linear transducers with
frequencies between 15 MHz and 18 MHz are preferred. Given the wide age range
encountered in paediatric imaging, it is vital to modify transducer selection so that an
appropriate size is used for the body part of interest. For example, using a “hockey-stick”
transducer would be appropriate to evaluate a finger in an adolescent but is unlikely to be
appropriate to examine the wrist, whereas for a 2-year old, a “hockey-stick” transducer is
much more appropriate than a standard 15 MHz linear transducer for wrist assessment.
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COMPOUND AND HARMONIC IMAGING
Compound ultrasound imaging is a technique where the transducer angles the beam over
several different angles of insonation and the resulting image is composed of the resulting
echoes from each of these. This leads to decreased speckle-, noise- and angle-related artefacts,
which have been shown to be of benefit in soft tissue imaging, particularly for structures
containing internal fibrillary structures such as tendons and muscles.21 The imaging of tendons
and muscles can be affected by the angle of insonation, with apparent reduced echogenicity
seen where the beam is not perpendicular to the fibres (anisotropy). Compound imaging is a
very useful tool in children who tend to wriggle and move, causing greater difficulty in
maintaining an ideal angle of insonation.
Harmonic imaging utilizes the phenomenon of non-linear propagation of ultrasound waves
through the body leading to multiples of the primary echo frequency returned from reflective
body interfaces (harmonics) around the primary transducer frequency. Using the second
harmonic in addition to the primary frequency to generate the ultrasound image leads to an
improved signal-to-noise ratio and increased axial resolution compared with conventional
ultrasound.
Taking into consideration the technical advantages described above, when performing MSK-
US in children, it is recommended to use an appropriately sized transducer for the body part
being examined, at as high a frequency as possible, with the addition of both compound and
harmonic imaging.
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NORMAL FINDINGS IN CHILDREN

One of the most challenging aspects of paediatric MSK-US is differentiating normal from
abnormal findings. Work carried out by Roth et al22 has provided the first ultrasound
definitions of joints in healthy children (Table 3). The growing skeleton is composed of an
initially cartilaginous epiphysis, physis (growth plate), metaphysis and diaphysis (Figure 3).
The age at which ossification begins within the epiphysis varies depending on the individual
bone involved, following (more or less) a well-described order,23 the discussion of which is
beyond the scope of this article.
Table 3.
Consensus definitions of the normal findings within joints on ultrasound examination22

Definition The hyaline cartilage will present as a well-defined anechoic structure (with/without bright
1 echoes/dots) that is non-compressible. The cartilage surface can (but does not have to) be detected
as a hyperechoic line

Definition With advancing maturity, the epiphyseal secondary ossification centre will appear as a hyperechoic
2 structure, with a smooth or irregular surface within the cartilage
Definition Normal joint capsule—a hyperechoic structure that can (but does not have to) be seen over bone,
3 cartilage and other intra-articular tissues of the joint

Definition Normal synovial membrane—under normal circumstances, the thin synovial membrane is
4 undetectable

Definition The ossified portion of articular bone is detected as a hyperechoic line. Interruptions of this
5 hyperechoic line may be detected at the growth plate and at the junction of two or more ossification
centres

Figure 3.

Lateral, longitudinal views of a normal knee joint: the image shows the potential joint space (star)
lined by the hyaline cartilage and linear and radial echoes (arrows) representing vascular channels
within the epiphyseal cartilage and the physeal cartilage (arrowhead).

