Fig. 4.

2 gross rheumatoid arthtritis at the carpus with ulnar deviation, subluxation and joint
narrowing at the metacarpo-phalangeal joints. Boutonniere deformities are present at the
index and little fingers.

Fig. 4.3 Rheumatoid arthtritis with narrowing of the metatarsophalangeal joint of the great
toe and a fine periostitis on the adjacent shafts (arrows).

Fig. 4.1 Marked soft-tissue swelling is present over the right ulnar styloid and adjacent carpus
in an early case of rheumatoid arthritis with no local erosion.

1. SOFT TISSUE CHANGES. These changes are best assessed clinically but may also
be shown radiologically in the hand, knee or foot and other joints. Soft tissue swelling
is due to oedemaof periarticular tissuesand to synovial inflammation in bursae, joint
space and along tendon sheaths. Joint distension also follows an increas in synovial
fluid.
In the han, fusiform swelling due to capsular distension and local oedema may be
seen over interphalangeal and metacarpophalangeal joints.soft tissue swelling over the
third and fourth metacarpophalangeal joints is seen as a local increase in density and
occasionally as soft tissue projection into adjacent web space. Soft tissue swelling
overthe ulnar styloid can be due to local involvement of the extensor carpi ulnaris
tendon sheath. Changes at the radial styiloid are related to local radiocarpal joint
synovial hyperthropy.
Soft tissue change are less well demonstrated in the foot. Changes over the firts ang
fifth metatarsophalangeal joints reflect synovitis in the bursae over the first and fifth
metatarsah heads, but swelling over the remaining metatarsophalangealjoints may be
seen as fusiform increases in density.
The achilles tendon insert into the back of the calcaneum below its upper margin. It is
sharply demarcated anteriorly by the pre-achilles fat pad and more inferiorly, by the
retrocalcaneal bursa. Local synovitis thickens the bursa and oedema obliterates the fat
and blurs out the tendon, which also thickens. Similar changes occur inferiorly, at the
plantar fascial origin at the base of the calcaneum.
Distension of the capsule of the knee joint is shown on the anteroposterior radiograph
as alateral bulging of the normally poorly seen fat lines over the distal femur. On a
lateral view of the knee the supra-patellar pouch is distended and its surrounding fat
lines blurred. Posteriorly, a distended joint capsule may give a local increase indensity
 and in this way a Bakers cyct is often identified. This can be confirmed by ultrasound
or artography.

On the lateral view of the elbow, the anterior and posterior fat planes are displaced in
a direction vertical to the long axis of the jointy, but may be obliterared by local oedema.

Swelling around an affected joint is symmetrical while in gout the swelling is eccentric. In
rheumatoid arthritis, however, a rheumatoid nodule may cause alocalized eccentric swelling,
and these often occur at pressure points.

2. OSTEOPOROSIS. Assessment of osteoporosis depends in part on film quality, and

comparison between normal and abnormal joints in the same patient may be helpful.
Interpretation is subjective and changes are seen only after loss of 25-50% of mineral.
Differences in assessment of osteoporosis may exist, both between different observers and
between the same observer at different times.

Osteoporosis in rheumatoid arthritis is of two types:

Generalized. This may be due to steroids or limitation of movement due to pain, or

muscle wasting. This type in uncommon and occurs late in the course of the disease. It may
also reflect coincidental bone loss in post-menopausal woman, commonly affected by this
disorder.

Local osteoporosis around joints occurs earlier and is due to synovial inflammation
and hyperaemia.

Osteoporosis increases in incidence with the duration of the disease and the age of the
patient. Some 30% of patients show it at presentation but two years after, 80% are affected.

Osteoporosis is a precursor of erosive disease and may mask early erosions.

Generalized or solitary sclerosis of one or more distal phalanges (terminal phalangeal
sclerosis) is often rendered more prominent because of osteoporosis elsewhere. This occurs in
some 35% of patients with rheumatoid arthritis and other arthropaties and may be present
before any other abnormality. In a woman, especially, it may prognosticate future disease, but
is seen in some normal patients.

