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Magnetic resonance imaging evidence of tendinopathy in early rheumatoid arthritis predicts tendon rupture at six years.

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ARTHRITIS & RHEUMATISM
Vol. 52, No. 3, March 2005, pp 744–751
DOI 10.1002/art.20947
© 2005, American College of Rheumatology
Magnetic Resonance Imaging Evidence of Tendinopathy in
Early Rheumatoid Arthritis Predicts Tendon Rupture at
Six Years
Fiona McQueen,1 Vaughan Beckley,2 Jeff Crabbe,3 Elizabeth Robinson,2
Sue Yeoman,4 and Neal Stewart5
at 6 years (r ⴝ 0.11, P ⴝ 0.5). The strongest predictor of
the 6-year tendinopathy score was the 1-year tendinopathy score (R2 ⴝ 0.36, P ⴝ 0.0003 [␤ ⴝ 1.28, SE ⴝ 0.31]).
In 4 patients, extensor tendon rupture had occurred by
6 years. Their baseline and 1-year tendinopathy scores
were higher than in the nonrupture group (medians 2.8
versus 1.0 [P ⴝ 0.04] and 4.3 versus 0.8 [P ⴝ 0.03],
respectively), as were their Health Assessment Questionnaire scores (1.33 versus 0.54 [P ⴝ 0.02], 1.18
versus 0.25 [P ⴝ 0.03], and 0.98 versus 0.37 [P ⴝ 0.01]
at 0, 1, and 6 years, respectively). For the group as a
whole, the baseline tendinopathy score was predictive of
rupture at 6 years (odds ratio [OR] 1.52, 95% confidence interval [95% CI] 1.02–2.32, P ⴝ 0.03), as was the
1-year score (OR 1.57, 95% CI 1.03–2.04, P ⴝ 0.02).
Conclusion. MRI can be used to quantify tendinopathy at the wrist in RA patients. High scores in early
disease were predictive of tendon rupture in a small
group of patients, but further studies are required to
determine whether this has clinical relevance.
Objective. To determine whether magnetic resonance imaging (MRI) evidence of tendinopathy in early
rheumatoid arthritis (RA) could be used to predict the
course of tendon involvement in later disease and
specifically the risk of tendon rupture.
Methods. The occurrence, pattern, and progression of tendinopathy were studied prospectively over 6
years in a cohort of patients who had presented with RA.
Of 42 patients enrolled, full MRI and clinical data were
available for 31 at 6 years. MRI scans of the dominant
wrist were scored for tendinopathy by 2 radiologists
using a validated system. These data were compared
with MRI synovitis, erosion scores, and disease activity
measures. Prognostic factors for tendon inflammation
and rupture were sought.
Results. Thirty-four patients (81%) had MRI evidence of tendinopathy at baseline, falling to 59% at 1
year and 68% at 6 years. The most commonly affected
site was the extensor carpi ulnaris. MRI tendinopathy
and synovitis scores were correlated at baseline (r ⴝ
0.37, P ⴝ 0.01) and 1 year (r ⴝ 0.45, P ⴝ 0.003) but not
Tendinopathy involving the extensor tendons of
the wrist is observed in 50–64% of patients with rheumatoid arthritis (RA) (1). An important complication is
tendon rupture, which has been related both to invasion
of the tendon by tenosynovial pannus and fraying of the
tendon against eroded bone margins (2,3). Studies of
invasive tenosynovium have revealed high levels of matrix metalloproteinases, proinflammatory cytokines, and
angiogenic factors, indicating a propensity for damage to
neighboring tissues (4). The importance of ongoing
tenosynovial inflammation in promoting tendon rupture
has been confirmed by observations that prophylactic
dorsal tenosynovectomy can prevent this complication in
many patients (5). However, the decision to perform
surgery is usually made in established cases of RA once
Supported by grants from the Health Research Council of
New Zealand, the Arthritis Foundation of New Zealand, the Auckland
Medical Research Foundation, Lotteries Health, New Zealand, the
Auckland Radiology Group, Sanofi-Winthrop, and the Auckland
Regional Rheumatology Research Trust.
