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Magnetic resonance imaging assessment of spinal inflammation in ankylosing spondylitisStandard clinical protocols may omit inflammatory lesions in thoracic vertebrae.

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Arthritis & Rheumatism (Arthritis Care & Research)
Vol. 61, No. 9, September 15, 2009, pp 1187–1193
DOI 10.1002/art.24561
© 2009, American College of Rheumatology
Magnetic Resonance Imaging Assessment of
Spinal Inflammation in Ankylosing Spondylitis:
Standard Clinical Protocols May Omit
Inflammatory Lesions in Thoracic Vertebrae
Objective. Radiologic assessment of spinal inflammation in patients with ankylosing spondylitis (AS) relies primarily
on magnetic resonance imaging (MRI), although little is known about the distribution of inflammatory lesions within the
structures of the spine. Our objective was to compare the distribution of inflammatory lesions centrally and laterally
within the thoracic and lumbar spine vertebral bodies.
Methods. We studied 49 patients with AS who were scanned with STIR and T1-weighted spin-echo MRI of the whole
spine. Scans were read by 2 musculoskeletal radiologists, with a third reader as the arbitrator. Controls included 6
age-matched individuals. We recorded bone marrow edema on STIR images from each vertebral body, separately
identifying central and lateral slices. The latter were defined as images that included or were lateral to the pedicle.
Interreader reproducibility was assessed by kappa statistics.
Results. Inflammation was present in 263 (45%) of 588 thoracic and 86 (35%) of 245 lumbar vertebrae; the mean number
of affected thoracic and lumbar vertebrae per patient were 5.4 and 1.8, respectively. Inflammation was present in the
lateral aspect of 219 (37%) of 588 thoracic vertebrae and 45 (18%) of 245 lumbar vertebrae (P < 0.001). Lesions were more
common laterally than centrally for all thoracic vertebrae except for T7. Involvement of only the lateral slices was
observed in as many as 19.6% of thoracic vertebrae.
Conclusion. Evaluation of spinal inflammation by MRI may omit lesions in up to 20% of inflamed thoracic vertebrae if
both scanning and image assessment do not include sagittal slices that extend to the lateral edges of all vertebrae.
Magnetic resonance imaging (MRI) is a sensitive imaging
modality for detection of inflammatory lesions in patients
with ankylosing spondylitis (AS) (1). Detailed histopathologic analyses of the sacroiliac (SI) joints and spine have
Mr. Maksymowych is recipient of a Scientist Award from
the Alberta Heritage Foundation for Medical Research.
Winston J. Rennie, MB, FRCR: University Hospitals of
Leicester, Leicester Royal Infirmary, Leicester, UK;
Suhkvinder S. Dhillon, MB, FRCR, Barbara Conner-Spady,
PhD, Walter P. Maksymowych, MB, FRCPC, Robert G. W.
Lambert, MB, FRCPC: University of Alberta, Edmonton, Alberta, Canada.
Mr. Rennie is employed for honorary consultancy and has
received speaking fees (less than $10,000) from DePuy (UK).
Address correspondence to Robert G. W. Lambert, MB,
FRCPC, Department of Radiology and Diagnostic Imaging,
University of Alberta, 2A2.41WMC, 8440-112 Street, Edmonton, Alberta, Canada T5T 1E3. E-mail:
Submitted for publication April 15, 2008; accepted in
revised form June 11, 2009.
shown that inflammatory lesions are particularly evident
within bone marrow beneath articular cartilage and adjacent to the attachment of ligaments and capsules to bone
(2). These regions are typically not amenable to biopsy,
which has restricted progress in our understanding of the
pathophysiology of disease and therefore the development
of new therapeutic agents. Biopsy of the costovertebral
joint is not feasible, and arthropathy of this joint is particularly difficult to identify with radiography, although it is
a well-recognized entity in AS causing thoracic spine pain
(3). Limitation in chest expansion due to costovertebral
joint involvement is an important diagnostic criterion in
the widely used modified New York criteria (4). Erosions,
sclerosis, and bony proliferation have been reported
within the costovertebral joint in AS, more pronounced on
the vertebral side of the joint (5–7).
The use of T2-weighted MR sequences that suppress the
signal from marrow fat (STIR, T2 with fat suppression)
allows detection of increased water signal, which is associated with active inflammation in bone marrow. These
sequences are now routinely used to image the spine and
SI joint, providing a noninvasive approach to the evaluation of inflammatory lesions within bone marrow and soft
tissues of the entire axial skeleton. Scoring systems have
also been developed to quantify the extent of inflammatory
change in the spine (8,9).
