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High-resolution magnetic resonance imaging for the assessment of hand osteoarthritis.

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ARTHRITIS & RHEUMATISM
Vol. 52, No. 8, August 2005, pp 2355–2365
DOI 10.1002/art.21210
© 2005, American College of Rheumatology
High-Resolution Magnetic Resonance Imaging for the
Assessment of Hand Osteoarthritis
Ai Lyn Tan,1 Andrew J. Grainger,1 Steven F. Tanner,1 David M. Shelley,1 Colin Pease,1
Paul Emery,1 and Dennis McGonagle2
Objective. To investigate the use of a novel surface
coil for clinically utilized magnetic resonance imaging
(MRI) scanners, in order to describe the microanatomic
basis for hand osteoarthritis (OA) at all stages of
disease.
Methods. MRI of proximal or distal interphalangeal joints was performed in 58 subjects: 16 patients
with early OA (symptom duration <12 months), 14
patients with chronic OA, 10 patients with clinically
normal asymptomatic joints adjacent to arthritic joints,
and 18 normal controls. High-resolution images were
obtained with displayed pixel dimensions of 80–100 ␮m
using a 1.5T scanner and a 23-mm–diameter surface
coil. All joint structures were evaluated.
Results. The high-resolution images of every joint
structure showed comparable abnormalities in both
early and chronic OA, including cartilage loss, bone
edema, synovial enhancement, osteophytosis, and erosions. Heberden’s and Bouchard’s node formation occurred at regions where soft tissue bulged through the
capsule between the dorsal tendons and collateral ligaments (CLs). Prominent CL thickening or disruption
(100% of OA patients) was evident even in joints where
cartilage was partially preserved. Clinically normal
joints adjacent to OA hand joints showed thickening
and enhancement of CLs which was the most common
abnormality seen (80% of OA patients). Older normal
subjects showed subtle changes within the CLs.
Conclusion. Obtaining high-resolution MR images from clinically utilized scanners represents a novel
way for exploring the microanatomic basis of hand
arthritis and may have considerable potential in the
clinical setting. In the present evaluation in nodal OA,
previously unappreciated CL abnormalities were especially common.
The hand is commonly involved in both inflammatory arthritis and osteoarthritis (OA), but the microanatomic basis for hand disease damage and localization
is unclear. While synovitis is the primary abnormality
in rheumatoid arthritis (RA), and enthesitis/osteitis and
synovitis are central to the pathogenesis of spondylarthropathy (SpA), the microanatomic basis for hand
OA, especially at the earliest stages of disease, is less
apparent.
Osteoarthritis has been viewed primarily in relation to cartilage loss, but the importance of bone abnormalities and joint inflammation in OA has also been well
documented (1,2), as has the need to consider the whole
joint organ in disease pathogenesis (3). Conventional
magnetic resonance imaging (MRI) has been used to
explore the anatomic sites of abnormality in large joint
OA, and has enhanced our understanding of disease
mechanisms in the knee and hip, where both subchondral bone edema and synovitis are associated with pain,
and bone edema itself is associated with progressive
disease (4–6).
Knee OA may be difficult to recognize at clinical
presentation and patients with knee pain but normal
radiographic findings would not normally be referred to
a rheumatologist. The clinical pattern of the early stages
of distal interphalangeal joint (DIP) and proximal interphalangeal joint (PIP) involvement in OA is often
diagnostic, and does not rely on radiographic criteria,
Supported by the Medical Research Council, UK and the
Arthritis Research Campaign, UK.
1
Ai Lyn Tan, MRCP, Andrew J. Grainger, MRCP, FRCR,
Steven F. Tanner, PhD, David M. Shelley, BSc, Colin Pease, FRCP,
Paul Emery, MA, MD, FRCP: Leeds General Infirmary, Leeds, UK;
2
Dennis McGonagle, PhD, FRCPI: Leeds General Infirmary, Leeds,
and Calderdale Royal Hospital, Halifax, UK.
Address correspondence and reprint requests to Dennis
McGonagle, PhD, FRCPI, Academic Unit of Musculoskeletal Disease,
2nd Floor, Chapel Allerton Hospital, Chapeltown Road, Leeds LS7
4SA, UK. E-mail: d.g.mcgonagle@leeds.ac.uk.