1
Fiona McQueen, MBChB, MD, FRACP: University of Auckland and Auckland District Health Board, Auckland, New Zealand;
2
Vaughan Beckley, Elizabeth Robinson, MSc: University of Auckland,
Auckland, New Zealand; 3Jeff Crabbe, MBChB, FRANZCR: Auckland Radiology Group, Auckland, New Zealand; 4Sue Yeoman: Auckland District Health Board, Auckland, New Zealand; 5Neal Stewart,
MBChB, FRANZCR: Auckland District Health Board and Auckland
Radiology Group, Auckland, New Zealand.
Address correspondence and reprint requests to Fiona McQueen, MBChB, MD, FRACP, Department of Rheumatology, Building 7, Auckland Hospital, Private Bag 92024, Auckland, New Zealand.
E-mail: f.mcqueen@auckland.ac.nz.
Submitted for publication July 6, 2004; accepted in revised
form December 2, 2004.
744
PREDICTING TENDON RUPTURE THROUGH MRI EVIDENCE
clinical or radiologic features of joint damage have
developed (6).
Magnetic resonance imaging (MRI) has been
shown to be a powerful tool in identifying early soft
tissue and bony change at sites in the hand and wrist in
early RA (7,8). At 4 months, as many as 90% of patients show MRI evidence of wrist synovitis (9). MRI is
an excellent modality for imaging tendons at the wrist
in view of its ability to identify characteristic signal
changes in tissues which have become inflamed or
damaged (7). Hypertrophy of the tenosynovium within
the tendon sheath is revealed as bright signal in thickened tissue surrounding a tendon on T1-weighted postcontrast and T2-weighted sequences, while an accompanying effusion within the sheath is low signal on early
T1-weighted postcontrast scans. Changes within the
tendon itself can be identified and include increased
signal on T2-weighted images implying inflammatory
change, as well as thinning and attenuation, which are
likely to precede rupture (7,10). MRI identification of
tendon rupture is highly correlated with surgical confirmation and has been shown to be more accurate than
clinical evaluation (3).
In this report we describe the progression and
complications of tendinopathy, as revealed by MRI of
the dominant wrist, in a cohort of RA patients who
have been studied prospectively over a 6-year period.
We investigated associations between tendinitis/
tenosynovitis, synovitis, and erosion, and sought prognostic indicators of tendon rupture.
PATIENTS AND METHODS
Patient population and clinical assessments. Patients
for this study have been studied longitudinally over a 6-year
period and have been previously described (9,11). Patients
were referred to an early arthritis clinic by primary care
physicians and specialist rheumatologists after a media campaign. Approval for the study was granted by regional ethics
committees. Enrollment proceeded from 1994 through 1996,
and then patients were followed with clinical assessments and
MRI scans of the dominant wrist at 0, 1, and 6 years. Disease
activity was assessed using tender and swollen joint counts,
erythrocyte sedimentation rate (ESR), and C-reactive protein
(CRP) levels. The Disease Activity Score (DAS) was derived
according to the method described by van der Heijde et al (12).
At the onset of the study the now-validated DAS28 measure
had not been developed, so the original DAS calculation was
used at each time point. Joint subluxation and malalignment
were not scored, but function was assessed using the Health
Assessment Questionnaire (HAQ) score (13).