In one report, MRI evaluation of inflammation in the
spine showed that the majority of inflammatory lesions in
patients with established disease were observed at the
thoracic level (10). However, this evaluation focused on
anterior spondylitis and spondylodiscitis, and foci of inflammation in the more lateral aspects of the vertebrae that
include the costovertebral joint may not have been fully
assessed. Complete nonvisualization of pathology at the
lateral edge of vertebrae may occur when scoliosis is
present because typical scanning protocols require that
sagittal sequences depict the entire spinal canal and the
majority of the vertebra/disc at each level, but do not
specify the need to include the lateral edges of the vertebral bodies. This may have important implications for the
approach to diagnostic evaluation as well as the assessment of treatment-refractory disease. In this study we
aimed to assess the frequency of involvement of lateral
structures of the spine in patients with AS by systematic
examination of the extent and distribution of inflammatory
lesions in the vertebral bodies using MRI.
Subjects. We studied 49 patients diagnosed with AS
according to the modified New York criteria (4). All patients had been recruited to a prospective, longitudinal
observational cohort, the Followup Research Cohort of AS
study, in which clinical and laboratory data are systematically collected every 6 months, and plain radiographic
imaging and MRI are obtained annually. Most patients
(83%) received nonsteroidal antiinflammatory drugs
and/or physical modalities of therapy. Of the 49 patients
with AS, 35 (71%) were male, with a mean ⫾ SD age of
42.3 ⫾ 11.7 years (range 21–70 years) and a mean ⫾ SD
disease duration of 19.4 ⫾ 11.4 years (range 2– 42 years).
The mean Bath AS Disease Activity Index score was 4.7
(range 2.7– 8.8) and mean Bath AS Functional Index score
was 4.1 (range 2.2– 8.4). We also included 6 controls, 3 of
whom had a history of nonspecific back pain. The controls
had a mean age of 36 years (range 24 – 47 years) and 4 were
male. All controls were imaged with an MRI protocol
identical to that for the patients with AS. The study was
approved by the University of Alberta Ethics Committee
and all patients provided informed consent.
MRI. All MRI of the spine was performed with 1.5T
systems (Siemens, Erlangen, Germany). Sagittal sequences
were obtained with 3– 4 mm slice thickness and 11–15
slices acquired. Sequence parameters were 1) T1-weighted
spin-echo (time to recovery [TR] 517– 618 msec, time to
echo [TE] 13 msec), and 2) STIR (TR 3,000 –3,170 msec,
time to inversion 140 msec, TE 38 – 61 msec). The field of
view was 380 – 400 mm and the matrix was 512 ⫻ 256
pixels. The spine was imaged in 2 parts: the upper half,
comprising the entire cervical and most of the thoracic spine,
Rennie et al
Figure 1. The transverse anatomy of the mid-thoracic spine illustrated with superimposed lines representing the location of 11
slices in a typical sagittal STIR magnetic resonance imaging sequence. The drawing includes minimal asymmetry and rotation of
the vertebra that is within normal limits. Central sagittal images
include the spinal canal (solid lines C). Lateral images include the
pedicle (solid lines L). In this study, one image on either side
immediately medial to the completely visualized pedicle at each
vertebral level was excluded from scoring, and images lateral to
the vertebral body were not evaluated (dotted lines). Note that the
left lateral edge of the vertebral body and the transverse processes
would not be included on this sagittal sequence.
and the lower half, comprising the lower portion of the
thoracic spine and entire lumbar spine. The specific MRI
parameters for acquiring spine images are provided on the
author’s Website (
MRI reading exercises. A unique MRI study number
was allocated to each patient and control, thereby ensuring
blinding to all patient demographics. Allocation was done
by a technologist unconnected with the study using computer-generated random numbers. Assessment was performed on a 3-monitor review station by 2 readers (WJR,
SSD) using computer software that is optimal for this type
of review (eFilm; Merge, Milwaukee, WI), and viewing
conditions were standardized. Each subject was only identified by the MRI study number, and scans were read in
random order by 2 fellowship-trained musculoskeletal radiologists, with a third musculoskeletal radiologist reader
as arbitrator (RGWL). Readers were unaware of the number
of control subjects included in the review.