Submitted for publication February 7, 2005; accepted in
revised form May 3, 2005.
2355
2356
TAN ET AL
which are of limited use in diagnosis of early hand
disease and disease at other sites prone to OA, including
the knee (7,8). Furthermore, patients with hand OA are
more likely to present to the early arthritis clinic than
are those with early knee symptoms; hence, there is the
potential to recognize and evaluate OA soon after
symptom onset. The spatial resolution limitation of
currently available MRI has precluded detailed highresolution imaging assessment of hand OA. However,
previous small pilot studies using custom-built highresolution MRI equipment showed that MRI was a valid
method for the assessment of small joint structures,
including the bone trabeculae, cartilage, ligaments, and
tendons (9,10). Dedicated high-resolution MRI scanners
have also been developed for animal research, where
they show considerable potential in the evaluation of
therapy for joint inflammation (11).
An anatomic understanding of the earliest stages
of hand OA may have important implications for elucidating its pathogenesis, and high-resolution MRI represents a potentially useful way for such a detailed assessment. This study optimized recently developed highresolution MRI coils, that can be fitted to existing
commercially available scanners routinely used in the
clinical setting, to explore the microanatomic basis for
hand OA.
PATIENTS AND METHODS
Patients. Fifty-eight subjects provided informed consent and participated in the study. The study was approved by
the local ethics committee at the Leeds Teaching Hospitals
National Health Service Trust. In total, images from 40
patients with hand OA and 18 normal control subjects were
scanned. All subjects were invited to participate in the study
either from rheumatology outpatient clinics or via leaflets and
posters about the study distributed in the clinics. Either a DIP
or a PIP joint was scanned. Sixteen female patients with a
mean age of 56 years (range 49–69 years) had early OA (8 DIP
joints, 8 PIP joints) defined by disease duration of ⱕ12 months
(mean 8 months). The disease duration was determined from
the onset of symptoms (pain, swelling, or tenderness) in any of
the finger joints with clinical OA. Fourteen patients (11
women, 3 men) with a mean age of 60 years (range 51–68
years) and OA symptoms termed chronic (duration ⬎12
months [mean 75 months]) were also imaged (9 DIP joints, 5
PIP joints). Findings on radiography of the hands can appear
normal at clinical presentation of OA, and therefore, radiographic depiction of OA was not mandatory for the diagnosis
of OA in this study. The patients with OA were diagnosed on
clinical grounds with DIP or PIP joint soft tissue swelling or
bony thickening and the absence of other arthropathies, including RA, psoriatic arthritis, and gout, or any traumatic
injury to the joint selected for imaging.
Ten patients (8 women, 2 men; mean age of 60 years
[range 46–72 years]) with hand OA (mean disease duration
120 months; 5 DIP joints, 5 PIP joints) and at least 1 clinically
normal joint were randomly selected from the OA cohort, for
MRI of the clinically normal joint that had never been
symptomatic. This group may represent the earliest stages of
OA, since disease tends to progress to affect the uninvolved
finger joints over time (7). This group of patients are henceforth referred to as the “latent OA” group.
Eighteen healthy volunteers who had no known OA
with asymptomatic finger joints also had 1 finger joint scanned
(10 DIP joints, 8 PIP joints). The healthy volunteer group was
divided into those ⱕ40 years old (mean 34 years [range 30–37
years]; 4 women, 4 men) and those ⬎40 years old (mean 55
years [range 42–72 years]; 5 women, 5 men). This group was
divided at age 40 years arbitrarily because clinical hand OA
usually presents at ⬃50 years of age.
MRI data acquisition. MR images were acquired using
a 1.5T Gyroscan ACS-NT scanner (Philips, Best, The Netherlands). Subjects were placed in the prone position with the
hand extended in front of the body. The surface coil was placed
on top of the relevant joint and held in place using sandbags.
The DIP and PIP joints are small in relation to most other
joints that are routinely studied using MRI. Examination of
these joints therefore required methods that measured the MR
data at adequate resolution to distinguish the relevant joint
features. In previous investigations this was achieved by studying fingers from cadavers, with long imaging times and/or use
of specialized imaging coils to obtain the required signal-tonoise levels (9,10,12,13). In the present study, a Philips 23mm–diameter surface “microscopy” coil was used to acquire
adequate signal levels from the small voxels required for
high-resolution study of the DIP and PIP joints.