In 31 patients, full clinical and MRI data were available
at 6 years. In an additional 3 patients, clinical assessments were
performed but MRI scans could not be obtained because of
745
Table 1. Medication profile of the study cohort at baseline and at 1
and 6 years*
NSAIDs
DMARDs
Sulfasalazine (1–3 gm/day)
Methotrexate (7.5–25 mg/week)
Prednisone (1–13 mg/day)
Baseline
(n ⫽ 42)
1 year
(n ⫽ 42)
6 years
(n ⫽ 34)
38 (90)
21 (50)
18 (43)
1 (2)
6 (14)
24 (57)
30 (71)
15 (36)
11 (26)
10 (24)
17 (50)
30 (88)
10 (29)
15 (44)
9 (28)
* Values are the number (%). Treatments received by the 4 patients in
whom extensor tendon rupture occurred during the study were as
follows: at baseline, patient 1 piroxicam (pirox.), patient 2 diclofenac,
sulfasalazine (SSZ), prednisone (pred.), patient 3 naproxen (naprox.),
methotrexate (MTX), pred., patient 4 pirox., SSZ, pred.; at 1 year,
patient 1 SSZ, patient 2 MTX, pred., patient 3 naprox., SSZ, MTX,
pred., patient 4 pirox., MTX, pred.; at 6 years, patient 1 ibuprofen,
SSZ, patient 2 MTX, patient 3 naprox., SSZ, MTX, azathioprine,
patient 4 MTX, pred., cyclosporine. NSAIDs ⫽ nonsteroidal antiinflammatory drugs; DMARDs ⫽ disease-modifying antirheumatic
drugs.
surgical placement of pins across the carpus (2 patients) or a
pacemaker in situ (1 patient). At surgery, 2 of these patients
were found to have tendon rupture and their data are included
in the analysis. Demographic information and disease activity
measures for the total group at baseline and at 1, 2, and 6 years
have been published (11). At 6 years, 65% of the cohort was
female with a mean age of 46 years. The median (range) for
the DAS at 0 and 6 years were 4.2 (1.3–7.6) and 2.7 (0.9–4.6).
Table 1 gives details of antirheumatic medication for the group
as a whole and for those in whom tendon rupture occurred.
MRI scans. An MRI scan of the dominant wrist was
obtained using a 1.5T MRI scanner (General Electric Signa,
Milwaukee, WI) with a dedicated wrist coil (Medical Devices,
Waukesha, WI). The hand was placed in the wrist coil where it
fitted snugly at the patient’s side with the palm facing the body,
thumb anteriorly. The field of view was 8 cm and included the
distal radioulnar, radiocarpal, and midcarpal joints as well as
the metacarpal bases. The small field of view was chosen to
optimize resolution and did not include metacarpophalangeal
joints. Coronal and axial T1 sequences were performed, followed by axial fat-suppressed fast spin-echo T2, then coronal
fat-suppressed T1 sequences after injection of gadolinium
diethylenetriaminepentaacetic acid (Gd-DTPA; Nicomed Omniscan, Amersham Health, Lindesnes, Norway), which acts as
a contrast agent. An axial fat-suppressed T1 post–Gd-DTPA
sequence was also included at 6 years. Slice thickness of 3 mm
was used throughout.
Scoring MRI scans. The system used to score MRI
scans has been previously described (9). Briefly, 9 tendon
groups were scored including extensor pollicis brevis and
abductor pollicis, extensor carpi radialis (ECR), extensor
pollicis longus (EPL), extensor digitorum and indicis (ED),
extensor digiti minimi, extensor carpi ulnaris (ECU), flexor
carpi radialis (FCR), flexor digitorum superficialis and profundus, and flexor carpi ulnaris. They were evaluated on axial
scans using T1-weighted and T2-weighted sequences. A score
of 0 (if absent) or 1 (if present) was given for inflammation in
the tendon sheath (increased bright signal around the tendon
746
McQUEEN ET AL
on T2-weighted images and ⬎1 mm thickness of sheath on 2
consecutive slices). Inflammation within the tendon itself was
also scored (0 ⫽ normal signal, 1 ⫽ increased signal on
T1-weighted and/or T2-weighted sequences). Tendon size was
scored as 0 (normal), 1 (thickened), or 2 (attenuated). The
definition of “normal” tendon size was determined by the
individual radiologists on the basis of their specialist experience. Scores were added for a total tendon/tendon sheath
score for the carpus (maximum possible score ⫽ 36).