To the best of our knowledge, there is no normal variant/normal developmental atlas for
paediatric MSK-US, and therefore becoming familiar with the appearances at different ages is
a large part of the learning curve when first contemplating performing these examinations.
Ultrasonographically, unossified cartilage, owing to its high water content appears
hypoechoic. Internal radial linear echoes may be seen within the cartilaginous epiphysis,
corresponding to blood vessels22 (Figure 3). The physis is also seen as a relatively linear, but
undulating, hypoechoic structure (being unossified cartilage also); the metaphysis and
diaphysis, being ossified, exhibit linear strongly reflective echoes. With increasing age, the
chondroepiphysis begins ossification, initially a central reflective echo with posterior acoustic
shadowing. This central echo is variable in appearance, but is frequently irregular in
outline.22 Over time, the cartilaginous epiphysis is progressively mineralized until ultimately
the whole epiphysis is ossified and covered by articular cartilage, which can be seen as a
hypoechoic rim overlying the bone. The inexperienced practitioner should be aware of the
possibility of mistaking this hypoechoic cartilage for joint fluid.
Establishing the range of normality in children is the key in standardising MSK-US and its
use in JIA, because identifying disease impacts therapy. Spannow et al24 evaluated the normal
range of articular cartilage thickness for a range of joints in healthy children, showing
decreasing cartilage thickness with age in their cohort of 6–17-year olds, with males having
thicker cartilage than females. A formula for calculating cartilage thickness according to age
was also derived by Spannow et al, who suggest it may be used in monitoring responses to
treatment.
When ultrasound-measured cartilage thickness is compared with MRI, good intermodality
agreement was found with a difference of <0.5 mm, with good overall agreement with the
exception of the wrist joint.25 An explanation for this may be the variability in ossification of
the abundant cartilage found in the carpus.26 Unfortunately, cartilage thickness is also affected
by confounding variables such as height, weight and skeletal maturation,24 likely making this
a difficult parameter for clinical use.
MRI studies in healthy children have highlighted the presence of bony depressions that
increase in number with age.27 Avenarius et al28 showed 75% of their healthy cohort had at
least one cortical depression. The depressions are thought to represent sites of ligamentous
insertion or vascular channels. In the clinical setting, knowledge of their presence is
important, since they may be mistaken for erosions on ultrasound. The most accurate way to
confirm a normal cortical depression is: (a) the anatomical location and (b) the presence of
cartilage at its base, which would not be present in the eroded bone.
Another unique feature of normal paediatric hands and wrists is that on MRI, joint fluid is
seen in at least one joint, with half of the children having >2 mm of fluid.29 Joint fluid is often
used as a marker of disease in adults,29 but this clearly demonstrates that joint fluid alone
cannot be used as a marker of JIA. Magni-Manzoni et al30 found ultrasound abnormalities in
nearly 36% of healthy children including joint effusions, synovial hyperplasia and a single
case of tenosynovitis. These are believed to be normal occurrences secondary to growth and
development of the paediatric skeleton. Power Doppler (PD) signal has been reported as a
common finding in the wrists of adults and children;18,31 these findings are more difficult to
explain in adults but may be due to detection of normal nutrient vessels in children.32
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ULTRASOUND FINDINGS IN JUVENILE IDIOPATHIC ARTHRITIS

As ultrasound technology has advanced, its use in rheumatology has become widespread. One
of the problems with ultrasound is that with technological improvements, practitioners are
visualizing more without knowing the implications of these findings. For example, as PD
becomes more sensitive to low flow, at what point is synovial vascularity abnormal? To begin
filling this validity and reliability void, the outcome measures in Rheumatology (OMERACT)
ultrasound special interest group was formed in 2004. They developed the first consensus
definitions for ultrasound pathologies in inflammatory joint diseases in adults. There are
limited data in children, although work on B mode and Doppler ultrasound is currently under
way.33 Ultrasound definitions of common lesions found in adult inflammatory arthritis (Table
4) were agreed upon in 2005 by the OMERACT group34 and are broadly adopted for use in
children.
Table 4.
Consensus definitions of joint abnormalities in adult inflammatory arthritis as seen on
ultrasound34

Rheumatoid An intra-articular discontinuity of the bone surface that is visible in two perpendicular
arthritis bone planes
erosion
Synovial fluid Abnormal hypoechoic or anechoic (relative to subdermal fat, but sometimes may be
isoechoic or hyperechoic) intra-articular material that is displaceable and compressible, but
does not exhibit Doppler signal

Synovial Abnormal hypoechoic (relative to subdermal fat, but sometimes may be isoechoic or
hypertrophy hyperechoic) intra-articular tissue that is non-displaceable and poorly compressible and
which may exhibit Doppler signal