Definitions were finalized after training. This consisted
of an initial pilot study of 15 scans of patients with AS
read by 2 observers and by consensus. The pilot results
were then discarded and these scans were not used in the
main study. Increased bone marrow signal denoting inflammation in vertebral bodies was assessed on STIR sequences. Bone marrow that was positive for inflammation
was defined as an appearance where the bone marrow
Assessment of Spinal Inflammation in AS with MRI
Table 1. Frequency and distribution (by subject) of inflammatory lesions in the spine of 49 patients with AS and 6 controls*
Group, spinal segment,
and slice location
Subjects with
abnormalities, no.
Effected levels per
patient, mean ⴞ SD
0.6 ⫾ 1.1
0 (0–1)
5.4 ⫾ 4.3
3.0 ⫾ 3.2
4.5 ⫾ 4.1
5 (0.5–9)
2 (0–5.5)
4 (0–8.5)
1.8 ⫾ 1.9
1.5 ⫾ 1.7
0.9 ⫾ 1.4
1 (0–3)
1 (0–3)
0 (0–1)
Patients with AS
Cervical, any
Cervical, any
Thoracic, any
Lumbar, any
Effected levels per
patient, median (IQR)
* AS ⫽ ankylosing spondylitis; IQR ⫽ interquartile range.
signal was greater than the signal from the center of an
adjacent normal vertebral body. We recorded inflammatory signal (as a dichotomous yes/no) on STIR images from
each vertebral body, and data sheets were designed to
separately identify inflammatory change from central and
lateral slices (Figure 1). Abnormalities in the pedicles,
other posterior elements of the vertebrae, or ribs were not
evaluated. Only the presence of vertebral body inflammation was recorded, and scoring did not include assessment
of lesion size, shape, or intensity of signal. Readers were
instructed to not distinguish between various possible
causes of inflammation. However, other lesions that may
be bright on T2-weighted sequences, such as hemangioma,
were excluded.
At each level of the thoracic and lumbar spine, the
sagittal images were defined as either a lateral slice (the
image of the vertebral body included or was lateral to the
pedicle) or a central slice (the image of the vertebral body
included the spinal canal or lateral recess). Often there is
one slice at the medial cortex of the pedicle that is also
partly through the lateral recess. To avoid variability of
assignation of this transitional slice, one slice on the left
side and one on the right side were discarded from the
analysis, defined as follows: the slice medial to the most
medial image clearly depicting the full length of the pedicle. It was not possible to apply these definitions to the
cervical spine, where the vertebral bodies are small with a
proportionately wider spinal canal, and assessment of cervical vertebrae did not distinguish between central and
lateral images. At each level, the number of central slices
varied mostly according to the size of the vertebra, and the
number of lateral slices varied according to the presence of
scoliosis. The central sections consisted of a minimum of
3 and a maximum of 5 slices, and the lateral sections
consisted of a minimum of 0 and maximum of 3 slices for
each side, with a combined minimum of 2 and maximum
of 6 lateral slices at each vertebral level.
Statistical analysis. The distribution of inflammatory
lesions according to spinal segment, vertebral level, and
lateral versus central slices was analyzed descriptively
and by Fisher’s exact test. Interobserver reliability was
assessed using kappa statistics. Kappa values of ⬎0.75,
0.40 – 0.75, and ⬍0.40 were designated as representing
excellent, fair to good, and poor reliability, respectively.
Table 2. Relative frequency and distribution (by vertebra) of inflammatory lesions in central and lateral slices of the
thoracolumbar spine in 49 patients with AS*
Location of inflammation
Thoracic vertebrae
(n ⴝ 588)
Lumbar vertebrae
(n ⴝ 245)
OR (95% CI)
P (Fisher’s exact)
Any slice
Central slice
Lateral slice
Central and lateral slices affected
Central slice only
Lateral slice only
No inflammation
263 (44.7)
148 (25.1)
219 (37.3)
104 (17.7)
44 (7.4)
115 (19.6)
325 (55.3)
86 (35.1)
72 (29.4)
45 (18.4)
31 (12.7)
41 (16.7)
14 (5.7)
159 (64.9)
1.50 (1.10–2.04)
0.81 (0.58–1.13)
2.64 (1.83–3.80)
1.48 (0.96–2.29)
0.40 (0.26–0.63)
4.01 (2.25–7.14)
0.67 (0.49–0.91)
⬍ 0.0001
⬍ 0.0001
* Values are the number (percentage) unless otherwise indicated. AS ⫽ ankylosing spondylitis; OR ⫽ odds ratio; 95% CI ⫽ 95% confidence interval;
NS ⫽ not significant.