Seven individual sites within the carpus were assessed
for synovitis: the distal radioulnar joint, radiocarpal joint
(ulnar aspect), radiocarpal joint (radial aspect), intercarpal
joint (between the proximal and the distal carpal row), carpometacarpal joints (second through fifth assessed together), first
carpometacarpal joint, and the pisotriquetral joint. Synovitis
was scored according to synovial thickening and postgadolinium enhancement. Erosions were defined as focal areas of
loss of low signal cortex, with sharply defined margins, identified on both T1-weighted and T2-weighted sequences in 2
planes, with a cortical break seen in at least 1 plane. Erosions
were scored at 15 sites according to number and size and
summed for a total carpal score (maximum possible score ⫽
90). Bone marrow edema was identified as poorly defined
regions of low signal within bone on T1-weighted images with
high signal on fat-suppressed T2-weighted images and was
scored at the same sites (maximum possible carpal score ⫽ 30).
MRI scans were scored independently by 2 experienced musculoskeletal radiologists (NS and JC) who were blinded to
clinical data. Their mean scores were used for data analysis.
Statistical analysis. Spearman’s correlation was used
to test for associations between tendinitis, other MRI scores,
and clinical measures. Mann-Whitney U tests were used to
investigate whether tendon scores differed between rupture
and nonrupture groups. Linear and exact logistic regressions
were used to determine predictors of tendinitis at 6 years and
rupture at 6 years, respectively. Generalized linear mixed
models, which allow for the correlations between data from the
same patients, were used to investigate changes over time in
tendinitis scores. Site-specific analysis was performed to determine whether tendon involvement was associated for each
case, first with synovitis in a neighboring joint and second with
erosion at an adjacent bone. For example, in the case of the
EPL tendon, relevant joints were the radiocarpal joint (radial
aspect) and first carpometacarpal joint, and adjacent bones
were the radial head, scaphoid, and trapezium (data available
on request).
RESULTS
Interobserver reliability for scoring tendinopathy. Interobserver reliability for tendinopathy scoring
was high with intraclass correlation coefficients (ICCs)
of 0.77 (95% confidence interval [95% CI] 0.60–0.87) at
baseline, 0.73 (95% CI 0.54–0.84) at 1 year, and 0.85
(95% CI 0.71–0.92) at 6 years. Reliability data for
erosion and synovitis scoring have been published elsewhere (11).
Figure 1. Box plots of the mean observer score for magnetic resonance imaging tendinopathy at baseline and at 1 and 6 years. Each box
represents the 25th to 75th percentiles. Lines outside the boxes
represent the 10th and 90th percentiles. Lines inside the boxes
represent the median. Circles indicate outliers and ⴱ indicates an
extreme data point.
Progression of tendinopathy over 6 years. The
total MRI tendon score comprised 3 measures; tendon
signal change, tendon size, and tendon sheath signal
change. The profile of tendon scores within the patient
group was examined at baseline and at 1 and 6 years
(Figure 1). Thirty-four patients (81%) had MRI evidence of tendinopathy at baseline, compared with 59%
at 1 year and 68% at 6 years. There was an indication
that the median MRI tendinitis score increased over the
3 time points (P ⫽ 0.08), and by 6 years there was a
greater spread of scores with 3 patients having very high
scores, indicating severe involvement.
Most common sites of tendon involvement. The
ECU tendon was most frequently involved at baseline
and at 1 and 6 years. At all time points, the highest
scores were obtained for the ECU tendon. In order of
decreasing total score, the following tendons were affected: at baseline ECU, FCR, ECR, at 1 year ECU,
FCR, ED, and at 6 years ECU, ED, and ECR.