3. JOINT SPACE AND ALIGNMENT DEFORMITIES. In the early stage a joint

space may be widened by synovial hypertrophy and an effusion. Later in the disease, joint
spaces narrow due to cartilage destruction by pannus (Fig. 4.2). Narrowing of joint spaces
may, however, be apparent rather than real in the presence of flexion deformities, so that an
oblique view is needed to assess the space. Alignment abnormalities at joints may result from
local synovitis weakening the capsule and tendinitis preventing normal musculotendinous
action. Tendons may also rupture in the region of roughened bone. Thus, rotator cuff tears
allow upward subluxation of the eroded humeral head.

The classic changes of alighnment in the rheumatoid hand are irreversible.

Subluxations at metacarpophal-angeal joints lead to ulnar deviation (Fig. 4.2) which occurs in
up to 50% of those with chronic disease. This change may result from ulnar deviation of
extensor tendons.

The boutonniere deformity (Fig. 4.2) results from proximal interphalangeal joint
flexion and distal interphalangeal joint extension, and the swam-neck deformity from the
reverse (peoximal interphalangeal joint extension and distal interphalangeal joint flexion).
The bouthonniere deformity is the more common.

Similarly, lateral deviation of the toes may be found. Hallux valgus is especially
common. The gallux sesamoids sublux between the first and second metatarsal heads and the
transverse arch flattens as local inflamation causes ligamentous laxity.

4. PERIOSTITIS. Local periosteal reactions occur either along the midshaft of a

phalanx or metacarpal as a reaction to local tendinitis, or at the metaphysis near a joint
affected by synovitis. Such changes are less near common in rheumatoid arthritis than in the
sero-negative arthropaties. They are difficult to identify, may be mistaken for lumbrical
impressions and are commoner in the feet (Fig. 4.3). Periostitis in the from of fluffy calcaneal
spurs, plantar and posterior, is also less common in reumathoid arthritis than in the
seronegative arthropathies (Fig. 4.4). When present, they are larger and more irregular than
the normal small well-corticated spurs of the elderly. Spurs may arise ab initio or may follow
healing of erosions.

5. EROSIONS. These are the most important diagnostic change but are not
necessarily present when the patient first attends. Their incidence rises from less than 40% of
patients at there months to up to 90% or 95% at ten years.

Classical periarticular erosions occur at the so-called bare arears of bone between
the edge of the articular cartilage an the attachment of the joint capsule (Fig.4.5).
 Erosions in rheumatoid arthritis should be sought for at the common sites.
Supplementary views, such as the Norgaard ball-catcher view (supine 25 oblique view),
may be needed. Erosions appear earlier and are more often seen in the feet, 90% of which
will eventually be affected, than in the hands (75%), and most often at the fifth
metatarsphalangeal joint. The hallux metatarsophalangeal is the least often involved. Erosions
affect typically the lateral side of the fifth metatarsal but the medial side of the others.

The metatarsal head erodes before the base of the distal phalanx. In the hand, the
second and third metacarpophalangeal joints are the earliest affected, initially on the radial
aspects. More distal erosions are inconstant. Erosions occur at the ulnar styloid, at the radial
styloid and at the proximal compartment of the distal radio-ulnar joint (Fig.4.6). Carpal
erosions occur throughout the wrist. An erosion is, for example, commonly seen on the lateral
scaphoid at its waist. Carpal disease may be followed by fusion, but this is uncommon
elsewhere in adult rheumatoid arthritis. On occasion, massive carpal destruction may be
found in the presence of virtually normal peripheral joints.

Tarsal erosions, other than at the posterior and inferior sorfaces of the calcaneum, are
uncommon and are also less common in rheumatoid arthritis than in the seronegative
spondyloarthropathies (Fag. 4.7). In rheumatoid arthritis, erosions are usually seen at or
above the insertion of the tendo achillis into the back of the calcaneum.