The examination protocol was designed to visualize the
different joint structures. This protocol included the acquisition of T1-weighted axial and coronal spin-echo (SE) images
for the assessment of the anatomy of most of the structures,
T2-weighted fat-suppressed SE images to identify areas of
edema and fluid in the joint space and cystic lesions, and
proton-density–weighted 2-dimensional SE images to study the
collateral ligaments (CLs). In addition, 3-dimensional
gradient-echo sagittal images were acquired using a waterselective radiofrequency excitation pulse to assess the cartilage
and tendons. After intravenous injection of 10 ml of the
contrast agent gadolinium diethylene tetrapentaacetic acid
(Gd-DTPA), axial and coronal T1-weighted fat-suppressed SE
images were also obtained, highlighting areas of inflammation
in the soft tissue and bone. The imaging sequences employed
a field of view of either 40 or 45 mm and a data acquisition
matrix of 256 ⫻ 204 with 512 ⫻ 512 Fourier transformed data
points. The measured slices were 1 mm thick, and the acquired
in-plane pixel dimension was therefore 160–200 ␮m with a
displayed pixel dimension of 80–100 ␮m. The T1-weighted
measurements were made with repetition time (TR) and echo
time (TE) values of 475 msec and 18 msec, respectively, and 2
signal averages, while T2-weighted images were acquired using
a turbo spin-echo (TSE) sequence and 3 signal averages with a
TR value of at least 3,500 msec and a TE of 100 msec. The
proton-density–weighted data were obtained using a TSE
sequence with centric data acquisition, 2 signal averages, and
TR/TE values of 2,000 msec/15 msec. A flip angle of 45° and
HIGH-RESOLUTION MRI OF HAND OA
2357
Figure 1. a and b, Percentage of subjects with abnormalities in soft tissue structures (a) and bone (b) in the groups studied. Although virtually every
joint structure was affected in both chronic and early osteoarthritis (OA), the abnormalities observed in early OA tended to be relatively milder. The
joints scanned in the “latent OA” group were asymptomatic with no history of pain or swelling, as were the joints of the “normal” group, but
abnormalities were more frequent in the latent OA group, particularly abnormalities in the collateral ligaments and the extensor tendons, and
osteophyte formations. Additionally, cartilage abnormalities were less frequent than ligamentous or tendon abnormalities in the latent OA group.
This demonstrates that in OA, every joint structure is affected, consistent with the idea that OA is ultimately a failure of the joint. ⴱ ⫽ P ⬍ 0.05,
ⴱⴱ ⫽ P ⬍ 0.001, compared with the normal group. c, Percentage of subjects in the latent OA group, normal ⱕ40 years old group, and normal ⬎40
years old group with abnormalities in the various structures. The younger normal group had virtually no abnormality detected in the joints, but subtle
abnormality of the ligaments, the extensor tendon, and bone edema were observed in the normal ⬎40 years old group. † ⫽ P ⬍ 0.05 compared with
the normal ⱕ40 years old group.
TR/TE values of 3,000 msec/12 msec were used to obtain the
gradient-echo images. The total examination time was ⬃50
minutes.
MRI analysis. MR images were read at a workstation
(Philips Easy Vision) by 2 readers, including an experienced
musculoskeletal radiologist. All groups (early OA, chronic OA,
latent OA, and normal control) were analyzed in a random
order. The observers were blinded to the clinical status and the
category of the subjects. The scoring was performed by consensus between the 2 readers. The features of the following
anatomic structures were described and evaluated in a dichotomous manner: cartilage, bone cortex, CL, extensor expansion,
bone edema, cysts, erosions, osteophytes/nodes (Heberden’s or
Bouchard’s), joint fluid, and capsule/synovium. Where determination of the location of the abnormality (such as bone
edema, cysts, erosions, or osteophytes) was possible, this was
also recorded.
MRI-determined joint erosions were recorded when a
cortical break was evident on T1-weighted images on both
coronal and axial images. In contrast, a well-circumscribed
area of trabecular absence within the bone was termed a cyst.
Osteophytes at either ligament origins or insertions or at
tendon insertions were termed enthesophytes.