Correlations between MRI tendinopathy scores
and clinical measures. Correlations between MRI tendinopathy scores and clinical measures were investigated
at baseline and at 1 and 6 years (Table 2). At baseline,
the total tendon score correlated with the swollen joint
PREDICTING TENDON RUPTURE THROUGH MRI EVIDENCE
747
Table 2. Correlations of magnetic resonance imaging (MRI) tendon scores with clinical measures and
other MRI scores*
Correlation, r (P)
Baseline
Clinical measures
CRP level
ESR
Pain score
Ritchie articular index
Swollen joint count
DAS
HAQ score
Other MRI scores
Synovitis
Bone edema
Bone erosion
1 year
6 years
0.190 (0.2)
0.272 (0.08)
0.047 (0.7)
0.121 (0.4)
0.386 (0.01)
0.334 (0.03)
⫺0.149 (0.3)
0.501 (0.001)
0.313 (0.05)
0.274 (0.08)
0.225 (0.1)
0.352 (0.02)
0.387 (0.01)
0.219 (0.1)
0.148 (0.4)
0.372 (0.03)
0.401 (0.02)
0.369 (0.04)
0.459 (0.009)
0.458 (0.009)
0.344 (0.05)
0.368 (0.01)
0.224 (0.1)
0.308 (0.04)
0.450 (0.003)
0.138 (0.3)
0.349 (0.02)
0.114 (0.5)
0.113 (0.5)
0.118 (0.5)
* CRP ⫽ C-reactive protein; ESR ⫽ erythrocyte sedimentation rate; DAS ⫽ Disease Activity Score;
HAQ ⫽ Health Assessment Questionnaire.
count and DAS (r ⫽ 0.39, P ⫽ 0.01 and r ⫽ 0.33, P ⫽
0.03, respectively). At 1 year, these associations remained significant and additional clinical factors were
also associated, including the CRP level and ESR (r ⫽
0.50, P ⫽ 0.001 and r ⫽ 0.31, P ⫽ 0.05, respectively). By
6 years, all scores correlated with MRI tendinopathy
scores except the CRP level. The strongest correlations
were with the DAS and swollen joint count (r ⫽ 0.46,
P ⫽ 0.009 for both).
Correlations between tendinopathy scores and
synovitis and erosion scores. Correlations between tendinitis and other available MRI scores at each time point
are shown in Table 2. Interestingly, the associations with
synovitis and erosion scores were similar at baseline and
1 year but were no longer apparent at 6 years. The bone
edema score did not correlate with tendinopathy at any
time.
Synovitis and erosion adjacent to tendinitis. Sitespecific analysis was undertaken to investigate for any
relationship between tendinitis and synovitis in the tissues adjacent to each of the 9 carpal tendon groups
scored on MRI. At baseline, there were a total of 71 of
378 “sites” (tendon groups) in the cohort with a positive
tendinitis score, compared with 48 of 369 sites at 1 year
and 60 of 306 sites at 6 years. At baseline, 97% of
affected tendons were adjacent to inflamed joints, while
1- and 6-year images showed a slightly lower percentage
(91%). A similar analysis was performed investigating
Figure 2. Scatterplots showing relationship of 6-year magnetic resonance imaging tendinitis scores to baseline scores (A) and 1-year scores (B).
748
whether there were erosions near involved tendons. At
baseline, 37 of the 71 tendinitis sites (52%) had positive
erosion scores at adjacent carpal bones. By 6 years, this
number had increased to 92%, and in only 6 sites (8.3%)
were there no erosions present in adjacent bones.
Early MRI tendinitis scores are predictive of
6-year scores. Linear regression was used to measure the
ability of the baseline and 1-year MRI tendinitis scores
to predict the 6-year score. Baseline scores were moderately predictive of tendinitis (R2 ⫽ 0.12, P ⫽ 0.05 [␤ ⫽
0.69, SE ⫽ 0.34]), but less so than 1-year scores, which
were highly predictive of 6-year tendinitis (R2 ⫽ 0.36,
P ⫽ 0.0003 [␤ ⫽ 1.28, SE ⫽ 0.31]) (Figure 2).
Tendon rupture in patients with high tendinitis
scores. At 6 years, full-thickness tendon rupture at the
ECU was diagnosed from wrist MRI scans in 2 patients
(1 man and 1 woman, ages 36 and 59 years, respectively,
at baseline). Rupture of extensor tendons to the index
and little fingers was also diagnosed in 1 male patient
(age 54 at baseline) on surgical exploration of the wrist
prior to fusion at 5 years. Another female patient (age 42
years at baseline) needed wrist surgery 1 year after
enrollment and was found to have a ruptured EPL.