Rennie et al
Descriptive data by patients. The number of patients
with MRI evidence of spinal inflammation in any vertebral
body was 39 (80%); 16 patients (33%) had inflammation in
the cervical spine, 37 patients (76%) had inflammation in
the thoracic spine, and 28 patients (57%) had inflammation in the lumbar spine. Of the patients who had inflammation in any vertebra, 41% involved the cervical spine,
95% involved the thoracic spine, and 72% involved the
lumbar spine. There were somewhat more patients with
lateral involvement (34 [70%] of 49) of the thoracic spine
compared with central involvement (32 [65%] of 49). In
contrast, more patients had involvement centrally (26
[53%] of 49) compared with laterally (21 [43%] of 49) in
the lumbar spine. Four of the 6 controls had evidence of
vertebral inflammation in either lumbar or thoracic vertebrae. Two controls had inflammation in the thoracic spine
and 4 had involvement of the lumbar spine, although only
a small number of vertebrae were affected (Table 1). All 3
of the controls with a history of nonspecific back pain
demonstrated minor foci of inflammation in the lumbar
Descriptive data by vertebrae. A total of 343 (7 per each
of the 49 subjects) cervical vertebrae, 588 (12 ⫻ 49) thoracic vertebrae, and 245 (5 ⫻ 49) lumbar vertebrae were
assessed for inflammation. Inflammation was present significantly more frequently in thoracic vertebrae (263 [45%]
of 588) than in cervical vertebrae (30 [9%] of 343; P
⬍ 0.0001) or lumbar vertebrae (86 [35%] of 245; P ⫽ 0.01)
(Table 2). Inflammation was also recorded in a total of 2
thoracic and 7 lumbar vertebrae from controls. The abnormalities identified in the control subjects were all small
and were adjacent to either a small tear of the annulus
fibrosus or a degenerate disc. In the thoracic vertebrae of
the AS group, involvement of lateral slices (37%) was
more common than involvement of central slices (25%)
(odds ratio [OR] 1.76, 95% confidence interval [95% CI]
1.37–2.27; P ⬍ 0.001), and lateral involvement was observed in a higher proportion of thoracic (37%) than lumbar (18%) vertebrae (P ⬍ 0.0001). Involvement of only the
lateral slices was observed in as many as 19.6% of thoracic
vertebrae versus only 5.7% of lumbar vertebrae (P
⬍ 0.0001). In contrast, involvement of only the central
slices was more common in lumbar vertebrae (P ⫽ 0.0001).
Moreover, the frequency of both lateral and central slice
inflammation in the same thoracic vertebra (17.7%) was
significantly more frequent than central slice inflammation
alone (7.4%) (OR 2.66, 95% CI 1.83–3.86; P ⬍ 0.0001), but
was not more frequent than lateral slice inflammation
alone (19.6%).
The distribution in the lumbar spine was different
where involvement of central slices (29.4%) was more
common than lateral slices (18.4%) (OR 1.85, 95% CI
1.21–2.83; P ⫽ 0.006), and where the frequency of both a
lateral and central slice lesion in the same lumbar vertebra
(12.7%) was similar to the frequency of central slice inflammation alone (16.7%) and significantly greater than
the frequency of lateral slice inflammation alone (5.7%)
Figure 2. Sagittal STIR magnetic resonance image in a 40-year-old
man with clinically proven ankylosing spondylitis and mild scoliosis. The lateral aspect of the lower thoracic vertebrae demonstrates a typical oval area of inflammation at the posterolateral
corner of the T9 inferior end plate and the T10 superior end plate
that constitutes the vertebral side of the tenth costovertebral joint
(long arrow). Inflammation is noted to extend posteriorly through
the pedicle. Intense inflammation is present in the head of the
eighth rib (short arrow).
(OR 2.39, 95% CI 1.24 – 4.62; P ⫽ 0.01). As a proportion of
all levels demonstrating inflammation, involvement of lat-
Assessment of Spinal Inflammation in AS with MRI
eral slices was recorded in 219 (83.3%) of 263 thoracic and
in 45 (52.3%) of 86 lumbar vertebrae. Typical lesions are
illustrated in Figures 2 and 3. Inflammation in lateral
slices was evident throughout the thoracic spine, being
most frequent at T8 and T11 thoracic vertebrae (data not
shown). Inflammation in central slices was most frequent
at T7 in the thoracic spine and was broadly distributed in
the lumbar spine.