Tenosynovitis Hypoechoic or anechoic thickened tissue with or without fluid within the tendon sheath,
which is seen in two perpendicular planes and which may exhibit Doppler signal

Enthesopathy Abnormally hypoechoic (loss of normal fibrillar architecture) and/or thickened tendon or
ligament at its bony attachment (may occasionally contain hyperechoic foci consistent with
calcification), seen in two perpendicular planes that may exhibit Doppler signal and/or
bony changes including enthesophytes, erosions or irregularity

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INFLAMMATORY CHANGES
The primary pathology in JIA is centred on the synovium, and therefore synovial hypertrophy
and hyperaemia are the primary sonographic correlates. Synovitis leads to synovial
proliferation (Figure 4) and accumulation of inflammatory tissue (pannus), which is typically
hypoechoic on B mode imaging. This is a potential pitfall for the inexperienced, as it may be
misinterpreted as unossified cartilage, joint fluid (Figure 5) or effusion within a tendon sheath
(Figure 6). Although typically low in reflectivity, synovial hypertrophy may also show mixed
or increased echogenicity. There may be exudation of fluid accompanying synovitis. Such
effusions are readily delineated on ultrasound, typically as hypoechoic collections, often, but
not exclusively, in association with synovial thickening.
Figure 4.

An anterior longitudinal image of the suprapatella recess of the knee: active nodular synovitis (double-
headed arrow) in the suprapatella recess and synovial thickening (arrowhead) in the visualized joint is
shown. An anechoic joint effusion (x) is seen above the prefemoral fat pad (star), which was also
hyperaemic (not shown). The unfused physis (arrow) is also demonstrated in this child with juvenile
idiopathic arthritis

Figure 5.
An anterior longitudinal image of the hip joint: a mildly echogenic normal epiphyseal cartilage
(curved arrow) is shown. When this is compared with the adjacent anechoic joint effusion (arrow),
synovial proliferation is just visible at the femoral head–neck junction (arrowhead), which is similar in
echogenicity to the unossified cartilage. Power Doppler interrogation of the synovium (not included)
did not show any active synovitis.

Figure 6.

Axial views of the medial ankle tendons in a patient with juvenile idiopathic arthritis: the tibialis
posterior tendon (arrowhead) surrounded by hypoechoic fluid (arrow) and mildly echogenic
tenosynovitis (curved arrows) (a) and the power Doppler signal in keeping with active tenosynovitis
(b).

