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Clinical features
The main presenting symptoms are pain and functional restriction in a
patient over the age of 45, but more often over 60 years. The causes of
pain in OA are not completely understood but may relate to increased
pressure in subchondral bone (mainly causing night pain), trabecular
microfractures, capsular distension and low-grade synovitis, or may
result from bursitis and enthesopathy secondary to altered joint
mechanics. Typical OA pain has the following characteristics
for pain :
• Insidious onset over months or years
• Variable or intermittent over time (‘good days, bad days’)
• Mainly related to movement and weight-bearing, relieved
by rest
• Only brief (< 15 mins) morning stiffness and brief (< 5 mins)
‘gelling’ after rest
• Usually only one or a few joints painful
And with the following clinical sign:
• Restricted movement due to capsular thickening, or blocking
by osteophyte
• Palpable, sometimes audible, coarse crepitus due to rough
articular surfaces
• Bony swelling around joint margins
• Deformity, usually without instability
• Joint-line or periarticular tenderness
• Muscle weakness and wasting
• Synovitis mild or absent
Generalised nodal OA
Characteristics of this common form of OA are
• Polyarticular finger interphalangeal joint OA
• Heberden’s (Bouchard’s) nodes
• Marked female preponderance
• Peak onset in middle age
• Good functional outcome for hands
• Predisposition to OA at other joints, especially knees
• Strong genetic predisposition
Some patients are asymptomatic whereas others develop pain, stiffness
and swelling of one or more PIP joints of the hands from the age of
about 40 years onward. Gradually, these develop posterolateral
swellings on each side of the extensor tendon that slowly enlarge and
harden to become Heberden’s (DIP) and Bouchard’s (PIP) nodesTypically,
each joint goes through a phase of episodic symptoms
(1–5 years) while the node evolves and OA develops. Once OA is fully
established, symptoms may subside and hand function often remains
good. Affected joints are enlarged as the result of osteophyte formation
and often show characteristic lateral deviation, reflecting the
asymmetric focal cartilage loss of OA Involvement of the first
carpometacarpal joint (CMC) is also common, leading to pain on trying
to open bottles and jars and functional impairment. Clinically, it may be
detected by the presence of crepitus on joint movement, and squaring of
the thumb base.Generalised nodal OA has a very strong genetic
component: the daughter of an affected mother has a 1 in 3 chance of
developing nodal OA herself. People with nodal OA are at increased risk
of OA at other sites, especially the knee.
Knee OA
OA principally targets the patello-femoral and medial tibio-femoral
compartments at this site but eventually spreads to affect the whole of
the joint (Fig. 25.18). It may be isolated or occur as part of generalised
nodal OA. Most patients, particularly women, have bilateral and
symmetrical involvement. With men, trauma is a more important risk
factor and may result in unilateral OA. The pain is usually localised to the
anterior or medial aspect of the knee and upper tibia. Patello-femoral
pain is usually worse going up and down stairs or inclines. Posterior knee
pain suggests the presence of a complicating popliteal cyst (Baker’s
cyst). Prolonged walking, rising from a chair, getting in or out of a car, or
bending to put on shoes and socks may be difficult. Local examination
findings may include:
• a jerky, asymmetric (antalgic) gait with less time weight-bearing on
the painful side
• a varus less commonly valgus, and/or fixed flexion deformity
• joint-line and/or periarticular tenderness (secondary anserine bursitis
and medial ligament enthesopathy), causing tenderness of the upper
medial tibia)
• weakness and wasting of the quadriceps muscle
• restricted flexion/extension with coarse crepitus
• bony swelling around the joint line.
Calcium pyrophosphate dihydrate (CPPD) crystal deposition in
association with OA is most common at the knee. This may result in a
more overt inflammatory component (stiffness, effusions) and super-
added acute attacks of synovitis which may predict more rapid
radiographic and clinical progression.