Regions of synovitis or capsulitis were defined on
images acquired after the injection of the contrast agent. The
T2-weighted fat-suppressed SE images were used to identify
bone marrow edema–like lesions, henceforth referred to as
bone edema, and the images were compared with the Gd-DTPA–
enhanced images to distinguish between bone edema (showing
enhancement) and cysts filled with fluid (nonenhancing).
Statistical analysis. Fisher’s exact test was used to
compare the proportion of abnormalities between the groups.
Because this was a pilot study, no correction for multiple
testing was performed, and the results of significance tests are
presented as a guideline only. All analyses were performed
with SPSS version 11.0 (Chicago, IL).
2358
TAN ET AL
Figure 2. Sagittal gradient-echo water-selective excitation imaging. a, The articular cartilage (arrows) in the proximal interphalangeal (PIP) joint
and the normal extensor tendon (arrowhead) of a normal subject. b, The PIP joint of a patient with severe chronic osteoarthritis, demonstrating
complete loss of the articular cartilage. Note the thickening and high signal change in the extensor tendon close to its insertion (arrow). Note also
the high signal in the bone marrow representing edema at the tendon enthesis site (arrowhead) and the large dorsal osteophyte (ⴱ). c, A commonly
seen pattern of cartilage loss predominantly affecting the volar aspect articular surfaces, with more dorsal cartilage preservation. Severe soft tissue
swelling around the dorsum of the joint is also present along with prominent dorsal osteophytes (arrowheads). V ⫽ volar aspect of joint.
RESULTS
Early and chronic OA. All MR studies were
satisfactory, with no subject having to be excluded on the
basis of technical failure. Virtually every joint structure
evaluated showed abnormalities in all patients with
either early or chronic OA, reflecting the known fact
that OA is a whole organ disease and ultimately a
disease of joint failure (Figure 1). The findings in early
and chronic OA are compared before presenting the
features of latent OA and the normal group.
Articular cartilage. On coronal and sagittal imaging, generalized full-thickness loss of articular cartilage
was evident in 4 of the 30 subjects, occurring in both the
early (3 of 16) and chronic OA (1 of 14) groups,
indicating marked cartilage loss at clinical presentation.
A further 5 subjects had generalized full-thickness loss
visible only on the coronal plane (2 with early OA and 3
with chronic OA). In the remaining 21 subjects in whom
cartilage loss was incomplete and variable, an ulnar
predilection for cartilage loss was observed, with 10 of 21
patients (48%) experiencing ulnar loss, as compared
with 5 of 21 (24%) experiencing radial loss and 6 of 21
(29%) patients experiencing symmetric but not fullthickness loss. On sagittal imaging, cartilage loss was
most pronounced on the volar joint surfaces (Figure 2).
MRI-determined subchondral bone sclerosis,
seen as low signal change in the subchondral bone on all
sequences, was evident on the distal side of the PIP and
DIP joints in 9 of 16 patients with early OA (56%) and
in 13 of 14 with chronic OA (93%) (P ⫽ 0.04). The
trabecular architecture appeared normal and discrete
breaks in the subchondral bone, suggestive of microfractures, could not be identified with the imaging resolution
obtained in this study.
Collateral ligaments. Ligament abnormalities
were universal in both chronic and early disease.
Changes seen ranged from thickening and increased
signal within the ligament to complete disruption (Figure 3), with Gd-DTPA enhancement evident in the
abnormal ligaments (Figure 4). Complete disruption of
both CLs was evident in 16 of 30 patients (9 of 16 with
early OA and 7 of 14 with chronic OA). While ligament
disruption was common in the ligament midsubstance,
increased signal was evident throughout the abnormal
HIGH-RESOLUTION MRI OF HAND OA
2359
Figure 3. Coronal proton-density–weighted images showing the collateral ligaments. a, The proximal interphalangeal (PIP) joint in a 37-year-old
normal volunteer. The collateral ligaments are seen as thin low-signal bands identified at either side of the joint (arrowheads). b, An asymptomatic
distal interphalangeal (DIP) joint in a patient with clinical and symptomatic osteoarthritis (OA) in adjacent joints. There is subtle collateral ligament
thickening with increased signal within the ligaments (arrows). This was the sole abnormality. c, Involved DIP joint in a patient with early OA. There
is thickening and some increase in signal in the collateral ligaments on both sides of the joint (arrowheads). The changes are seen centered close
to the proximal ligament enthesis sites. An erosion is also seen close to the proximal origin of the radial collateral ligament (arrow). d, The PIP joint
of a patient with severe chronic OA. The ligaments show severe disruption particularly on the radial side (arrowhead), and there is associated ulnar
deviation of the intermediate phalanx.