One of the most useful contributions of ultrasound is not only delineating exactly which joints
are involved, but also differentiating joint from tendon sheath involvement, which can be seen
as increased tendon sheath thickness, tendon sheath effusions and hyperaemia (Figure 6).
When examining superficial structures such as tendons, care must be taken with regard to the
amount of pressure applied when performing ultrasound, as compression can displace tendon
sheath effusions, deform synovial thickening and compress vessels, spuriously decreasing
hyperaemia, all of which may lead to confusion. In such situations, the gel stand-off technique
is useful. This is where a mound of gel is maintained between the probe and skin so as to
apply minimum pressure to structures being evaluated.
Rooney et al35 observed that clinical differentiation of ankle joint swelling from ankle
tenosynovitis is difficult. In their sample of 34 children who suffered from OJIA or PJIA, a
total of 49 ankles were oedematous. Only 29% of ankles had a joint effusion alone on
ultrasound, whereas 39% ankles had tenosynovitis alone and 71% ankles showed both joint
synovitis and tenosynovitis. Interestingly, this study and a subsequent prospective study
showed tibialis posterior involvement to be commoner in OJIA, and peroneal tenosynovitis to
be commoner in PJIA.36 It has been postulated that the common coexistence of joint and
tendon sheath synovitis may be due to the increased biomechanical stresses put upon tendons,
as they cross and turn around joints such as the ankle. McGonagle37 suggested that these sites
of stress should be considered as “functional entheses”, and this may account for the high
prevalence of flexor tenosynovitis in psoriatic JIA.
Shenoy and Aggarwal37 have also shown that ultrasound has better sensitivity in detecting
enthesitis than clinical examination in the form of increased vascularity on Doppler imaging.
In a study of 27 patients with JIA, enthesitis was most commonly detected at the distal patella
and Achilles tendon insertions with rare involvement of the plantar fascia. However, it
remains difficult to interpret the validity of such changes on ultrasound, with up to 50% of all
sites sonographically showing enthesitis being clinically normal in one study.38 In addition,
enthesitis changes were not confined to enthesitis related Juvenile Idiopathic arthritis alone,
being seen in patients with OJIA and PJIA.
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DESTRUCTIVE CHANGES
Joint cartilage is a late target in arthritis, leading to joint space narrowing. High-frequency B
mode ultrasound is suited to assessing the integrity of paediatric cartilage, being able to
visualize the unossified physis as well as the articular cartilage contour.
In 2013, Pradsgaard et al39 performed cartilage measurements of five joints in patients with
JIA and confirmed they had thinner cartilage than controls but also that JIA cases had
significantly thinner cartilage regardless of whether the joints were previously affected by
arthritis or not.
In 2015, investigators from the same group performed a validation study to confirm accurate
measurements of the knee joint cartilage, with ultrasound using MRI as the reference
standard.40 They identified the intercondylar notch of the distal femur of a flexed knee as the
easiest site for reproducibility and confirmed good reliability. Given the good reliability of
cartilage assessment by ultrasound, there is a prospect that examination of the knee with
ultrasound could be used as a marker of disease activity.
As cartilage is degraded by joint inflammation, there is exposure of the underlying
subchondral bone, which, if unchecked, goes on to become eroded (Figure 7). Since
ultrasound is dynamic, it is possible to examine symptomatic joints in several planes,
potentially visualizing erosions that would have gone unnoticed on plain radiographs. It is
known that erosions are more common in females, patients with PJIA, early disease onset,
with elevated inflammatory markers and if rheumatoid factor is positive.41 Ultrasound
practitioners should be aware of the potential pitfalls when assessing for cortical erosions that
include physiological irregularities such as secondary ossification centres, cortical
depressions, growth plates at the epiphyseal cartilage and newly ossifying bone.
Figure 7.

Longitudinal (a) and axial (b) images of a damaged third and normal fourth metacarpophalangeal joint
in a patient with juvenile idiopathic arthritis: the preserved chondroepiphysis and hyaline cartilage
(star) as compared with the deformed third metacarpal head, which contains erosions (arrows),
synovial thickening/pannus (curved arrows) and oedema in the soft tissues (thick double-headed
arrow), blurring boundaries between the normal tissue layers (thin double-sided arrow), can be noted.

Ultrasound has a limited role in depicting growth deformities, which are better evaluated by
modalities that provide more global assessment.
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DISEASE ACTIVITY ASSESSMENT AND COMPARISON WITH CLINICAL

ASSESSMENT
In adults, disease activity has traditionally been assessed upon clinical and serological
markers. Current criteria to assess disease remission in adults are based on the “modified
Wallace criteria”,42 which does not include imaging. Given the increased periarticular soft
tissue, potential compliance difficulties in examining children and reluctance to routinely take
blood samples, this is more of a challenge in JIA.
Ultrasound has therefore been suggested as a means of evaluating disease activity in
JIA.20 Shahin et al43 and others have shown an association with circulating Interleukin 6
(amongst other cytokines) and the amount of joint vascularity demonstrated on PD. Colour
and PD techniques can potentially be used in addition to B mode imaging to assess synovitis
and thus disease activity.
Using a combination of synovial thickening, effusion and vascularity, it has been shown that
ultrasound is more sensitive for the detection of disease-affected joints in JIA and detects a
greater number of involved joints than physical examination.19,32,44 Imaging only-detected
disease activity or subclinical synovitis has been shown to correlate with progression of joint
damage in adults with rheumatoid arthritis (RA).45 Magni-Manzoni et al30 showed that
although subclinical synovitis in their cohort of 39 children was common (77%), 67% of
children remained in clinical remission after 2 years, concluding that subclinical synovitis
does not predict subsequent flare. Given the complexity of JIA and its subtypes, the
significance of subclinical synovitis in JIA remains undetermined.
There are other important issues raised by subclinical synovitis, as the number of disease
involved joints influences not only the diagnosis (e.g. OJIA or PJIA) but also treatment
decisions, in particular whether or not to institute biologic agents.14,46,47
Historically, disease follow-up has been performed using JIA-specific scoring systems based
on conventional radiographs.48 It has been shown that ultrasound can be reliably used to assess
cartilage thickness, synovitis and joint effusions. Although MRI is superior, ultrasound is at
least as good if not better than plain radiography for detection of cortical erosions in
accessible regions.49 Semi-quantitative scoring systems have been applied to only adults with
RA where PD signal in synovitis showed good correlation with histopathology and
intraoperative appearances.50
Ultrasound can locate the anatomical abnormality and guide injection of intra-articular steroid
with reduced rates of complications such as subcutaneous atrophy. On follow-up, ultrasound
can demonstrate normalization or regression of hyperaemia and synovial
hypertrophy.20,51 Similar findings have been shown when ultrasound is used to follow up
disease response to antirheumatic drugs52 and biologic therapies53 in adults.
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FUTURE OF ULTRASOUND IMAGING IN JUVENILE IDIOPATHIC