Erosions are first seen as an area of local demineralization beneath the cortex which
eventually venishes, leaving irregular underlyng trabeculae. The destroyed area increases in
size and, as pannus spreads over articular serfaces, the entire articular cortex may be
destroyed, leaving a pointed bone end. Chronic trauma, in weightbearring or due to abnormal
tendon alignment, may further collapse articular surfaces. Steroids and analgesics also
modify the disease so that neuropathic-type destructive changes may result. Healing rarely
reverses erosions and so it not often that a normal appearance returns. Usually the margins of
healed erosions become corticated and they do not enlarge on follow-up.

Erosive change is less common at the larger joints but often bone destruction is
greater owing to the greater stresses placed on kness, elbows and shoulders. On occasion,
intraoseous defects-cysts or geodes-up to 2-3cm in diameter, may be seen beneath joint
surfaces (Fig. 4.8). An alternative form of change at large articul;ar sorfaces is a superficial
surface irregularity with a little reactive sclerosis in the presence of much joint narrowing.
This changeis seen at the elbow, knee and hip. In the hip joint it is characteristically the
medial joint space which is narrowed and eroded (as opposed to the superior in osteoartritis).
Muscle pull on adjacent irregular articular surfaces leads to medial migration of the femoral
head and acetabular resorption, causing protrusio acetabuli. This is classical , but not
pathognomonic of rheumatoid arthritis, at it also occurs in osteoarthritis, in conditions with
bone softening,and in an idiopathic inherited form. Gross loss of bone, especially at the
femoral head, may result in a birds beak appearance. Marked loss of bone around articular
surfaces is also common at the elbow and shoulder, and deformities of alignment follow.
Bone loss at the acromioclavicular joint may often be seen on a chest radiograph, with
pointing of adjacent bone ends and scaloping of the undersurface of the acromion (4.11).
Erosions of the superior aspects of the upper ribs are seen in patients with long-standing
disease and muscle wasting, and are probably due to the adjacent scapula rubbing on the rib.

Rheumatoid change in The Axial Skeleton.

Sacroiliac joints: changes are less common and less severe than in seronegative
disease but may be seen in up to 30% of those with long standing disease. The changes are
more common in women (cf. Ankylosing spondylitis) and rarely end in fusion.

Spinal change Rheumatoid change are common in the cervical spine but uncommon
in the thoracic and lumbar regions.

Osteoporosis disc narrowing and end-plate irregularity are seen with only a little
reactive new bone formation at the upper cervical vertebrae. Osteoarthritis, in distinction, is
seen more inferiorly. Facet joint erosions may result in subluxation, so that nerve entrapment
follows. Subluxation and erosion also accur at the synovial joint between the odontoid peg
and arch of atlas, and are potentiated by laxity of ligaments around the peg.separation in
flexion of more than 2,5 mm in adults or 5 mm in children is held to be abnormal. This
instability can be seen in up to 30% of patients with chronic rheumatoid arthritis. The eroded
odontoid may also fracture.

Resoption of bone at non articular surfaces occurs in the cervical spine at the spinous
processes which become short, sharp and tapered in patients with chronic disease.

6. SECONDARY OSTEOARTHRITIS. Weight bearing joints affected by

rheumatoid arthritis often develop secondary osteoarthritis. Indeed, at the hips, osteoarthritic
change may be superimposed on a previously unrecognized rheumatoid arthritis. Reactive
sclerosis and new bone formation in osteoarthritis is not marked in those whose underlying
disease has characteristic features of osteoporosis and bone destruction.

Arthritis in Children

There aremany causes of polyarthritis in children, the most common being viral
infection. It is now recognized that chronic childhood polyarthritis is a heterogenous group
disorders, the genericterm for whichisjuvenile chronic polyarthritis. Some 10% of the total
eventually have a seropositive form of disease similar to, or identical with, adult rheumatoid
arthritis, that is, an essentially peripheral arosive polyarthritis. The remaining patients have
seronegative chronic arthritis for which definite clinical and histological diagnostic criteria
axits.