2360
TAN ET AL
Figure 4. a, Coronal gadolinium-enhanced T1-weighted image with fat suppression, showing the distal interphalangeal (DIP) joint of a normal
subject. No enhancement of either the ligaments (arrowheads) or the adjacent structures is shown. This is in contrast to the findings in b, in which
florid enhancement and thickening is seen within the ligaments and surrounding soft tissues (arrows) in a patient with severe chronic osteoarthritis.
c, Clinically normal and asymptomatic DIP joint adjacent to an osteoarthritic joint. There is subtle enhancement and mild thickening in the ligaments
of this joint (arrows), which otherwise appeared normal.
ligaments, being seen at their origin, midregion, and
insertions. This increased signal was seen on both T1and T2-weighted imaging and would be consistent with
myxoid degeneration of the ligament, such as that seen
in other ligamentous and tendinous structures. Edema
was seen in the adjacent extracapsular tissues.
In 14 of 30 patients in whom complete CL
disruption was not a feature, the CLs were abnormal,
appearing thickened or with an indistinct appearance,
particularly at the proximal attachment. Furthermore, 6
of 14 patients showed Gd-DTPA enhancement of both
CLs, with only 1 of the CLs enhanced in 5 of 14. Three
patients with chronic OA had no enhancement in the
abnormally thickened CLs. In general, all patients with
early and chronic OA had some degree of ligament
abnormality, and all those with early OA showed GdDTPA enhancement (16 of 16), whereas 11 of 14 with
chronic OA had signs of enhancement (P ⫽ 0.09).
When the pattern of ligament abnormality was
compared with the articular cartilage damage in the
joint, it was noted that among the 21 of 30 subjects who
had cartilage that was partially preserved, 10 of 21
subjects had complete bilateral CL destruction, indicat-
ing end-stage ligament disease despite reasonable cartilage preservation. Two of the 4 subjects with complete
cartilage loss had complete bilateral ligament disruption.
Along with the ligament disruption, joint subluxation
was seen in 14 of 30 patients with OA. When present,
subluxation was more commonly seen toward the ulnar
side (varus subluxation); 11 of 14 patients (79%) had
ulnar subluxation, compared with 3 of 14 (21%) with
radial subluxation (Figure 3d).
Tendons. Thickening of the extensor tendons was
noted close to their enthesis site in almost all of the OA
patients (14 of 16 with early OA, 11 of 14 with chronic
OA) (Figure 2). All affected tendons had signs of enhancement. In the absence of severe cartilage loss (n ⫽ 21), only
16 of 21 subjects had extensor tendon abnormalities,
despite the CLs being universally abnormal.
Bone edema. Four major patterns of bone edema
were noted. The most common pattern was focal subchondral edema in 8 of 16 patients with early OA and 5
of 14 with chronic OA. Most of these subchondral
regions of bone edema (10 lesions in 9 subjects) were on
the proximal side of the joints, directly adjacent to sites
where the CLs exert pressure on the proximal phalanx.
HIGH-RESOLUTION MRI OF HAND OA
2361
Figure 5. Images illustrating how the expression of small joint osteoarthritis (OA) is influenced by the collateral ligaments. a, Perientheseal bone
edema on a T2-weighted fat-suppressed coronal image, appearing as high signal adjacent to the ligament insertion (arrow). b, An erosion seen at
the proximal origin of the radial collateral ligament (ⴱ). Both of the collateral ligaments are abnormally thickened and show high-signal
intrasubstance change. c, The appearance of acute Heberden’s nodes, seen as bulging enhanced soft tissue (arrowheads) on this axial
gadolinium-enhanced T1-weighted image through the distal intermediate phalanx close to the distal interphalangeal joint. The bulging soft tissue
appears to occur at points of “weakness” between the extensor tendon (black arrow) and ligaments (white arrows). d, Osteophyte formation in
chronic OA occurring on the dorsum of the phalanx (arrows) at a site corresponding to that where acute Heberden’s nodes are evident in c.