Reliability. The mean kappa for thoracic lateral and
central slices was 0.56 (range 0.35– 0.74) and 0.38 (⫺0.30
to 1.00), respectively (Table 3). The kappa values for assessment of thoracic lateral slices were fair to good (0.40 –
0.74) for 11 of the 12 thoracic vertebrae. Percentage agreement ranged from 67– 87% and from 53–100% for
assessment of thoracic lateral and central slices, respectively. Mean kappa values for lumbar lateral and central
slices were 0.72 (range 0.44 –1.00) and 0.20 (0.05– 0.44),
respectively. The kappa values for assessment of lumbar
lateral slices were excellent (⬎0.75) for 2 of the 5 lumbar
vertebrae. Percentage agreement ranged from 73–100%
and from 47–73% for the assessment of lumbar lateral and
central slices, respectively.
Our systematic evaluation of inflammatory lesions observed on MRI in thoracic and lumbar vertebrae of subjects
with established AS shows that such lesions in the lateral
slices occur in approximately one-third of all thoracic and
one-sixth of all lumbar vertebrae, that such lesions are
more common in lateral versus central slices in the thoracic but not the lumbar spine, and that approximately
one-fifth of all thoracic vertebrae display lesions only on
the more lateral images. Consequently, it is possible that a
diagnostic examination or an MRI scoring system that does
not include all the appropriate lateral images of the spine
or does not systematically analyze the lateral images could
omit nearly half (44%) of all inflamed vertebrae in the
thoracic spine and 16% of all inflamed vertebrae in the
lumbar spine.
The inflammatory abnormalities identified in the central
slices were usually typical Romanus lesions, central end
plate erosion with edema or diffuse vertebral inflammation, and, not surprisingly, occurred with similar frequency in the thoracic and lumbar spine. At levels where
inflammation was seen on both central and lateral images,
often these abnormalities were clearly separate lesions.
However, frequently contiguous pathology was noted, and
then it was not possible to specify the precise source of
inflammation. Lateral inflammation was identified much
more frequently in the thoracic spine and at many levels
was particularly common in, or immediately adjacent to,
the vertebral portion of the costovertebral joint. At a few
levels, inflammation appeared to be arising from the posterior elements and extending through the pedicle into the
vertebral body. However, this is not likely to be the primary source of lateral inflammation in the vertebral bodies, and it would not explain the striking difference in
lateral predominance between the thoracic and lumbar
Figure 3. From the same scan as Figure 2. Inflammation arising
from the eleventh costovertebral joint involves both adjacent vertebral end plates (short white arrow ). Inflammation from the twelfth
costovertebral joint involves only the T12 vertebra (long white arrow). The anatomy of this rib is different, and the head of the twelfth
rib does not articulate with the T11 inferior end plate. Some edema
in the pedicles of the lumbar spine is due to facet joint inflammation
with minimal or no extension into the vertebral bodies (black arrow). Posterior element changes were not scored in this study.
spine. We also noted in some cases of scoliosis (with
additional MRI slices on one side) that the typical pattern
Rennie et al
Table 3. Interobserver reliability between 2 readers of detection of inflammatory lesions in the thoracic and lumbar vertebrae
of 49 patients with AS*
Location of
Any slice
Any slice
Kappa, mean
Fair to good:
Agreement, mean %
0.59 (0.35–0.74)
0.38 (⫺0.30 to 1.00)
0.56 (0.35–0.74)
1 (8)
10 (83)
3 (25)
11 (92)
2 (17)
8 (67)
1 (8)
79 (67–87)
73.8 (53–100)
77.8 (67–87)
0.33 (0.22–0.48)
0.20 (0.05–0.44)
0.72 (0.44–1.00)
2 (50)
2 (40)
1 (20)
2 (50)
3 (60)
4 (80)
62.6 (53–73)
54.6 (47–73)
88 (73–100)
* Values are the number (percentage) unless otherwise indicated. AS ⫽ ankylosing spondylitis.
† No variation for 1 rater at L2.
of edema in the posterolateral aspects of 2 adjacent end
plates was associated with bone edema in the head of the
corresponding rib (Figure 2).