ARTHRITIS
Ultrasound imaging has advanced rapidly in the past 10 years with improvements in software
and hardware. Near-field imaging as used in the majority of rheumatological indications has
seen use of higher frequency probes with resolution up to 0.1 mm.54 The sensitivity of colour
Doppler has increased with manufacturers claiming it to be more sensitive to low flow than
PD.55
Colour and PD have a limited sensitivity in detecting the neomicrovascularity of synovitis, the
detection of which may be increased by performing i.v. microbubble contrast-enhanced
ultrasound to depict synovial enhancement. Time–intensity curves could provide an objective
measure of vascularity and hence inflammation which could be useful in grading disease
severity and response to treatment.56 Unfortunately, the requirement for peripheral venous
access and limited standardization make this technique less attractive in the general outpatient
paediatric population.
Conventional two-dimensional ultrasound imaging visualizes a limited slice of anatomy;
however, three-dimensional imaging can depict a whole joint. Using post-processing
software, computerized quantification of proliferative synovitis can be obtained, as has been
shown in synovitic knees.57 Three-dimensional ultrasound has not reached routine clinical
practice because its resolution remains poorer than that of B mode and Doppler imaging.
Real-time elastography has been shown to demonstrate that degenerative tendons are softer
than healthy tendon. This has gained much interest in the evaluation of lateral epicondylitis
and Achilles tendinopathy,58 and conceivably there may be a role in detecting enthesitis which
could be considered as the inflammatory homologue of “overuse” enthesitis.
Fusion imaging superimposes cross-sectional imaging data onto real-time ultrasound imaging.
It is already in use in nuclear medicine, radiotherapy and neurosurgery. The system uses an
electromagnetic field around the patient. A small receiver on the ultrasound probe provides
information about position and orientation. As the probe moves, the magnitude of electrical
current in the sensor changes within the magnetic field enabling the sensor unit to locate the
transducer. Images are displayed by extracting CT or MRI slices at the location parallel to the
ultrasound beam.59,60 Potential applications include ultrasound-guided injections into difficult-
to-access regions such as the sacroiliac joints with real-time needle placement on previously
acquired cross-sectional data, thereby limiting radiation exposure in the CT or fluoroscopy
suite.60
As described above, several advanced ultrasound applications have potential use in JIA
imaging but require further investigation before these can be clinically implemented.
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CONCLUSION
In summary, the literature supports the use of ultrasound in JIA but with the proviso that
practitioners should be aware of the complex anatomy that can demonstrate a wide range of
normal findings including “joint abnormalities” that are also detectable in healthy children.
Evidence shows ultrasound to be superior to the clinical examination alone, but the lack of
validated sonographic findings, scoring systems and treatment algorithms exposes the need
for further research. Initial steps should include addressing the sonographic definitions of the
normal paediatric joint and validating ultrasound protocols used in evaluating juvenile
arthritis.