Neither of these patients was able to have MRI scanning
performed at 6 years, due to metal pins at the carpus.
Figure 3 shows the baseline and 1-year scans from 1 of
the tendon rupture patients, revealing early tenosynovitis followed by swelling and partial rupture of the tendon
at 1 year, probably associated with invasion by pannus.
Scans at 6 years did not reveal the ECU tendon at all,
and it was assumed to have ruptured. The median
tendon score in the rupture group was higher than that
in the nonrupture group at baseline (2.8 versus 1.0; P ⫽
0.04) and 1 year (4.3 versus 0.8; P ⫽ 0.03). Exact
conditional logistic regression analysis revealed that
both baseline and 1-year MRI tendinitis scores were
predictors of tendon rupture by 6 years (odds ratio [OR]
1.52, 95% CI 1.02–2.32, P ⫽ 0.03 and OR 1.57, 95% CI
1.03–2.04, P ⫽ 0.02, respectively).
Patients with tendon rupture had higher DAS
and HAQ scores than those without rupture. The DAS
in the tendon rupture group was higher than in the
nonrupture group only at the 1-year examinations (3.59
versus 2.32; P ⫽ 0.04), but the HAQ score was higher in
the tendon rupture group at all 3 time points (1.33 versus
0.54 [P ⫽ 0.02], 1.18 versus 0.25 [P ⫽ 0.03], and 0.98
versus 0.37 [P ⫽ 0.01] at baseline, 1 year, and 6 years,
respectively). Medical management of tendon rupture
was relatively aggressive (but did not include anti–tumor
necrosis factor ␣ [anti-TNF␣] therapy) and is detailed in
Table 1.
McQUEEN ET AL
DISCUSSION
This is the first prospective MRI study to investigate the progression of tendinopathy at the wrist in
RA. Tendon rupture is a serious complication of RA
with an estimated incidence of 1 in 100 patients (14). It
occurs more frequently in those with aggressive disease
(15), who may have been overrepresented in our group
(fulfilled American College of Rheumatology [formerly,
the American Rheumatism Association] criteria for RA
at presentation) (16), and is frequently insidious in onset
and painless (15). Rubens et al clinically identified
extensor tendon rupture in only half of their patients
who had tendon rupture as confirmed by surgical inspection, whereas tendon rupture was identified by MRI
scanning in 9 of 10 (3). Thus, MRI evaluation of
tendinopathy may be superior to clinical examination,
and could be useful in planning management of disease.
In our study, those with tendon rupture had higher MRI
tendinopathy scores at baseline and 1 year than the
nonrupture group, and higher HAQ scores at baseline, 1
year, and 6 years. However, specific tendon changes
prior to rupture were variable, and included examples of
florid tenosynovitis, tendon enlargement, and signal
change as well as tendon attenuation.
We developed a scoring system for quantifying
MRI findings of soft tissue and bony pathology in 1996,
and we have applied this score to this cohort consistently
over a 6-year period (9). Our system was developed
before the Outcome Measures in Rheumatology Clinical
Trials (OMERACT) RA-MRI scoring system (RAMRIS) was published (17). The 2 scores are very similar,
but in our system erosions were scored by number and
size, rather than percent of involved bone as in RAMRIS. A score for tendinopathy was omitted from the
RAMRIS because of concerns about feasibility (18), but
we have shown that in the hands of experienced radiologists, scoring reliability was high (ICCs ranging from
0.73 to 0.85 at 3 time points). Whether a 3-point scale is
sufficiently sensitive to describe the range of severity of
tendinopathy in RA has not been determined, and
others may develop the system further. Ostendorf et al
recently described their own tendinopathy scoring system as an add-on to the OMERACT score when describing pathology at the metatarsophalangeal joints in
patients with very early RA (8). MRI features of tenosynovitis have also been described in other conditions
including spondylarthropathies (19) and systemic lupus
erythematosus (20). An interesting point of difference
between lupus-associated Jaccoud’s arthropathy and RA
is that the flexor tendons are more often involved in the
PREDICTING TENDON RUPTURE THROUGH MRI EVIDENCE
749
Figure 3. A, Baseline axial T1-weighted magnetic resonance imaging scan of the wrist, showing thickening of the extensor carpi ulnaris (ECU) tendon
sheath (arrow). B, Increased signal on the equivalent T2-weighted image (arrow). C, Axial T1-weighted scan at 1 year, showing extensive tenosynovitis
within the ECU tendon sheath (thick arrow) and a partial tear within the substance of the ECU tendon with likely pannus invasion (thin arrow). D,
T2-weighted image corresponding to C, confirming the extensive ECU tenosynovitis (thick arrow) and the partial ECU tear with likely pannus invasion
(thin arrow).