The second pattern occurred at the CL attachment (14 lesions in 9 patients) (Figure 5a). Bone edema
at the CL entheses was seen in 4 of 16 patients with early
OA and 5 of 14 with chronic OA patients. In these 14
regions of bone edema at the CL entheses, all except 1
were at the CL insertion on the distal phalanges of either
the PIP or DIP joints. Enthesophytes were present in 8
of 14 sites of CL enthesis bone edema. Only 2 of 14 bone
edema lesions at the CL entheses (14%) were related to
bone erosions, while 7 of 10 of the subchondral bone
edema lesions (70%) were associated with bone erosions
(P ⫽ 0.01).
Diffuse edema on both sides of the joint, where
cartilage was lost (representing a “kissing edema” pattern as described for large joints), was seen in 5 of 16
patients with early OA and 4 of 14 with chronic OA.
Lastly, small regions of focal edema present elsewhere
and not related to subchondral bone or enthesis were
2362
TAN ET AL
Figure 6. Coronal T1-weighted (a) and gadolinium-enhanced T1-weighted (b) images through the distal interphalangeal joint of an asymptomatic
normal control subject 64 years of age. The only abnormal finding is thickening of the collateral ligaments, which show increased signal within their
substance on unenhanced T1 imaging (arrows) and intrasubstance enhancement following intravenous gadolinium administration (arrowheads).
seen in 1 of 16 patients with early OA and 1 of 14 with
chronic OA.
Erosions and cysts. Erosions, as defined by bone
cortex disruption in 2 planes, were evident in 11 of 16
patients with early OA (22 erosions) and 7 of 14 with
chronic OA (10 erosions). Two patterns of erosion were
evident. The most common type of erosion occurred
adjacent to the CLs, and was evident in 17 subjects (24
erosions) (Figure 5b). Less common were central joint
erosions, which were evident at sites of cartilage loss
in 6 patients with OA (8 erosions). Bone cysts were
also visible in a smaller proportion of patients, being
present in 3 of 16 patients with early OA and 4 of 14 with
chronic OA.
Osteophytes. The most common site for osteophyte development is at the bone–cartilage interface of
the more proximal phalanx in both PIP and DIP joints,
predominantly on the dorsal proximal side of the joint.
These generally appeared hook-like and pointed proximally (Figure 2c). The sites of osteophytes in chronic
disease also corresponded with the enhancing soft tissue
that was bulging through the joint at areas of least
resistance in early disease (Figures 5c and d). Some
osteophytes were associated with adjacent bone en-
hancement following Gd-DTPA administration; these
tended to occur in the early OA group.
Enthesophytes. New bone formation at ligament
origins or insertions (enthesophytes) was more common
in longer standing OA than in early disease, as evidenced by examples in 3 of 16 of patients with early OA
(19%) (5 enthesophytes), versus examples in 6 of 14
patients with chronic OA (43%) (9 enthesophytes), and
was invariably evident at ligament insertions but not
origins. Furthermore, all of the enthesophytes in the
patients with early OA (5 of 5) showed Gd-DTPA
enhancement in the CLs, while only 4 of 9 enthesophytes
in patients with chronic OA (44%) showed enhancement
(P ⫽ 0.09). Similarly, bone edema adjacent to or within
enthesophytes was more common in the early OA group,
with 4 of 5 cases (80%) in the early OA group, versus 4
of 9 cases (44%) in the chronic OA group (P ⫽ 0.30).
Synovium and joint capsule. Excess joint fluid
visible on the T2-weighted fat-suppressed SE sequence
was evident in the joint space in a majority of the OA
patients (n ⫽ 22 [73%]). Fluid and synovial enhancement was especially common in the dorsal recess of the
joint in OA. In the axial sequences the central extensor
tendon slip and the adjacent lateral bands appear to
HIGH-RESOLUTION MRI OF HAND OA
have been pushed outwards and apart by soft tissue
swelling in the PIP joints, and outward in the DIP joints
(12 of 16 patients with early OA, 12 of 14 with chronic
OA). The bulging of the soft tissue tended to occur
through areas of least resistance at sites of anatomic
weakness in the joint capsule, between the extensor
tendons and CLs, and the flexor tendons and CLs
(Figure 5c).