Classification of juvenile chronic polyarthritis

1. Adult-type rheumatoid arthritis (with Ig M rheumatoid factor)

2. Polyarthritis with ankylosing spondylitis type sacroiliitis
3. Stills disease
a. Systemic
b. Polyarticular
c. Pauciarticular, with or without chronic iridocyclitis
4. Psoriatric arthropathy
5. Arthritis associated with ulcerative colitis or regional enteritis (as in adult)
6. Polyartrhropathis associated with other disorders, such as systemic lupus
erythematosus or familial Mediterranean fever.

Children with seronegative juvenile chronic arthritis may be further subdivided:

1. Acute systemic onset type (true stills disease) with constitutional symptoms and
hepatosplenomegaly, but litleor no joint involvement.
2. Pauci-articular (not more than four joints involved) affecting especially the knees ,
wrists and ankles. This usually ends up as.
3. Polyarticular disease, which may also present at the onset. Radiologycal changes
are late and the disease in non-erosive.

In the carpus and tarsus the bones show accelerated maturation due to hyperemia,
crowding of bones with joint space narrowing and an abnormal angular shape (4.14).
in general early overgrowth of epiphyseal centres with squaring or angulation leads to
premature fusion and eventual hypoplasia. This occurs at metacarpal and metatarsal
epiphyses and around the knees, hips, elbows and shoulders. The abnormally
modelled bone ends cannot easily be distinguished from the similar changes of
synovial tuberculosis or haemophilia. Osteoporosis may result from hyperaemia or
steroid administration which,in large doses, also causes undergrowth. Pathological
fractures may result. Residual trabeculae along lines of stress are rendered very
prominent. At the elbow, marked radial head enlargement cervical spine is often
affected and indeed is the cause of presentation in 2% of cases. Diminution of neck
movement is followed by apophyseal joint changes, maximal at C2-3, where erosions
lead to ankylosis. The associated vertebral bodies fail to develop. Atlantoaxial
subluxation is said to occur only rarely in those patients with seronegative disease,
and neurocentral joint lesions do not occur in seronegative disease.

Juvenile ankylosing spondylitis has a characteristic onset at about 10 years of age.

It is five times more common in boys and presents initially with an asymmetric
peripheral arthrophy. Sacroiliac changes develop some 5-15 years later.

GOUT
Radiographic finding :
1. Erosions
These are caused by deposition of sodium biurate and are typically punched out in
appearance. They tend to appear near joint margins. As they enlarge, they tend to
involve more of the cortex of the shaft rather than the articular surface. Large
erosion extend to the articular cortex and diffusely in the shafts.
Cartilage destruction is a relatively late manifestation. Usually much bony
destruction is seen before cartilage loss supervenes. In the hand gouttends to
attack the distal and proximal interphalangeal joints, whereas rheumatoid arthritis
affects the metcarpophalangeal and proximal interphalangeal joints.

2. Osteoporosis
Osteoporosis is not seen expect in advance caseswhich have been immobilized.
3. Tophi
These are shown as soft tissue swelling eccentric in distribution, in
contradistrinction to the fusiform soft tissue wselling of rheumatoid arthritis .
Eventually, both soft tissue and intrasseous tophi may become calcified.

Differential diagnosis
Differential between gout and multiple enchondromas may be difficult
radiographically. The tendency of multiple enchondromas to spare bone ends is
an important diagnostic point. The clinicalfindings and history readily
differentiate the two conditions.
In practice, the most frequent difficuly is in differentiating gout from rheumatoid
arthritis. Important points are : the longer latent period of gout; its eccentric, often
gross soft tissue swelling;and tendency to attack distal interphalangeal joints.
Osteoporosis is found much more frequently in rheumatoid arthritis. Rheumatoid
erosions are not so sharply defined as those of gout. Calcified tophi are, of course,
diagnostic of gout. In difficult cases, differentiation will be made by laboratory
tests revealing a raised uric acid level in blood.