750
former condition, as opposed to extensor tendons in the
latter (20).
Although we did not investigate healthy subjects
in this study, MRI scans from normal subjects have been
studied by others (3,10). Small amounts of fluid in 1 or
more dorsal wrist compartments have been described,
with rare examples of increased signal intensity within
the substance of tendons, but pannus has not been
identified. Thus, it is possible that some of the lowpositive tendon scores from our cohort could have
occurred without significant tendinopathy. However, the
major conclusions of this study have been drawn from
patients with high tendinopathy scores, which are most
unlikely to occur in the absence of true tendon involvement.
Tendonitis was frequently found adjacent to regions of synovitis at the wrist, especially within the first
year of disease. This is consistent with an immunopathologic picture of early RA, in which inflammatory change
within the tenosynovium mirrors that of the synovial
membrane, as shown by Jain et al (4). In our cohort,
erosions were identified adjacent to tendinitis/
tenosynovitis in only half of patients at baseline, but in
92% at 6 years. Friction of tendons against sharp, eroded
bony margins could promote inflammatory change and
eventually lead to tendon attrition and rupture. However, in many instances the erosions, although involving
adjacent bones, were not directly under the path of the
tendons in question, and a causal relationship between
erosion and tendon rupture could not be established
with certainty.
Swen et al compared MRI with the gold standard
of surgical inspection for the diagnosis of partial tears of
the finger extensor tendons in RA (14). They found MRI
to have high specificity for partial tears (0.83), but low
sensitivity and positive predictive value. It is difficult to
compare our study with theirs, as our MRI imaging
protocol was different, using a more powerful 1.5T
scanner and the addition of postcontrast T1-weighted
coronal and axial sequences to T2-weighted axial sequences for better resolution of tendon pathology. Our
MRI assessment of tendinopathy also differed, in that it
was graded on a continuous scale. Higher grades would
have included partial tears, but these were not specifically documented. However, complete tears, which were
more easily verifiable, were recorded and used as an end
point for our analysis.
In conclusion, MRI appears to be a useful imaging modality in the evaluation of tendon pathology at the
wrist in patients with RA. Our data suggest that while
tenosynovitis parallels synovitis in early disease, other
McQUEEN ET AL
factors, including bone erosion, may contribute to tendon attrition and rupture in more advanced RA. If MRI
evidence of high-grade tendinopathy is identified in
patients within a year of presentation, they are likely to
have ongoing tendon disease, which in some cases may
result in tendon rupture. Prophylactic surgical intervention might be planned for these patients, or local steroid
injections to the dorsal sheath (21,22) may be useful in
controlling tenosynovitis. TNF␣ inhibitors can reduce
collagenase concentrations in tenosynovial tissue (23),
and could also play a role in the early treatment of these
at-risk patients. Further prospective studies are required
to explore these possibilities and clarify the clinical
relevance of these MRI findings.
ACKNOWLEDGMENTS
The authors wish to acknowledge the assistance of the
Auckland rheumatologists who referred patients for this study.
We are also most grateful to the technical staff at the Auckland
Radiology Group (in particular Ms Rika Nel), who supervised
the performance of the MRI scans.
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