Asymptomatic joint in an OA-affected hand (latent OA). Although the joints scanned in the group of 10
OA patients were apparently unaffected and completely
asymptomatic, with no history of pain or swelling, and
were clinically normal, these joints showed abnormalities on MRI (Figure 1c). The CLs were the most affected
structure (n ⫽ 7 [70%]), although abnormalities were
often mild with only thickening of the ligament, particularly at the proximal attachment (associated with intrasubstance increased signal and Gd-DTPA enhancement
in all cases) (Figures 3b and 4c). Similarly, the extensor
tendon was also often affected to some degree, with
thickening at the distal attachment (n ⫽ 6 [60%]). Three
of the 7 patients with ligament abnormalities also had
associated bone edema. Four patients with ligament
abnormalities had subtle cartilage loss, 1 of whom also
had a bone erosion at the site of cartilage loss. Small
osteophytes were observed in 5 patients with ligament
abnormalities, located mainly on the dorsal phalanx
proximal to the joint. Cartilage damage without ligament
change was not seen.
Normal subjects. All of the younger control
subjects had completely normal joints including ligaments, cartilage, and bone, with a small region of normal
synovial fluid evident at the articular margins. However,
5 of 10 older control subjects had subtle abnormality of
the CLs, with thickening, and 3 of the 5 had Gd-DTPA
enhancement (Figures 1c and 6). Two subjects also had
small regions of bone edema, with 1 showing edema
adjacent to the abnormal CL. The tendons appeared
uniform, and the insertions did not show changes or
heterogeneity in signal intensity (Figure 2a). No cysts,
erosions, or soft tissue swelling were seen in any of the
normal finger joints. Consistent with reports of occasional osteophytes found on radiographs of older asymptomatic subjects, osteophytes were observed in 2 older
normal subjects in this study with preservation of joint
cartilage.
DISCUSSION
In this study we used a novel high-resolution
MRI coil that can be utilized in clinically available
2363
scanners to investigate the microanatomic basis for hand
OA. Hand OA was chosen for study because its microanatomic basis is less well defined compared with that of
RA and SpA. Consistent with the known features of OA,
every joint structure showed variable abnormalities.
Severe destructive and inflammatory changes, as suggested by Gd-DTPA enhancement, were evident in
every joint structure in early hand OA. Joint collateral
ligament abnormalities were especially common, and
subtle ligament changes were the most common changes
in normal joints adjacent to OA joints.
This study confirmed a number of interesting
observations in relation to hand OA and raised a
number of new issues. For example, subchondral bone
sclerosis was especially common in chronic OA, which
may support the recent assertion that subchondral bone
sclerosis represents secondary remodeling and is not
primarily responsible for cartilage damage as originally
suggested (14). The mechanism of bone edema in OA is
unknown but is considered to be related to bone microfracture or microcracks. The resolution of the images in
this study was not adequate for showing trabecular
microcracks or microfractures, but subchondral edema
without obvious trabecular fracture or damage to regions of adjacent cartilage was evident. Also, unlike
findings in RA, erosions were more commonly seen on
MRI in early OA, supporting the concept of the significant healing and remodeling that is known to occur in
OA as compared with RA. Joint inflammation as determined by Gd-DTPA uptake was common not only in the
synovium in OA but also in most other joint structures,
including ligaments, tendons, extracapsular tissues, and
bone marrow, and was comparable in degree and location in both patients with early disease and those with
painful chronic joint involvement.
The formation of Heberden’s and Bouchard’s
nodes is a characteristic clinical feature of OA. Soft
tissue was observed to bulge through the sites of relative
weakness of the joint capsule at the 4 locations bounded
by the medial and lateral CLs and the flexor and
extensor tendons, especially on the dorsal aspect of the
joint in early OA. In late OA, Heberden’s and Bouchard’s node formation was evident at the same sites,
suggesting that ossification of tissue at these sites was
related to prior inflammation and CL position as previously hypothesized (15), and further suggesting that the
phenotype of hand OA is related to the functional
anatomy of the joint. Longitudinal studies are needed to
confirm this theory.
Perhaps the most interesting result of this study
was the common occurrence of ligament abnormalities.