Clinical involvement of the costovertebral joint is
readily recognized as pain and stiffness in the thoracic
spine with restricted chest expansion. Histopathologic
studies of this joint reveal the presence of a fibrocartilaginous disc, and the presence of fibrocartilaginous tissue at
this location might explain the frequency with which inflammation is observed in the costovertebral joint (6). In
patients with AS, there is a predilection for inflammation
at sites rich in fibrocartilage, and it has been hypothesized
that a constituent of fibrocartilage may induce autoimmunity (11). Our observations would be consistent with this
hypothesis. However, even bony abnormalities of the costovertebral joint are not readily evident radiographically
due to the complexity of the anatomy and overlapping
structures that obscure these joints.
Bone marrow inflammation was seen in control subjects,
although the lesions were generally small and few in number. They occurred predominantly in the lower lumbar
spine and in association with disc degeneration. Of course,
some patients with AS also had disc degeneration and in
those cases, the vertebral inflammation observed may not
necessarily have been due to the spondylitis. However, the
pattern of bone edema is sometimes quite characteristic for
one or the other, and in the thoracic spine in particular, the
presence of vertebral inflammation at multiple levels may
be quite specific for spondylitis.
The interobserver reliability was only moderate overall.
The highest kappa values were recorded for readings of the
lateral slices, which may be surprising to those not familiar with MRI interpretation. However, there are several
factors that may explain this. All MRI scans are subject to
artifact and for some sequences this may be considerable.
The STIR sequence is very useful in this clinical setting
because it is quite reliable, even with different patients
and MRI units. A limitation of the sequence is its propensity to display phase-encoding artifacts caused by flowing
blood or cerebrospinal fluid, and this spurious signal tends
to be projected over the vertebral bodies near the midline,
so the lumbar vertebrae may be particularly affected (12).
This can make it quite difficult to interpret small or faint
abnormalities such as Romanus lesions. By comparison,
involvement of the costovertebral joint tends to affect a
broader area of the vertebral body and this may simplify
interpretation even in the presence of artifact (Figure 2).
The kappa values were particularly low in the central
slices of the lower lumbar spine, influenced by the variability of marrow signal at levels that are so frequently
affected by disc degeneration. Other contributing factors
include difficulty in interpreting small end plate erosions
versus Schmorl’s nodes, the small size of the upper thoracic vertebrae, and other MRI artifacts, although generally
the image quality was good.
The standard approach to MRI evaluation of the spine
focuses on sagittal and transverse sequences and on the
neurologic structures in the central spinal canal, lateral
recesses, and neuroforamina. It is neither practical nor
usually necessary to perform transverse imaging throughout the entire spine. So, regardless of indication, a typical
protocol usually involves doing sagittal sequences to find
the pathology, and then performing additional transverse
or other sequences through the identified levels of concern. The costovertebral joints are not generally the target
for neoplastic, degenerative, or neurologic disorders and,
therefore, neither are they the focus of routine clinical
MRI. Scoliosis compounds the imaging problem and scanning instructions to the MRI technologists usually run
along the lines of “spinal canal and lateral recesses must
be included.” However, inclusion of the lateral aspects of
all pedicles is not mandatory, let alone scanning lateral to
the pedicles. Thus, with even minor degrees of scoliotic
curvature, the pedicles are often only partially visualized,
and the lateral edges of the vertebral bodies may not be
seen at the middle or ends of the curvature. This problem
is exaggerated when scanning at large fields of view and
can only be overcome by adding more slices or making the
slices thicker with corresponding increase in scan time or
loss of resolution.
Our results have significant implications for the training
of radiologists and rheumatologists in the interpretation of
MRI from patients referred for both diagnostic evaluation
and assessment of activity in established disease. It has, for
example, been reported that at least one-quarter of patients
with AS who are sufficiently symptomatic to be recruited
to trials of anti–tumor necrosis factor ␣ (anti-TNF␣) therapies have no evidence of spinal inflammation on baseline
Assessment of Spinal Inflammation in AS with MRI
MRI scans (13). However, this assumption may have been
based on a limited assessment of sagittal images. Furthermore, scores for spinal inflammation on MRI have been
analyzed as both predictor variables for treatment response and structural damage and in correlation analyses
with clinical, laboratory, and biomarker variables. Our
data suggest that these analyses may be compromised if
assessment of MRI scans does not include the entirety of
the thoracic spine, extending to the costovertebral joints
Abnormalities in the lateral aspects of the vertebrae
appear to be more reliably detected, and scoring systems
that include assessment of lesions in consecutive sagittal
slices may possess advantages over those that focus on the
scoring of individual lesions in the anteroposterior dimension. In particular, inclusion of ⬎1 slice in the scoring of
lesions may improve responsiveness, and this may be advantageous in the evaluation of therapeutic agents that
possess structure-modifying properties but are less effective as antiinflammatory agents than anti-TNF␣ therapies.