Hip OA
Hip OA most commonly targets the superior aspect of the joint This is
often unilateral at presentation, frequently progresses with superolateral
migration of the femoral head, and has a poor prognosis. The less
common central (medial) OA shows more central cartilage
loss and is largely confined to women. It is often bilateral at presentation
and may associate with generalized nodal OA. It has a better prognosis
than superior hip OA and progression to axial migration of the femoral
head is uncommon. The hip shows the best correlation between
symptoms and radiographic change. Hip pain is usually maximal deep in
the anterior groin, with variable radiation to the buttock, anterolateral
thigh, knee or shin. Lateral hip pain, worse on lying on that side with
tenderness over the greater trochanter, suggests secondary trochanteric
bursitis. Common functional difficulties are the same as for knee OA.
Examination may reveal:
• an antalgic gait
• weakness and wasting of quadriceps and gluteal muscles
• pain and restriction of internal rotation with the hip flexed – the
earliest and most sensitive sign of hip OA; other movements may
subsequently be restricted and painful
• anterior groin tenderness just lateral to the femoral pulse
• fixed flexion, external rotation deformity of the hip
• ipsilateral leg shortening with severe joint attrition and superior
femoral migration.
Although obesity is not a major risk factor for development of hip OA, it
is associated with more rapid progression.
Spine OA
The cervical and lumbar spine are predominantly targeted by OA, then
referred to as cervical spondylosis and lumbar spondylosis, respectively
Spine OA may occur in isolation or as part of generalised OA.
The typical presentation is with pain localised to the low back region or
the neck, although radiation of pain to the arms, buttocks and legs may
also occur due to nerve root compression. The pain is typically relieved
by rest and worse on movement. On physical examination, the
range of movement may be limited and loss of lumbar lordosis is typical.
The straight leg-raising test or femoral stretch test may be positive and
neurological signs may be seen in the legs where there is complicating
spinal stenosis or nerve root compression.
Early-onset OA
Unusually, typical symptoms and signs of OA may present before the age
of 45. In most cases, a single joint is affected and there is a clear history
of previous trauma. However, specific causes of OA need to be
considered in people with early-onset disease affecting several
joints, especially those not normally targeted by OA, rare causes need to
be considered .
Erosive OA
This term is used to describe rare patients with hand OA who have a
more prolonged symptom phase, more overt inflammation, more
disability and worse outcome than those with nodal OA. Distinguishing
features include preferential targeting of PIP joints, subchondral erosions
on X-rays, occasional ankylosis of affected joints and lack of association
with OA elsewhere. It is unclear whether erosive OA is part of the
spectrum of hand OA or a discrete subset.
Investigations
A plain X-ray of the affected joint should be performed and often this will
show one or more of the typical features of. In addition to providing
diagnostic information, X-rays are used to assess the severity of
structural change, which is useful if joint replacement surgery is being
considered. Non-weightbearing postero-anterior views of the pelvis are
adequate for assessing hip OA. Patients with suspected knee OA should
have standing antero-posterior radiographs taken to assess tibio-
femoral cartilage loss, and a flexed skyline view to assess patello-femoral
involvement. Spine OA can often be diagnosed on plain X-ray, which
typically shows evidence of disc space narrowing and osteophytes. If
nerve root compression or spinal stenosis is suspected, MRI should be
performed. Routine biochemistry, haematology and autoantibody tests
are usually normal. Synovial fluid aspirated from an affected joint is
viscous with a low cell count. Radioisotope bone scans performed for
other reasons often show, as an incidental finding, discrete increased
uptake in OA joints due to increased bone remodelling. Unexplained
early-onset OA requires additional investigation, guided by the suspected
underlying condition.
X-rays may show typical features of dysplasia or avascular necrosis,
widening of joint spaces in acromegaly, multiple cysts and
chondrocalcinosis in haemochromatosis or disorganised architecture
inneuropathic joints.
Management