2364
To the best of our knowledge, there are no previous
studies implicating ligament diseases in hand OA. It is,
however, well recognized that trauma or disruption of
the ligament of large joints is associated with the subsequent development of OA in experimental and clinical
settings. Knee cruciate ligament disruption is associated
with subsequent canine OA (16). In humans, chronic
knee joint ligament instability is associated with OA
development (17–19). Therefore, large joint OA could
be seen as an inevitable consequence of ligament failure
(14). In the case of small joints it has been shown that
the PIP CLs are the primary restraint to varus and valgus
joint angulation (20), and that reconstruction of the
ligaments as opposed to other joint structures has the
greatest benefit in the amelioration of carpometacarpal
joint OA (19). While ligament laxity may be important in
knee OA, the relationship between joint laxity in the
small joints and associated OA remains controversial
(21–23). In this study we also noted that other MRIdetermined joint abnormalities, including erosion, bone
edema, and new bone formation, bore a close anatomic
relationship to the abnormal ligaments. Furthermore,
older normal subjects had subtle ligament abnormalities,
generally showing a lesser degree of enhancement without frank disruption compared with patients who had
clinically evident OA. The question arises, therefore,
whether the ligament changes are age related or if they
are in some way implicated in the pathogenesis of hand
OA. Further longitudinal studies specifically examining
ligaments in the early stages of hand OA are planned.
Based on the observation that enthesophytes
(new bone formation at ligament attachments) were
common in OA, it has been suggested that this supports
the importance of bone in the pathogenesis of OA (2).
However, hand OA is characterized by enthesopathic
changes especially in the soft tissue side of ligament
enthesis, and also with bone edema at ligament attachments. Therefore, entheseal new bone in OA could
simply reflect a reactive bone-forming process at the
enthesis, in a manner reminiscent of diseases such as
ankylosing spondylitis and psoriatic arthritis, rather than
an intrinsic bone disorder (1).
There were a number of limitations to this study.
Although we identified the ligament as a prominent site
of abnormality in hand OA, we could not obtain histologic proof of ligament disease, since an in vivo study of
ligaments precludes the comparison with equivalent
sections obtained for histopathologic study. Identification of image features is possible, however, due to good
anatomical detail and analogy to findings described in
previous reports involving cadaver specimens and ani-
TAN ET AL
mal models (9,10,12,13,24). Although we studied the
early symptomatic phases of OA, it is clear that it is
virtually impossible to study the early pathologic phases
of hand OA, since patients with symptoms of a few
months’ duration often had joint abnormalities comparable with those in patients who had chronic disease.
This is well described for other sites of OA presentation,
including the hip joint (25). However, we referred to
these patients as having early OA, because they were
assessed following a first symptomatic episode, and we
also assessed uninvolved joints that may develop clinical
OA at a later stage. Furthermore, we divided the normal
subjects into a younger group and an older group, more
closely age-matched with the patients.
Because OA is a disease of aging, it is possible
that it represents an aberrant age-related process. It was
clear that older normal subjects had ligament abnormalities that younger normal subjects did not have. Although the sample sizes of the groups were comparatively small in this pilot study, and multiple tests were
performed, the findings consistently indicated prominent ligament damage, particularly in early and chronic
OA. Finally, the demonstration of ligament abnormalities in the small joints could reflect the unique anatomy
and biomechanics of these joints, and it remains to be
proven whether ligament changes are common in other
generalized OA-prone sites, including the spine, hip, and
knee.
In conclusion, this study used high-resolution
MRI in patients with OA to better define the microanatomic basis for early hand joint involvement. The results
of the study reaffirm some longstanding concepts relating to OA, in particular the concept of whole joint organ
involvement, even at disease onset. The findings also
raise important questions about the role of ligaments in
hand OA. This MRI technique should become widely
available to rheumatologists to investigate the microanatomic basis for OA and other diseases in the clinical
setting. In particular, the findings of this study highlight
the need for more research into ligament abnormalities
in the early stages of OA.
ACKNOWLEDGMENTS
We would like to thank all who volunteered or referred
patients for the study. We would also like to thank all the staff
at the Leeds General Infirmary MRI Unit for their services
with regard to the study, and Dr. Elizabeth Hensor for advice
on statistical analysis.
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