In conclusion, this systematic analysis of inflammatory
lesions evident on MRI in the thoracic and lumbar spine
demonstrates that the majority of lesions in thoracic vertebral bodies are present in the more lateral aspect of the
vertebrae and that lateral lesions in general are more reliably detected than those closer to the midline. Lateral
lesions may not be fully assessed on the sagittal images of
standard MRI protocols, especially in the presence of scoliosis, and so it is recommended that diagnostic evaluation
and assessment of disease activity in spondylarthropathy
should include assessment of sagittal images that extend to
the lateral edges of all thoracic vertebrae as a minimum
All authors were involved in drafting the article or revising it
critically for important intellectual content, and all authors approved the final version to be submitted for publication. Mr.
Lambert had full access to all of the data in the study and takes
responsibility for the integrity of the data and the accuracy of the
data analysis.
Study conception and design. Rennie, Dhillon, Maksymowych,
Acquisition of data. Rennie, Dhillon, Maksymowych, Lambert.
Analysis and interpretation of data. Rennie, Dhillon, ConnerSpady, Maksymowych, Lambert.
1. Maksymowych WP, Lambert RG. Spinal inflammation in ankylosing spondylitis: how and why should it be measured by
MRI? [editorial]. Nat Clin Pract Rheumatol 2006;2:232–3.
2. Francois RJ, Gardner DL, Degrave EJ, Bywaters EG. Histopathologic evidence that sacroiliitis in ankylosing spondylitis is not merely enthesitis: systematic study of specimens
from patients and control subjects. Arthritis Rheum 2000;43:
3. Pascual E, Castellano JA, Lopez E. Costovertebral joint
changes in ankylosing spondylitis with thoracic pain. Brit
J Rheumatol 1992;31:413–5.
4. Van der Linden S, Valkenburg HA, Cats A. Evaluation of
diagnostic criteria for ankylosing spondylitis: a proposal for
modification of the New York criteria. Arthritis Rheum 1984;
27:361– 8.
5. Hart FD, Emmerson PA, Gregg I. Thorax in ankylosing spondylitis. Ann Rheum Dis 1963;22:11– 8.
6. Fassbender HG. Pathology of the rheumatic diseases. Berlin:
Springer-Verlag; 1975. p. 221–58.
7. Dihlmann W. Current radiodiagnostic concept of ankylosing
spondylitis. Skelet Radiol 1979;4:179 – 88.
8. Braun J, Baraliakos X, Golder W, Brandt J, Rudwaleit M,
Listing J, et al. Magnetic resonance imaging examinations of
the spine in patients with ankylosing spondylitis, before and
after successful therapy with infliximab: evaluation of a new
scoring system. Arthritis Rheum 2003;48:1126 –36.
9. Maksymowych WP, Inman RD, Salonen D, Dhillon SS, Krishnananthan R, Stone M, et al. Spondyloarthritis Research Consortium of Canada magnetic resonance imaging index for assessment of spinal inflammation in ankylosing spondylitis.
Arthritis Rheum 2005;53:502–9.
10. Baraliakos X, Landewe R, Hermann KG, Listing J, Golder W,
Brandt J, et al. Inflammation in ankylosing spondylitis: a
systematic description of the extent and frequency of acute
spinal changes using magnetic resonance imaging. Ann
Rheum Dis 2005;64:730 – 4.
11. Maksymowych WP. Ankylosing spondylitis: at the interface
of bone and cartilage. J Rheumatol 2000;27:2295–302.
12. Maksymowych WP, Lambert RG. Magnetic resonance imaging
for spondyloarthritis: avoiding the minefield [editorial].
J Rheumatol 2007;34:259 – 65.
13. Braun J, Landewe R, Hermann KG, Han J, Yan S, Williamson
P, et al, for the ASSERT Study Group. Major reduction in
spinal inflammation in patients with ankylosing spondylitis
after treatment with infliximab: results of a multicenter, randomized, double-blind, placebo-controlled magnetic resonance imaging study. Arthritis Rheum 2006;54:1646 –52.
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