Rheumatology 6 - Clinical Features of Osteoarthritis
Anil Chopra
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Describe the causal factors of osteoarthritis
Outline the general symptoms of arthritis
Have a basic understanding of how to examine joints.
List at least 3 radiological features helpful in the diagnosis of osteoarthritis
Outline the diagnosis and treatment of osteoarthritis
Osteoarthritis is a disease of cartilage not of bone. It is caused by:
– Breakdown of proteoglycans and collagen
– Change in water content
– thinning and fibrillation of cartilage (where the cartilage has more fibrous as
opposed to smooth structure)
This results in bony changes (sclerosis and osteophytes) and is not related to
osteoporosis. They occur as the body tries to compensate for loss of cartilage
Risk factors for the development of osteoarthritis include:
• Increasing age
• Genetics
• Joint damage
– Obesity (weight bearing joints)
– Congenital dysplasia (hips)
– Sports injuries (knees)
– Surgery (meniscectomy)
– Previous rheumatoid arthritis as
joint will be damaged.
Osteoarthritis is not the same as ageing, it is a metabolic process
Osteoarthritis
Ageing
- Increased cartilage Hydration
- Decreased cartilage hydration
- Decreased proteoglycan
- Constant proteoglycans
- Decreased collagen
- Constant collagen
- Increased chondrocytes proliferation
- Constant chondrocytes proliferation
- Increased metabolic activity
- Constant metabolic activity
- Increased sub-chondral bone thickness
- Normal sub-chondral bone thickness
Pathogenesis of Osteoarthritis
The breakdown of proteoglycans caused by age and trauma has a number of effects.
Early Changes:
– Swelling of cartilage
– Loosening of collagen framework
– Chondrocytes increase proteoglycan synthesis but also release degradative
enzymes
– Increased water content
Later Changes:
– Proteoglycan broken down faster than produced
– Cartilage thins and softens with fissuring and cracking
– Repair attempted but inadequate
– Bone exposed
– Remodelling and hypertrophy of subchondral bone
Healthy cartilage
The diagram above is a representation of what healthy cartilage looks like (in terms of
its structure). The proteoglycan contains many side chains and is very sulphated. This
makes the proteoglycans extremely hydroscopic (i.e. they take up lots of water). This
gives the cartilage huge tensile strength – the structure is very strong mainly due to
the water content of it, and this is due to the hydroscopic nature of the proteoglycans
involved.
The diagram below shows the effect of trauma on the cartilage matrix.
As you can see, trauma to the matrix induces the release of growth factors from the
matrix which in turn cause release of metalloproteinases (from chondrocytes) which
cause rapid joint destruction via collagen and proteoglycan breakdown in the cartilage
of the joint.
Unhealthy Cartilage in OA
In OA, the proteoglycans (which are a key part of the normal structure) break down
and become fragmented, and therefore, the water content of the cartilage diminishes.
As a result, the collagen (supporting network) also degenerates. This causes the
cartilage to thin, and as a result, the bones are able to get closer together – in some
extreme cases, they may touch and rub together – this will cause pain in the joints,
and as the osteophytes generate more bone to compensate for the cartilage lost, the
condition worsens.
This diagram shows the secondary effects of cartilage
matrix breakdown. The cartilage has already started
to degenerate, and at the centre of all of the action are
chondrocytes.
The
chondrocytes
release
metalloproteinases which activate the synoviocytes to
release pro-inflammatory cytokines and synovial
fluid. The cytokines mediate the inflammation of
arthritis and the release of synovial fluid and also
inflammatory response will cause local swelling
(oedema).
Epidemiology
• Aged 50, 50% population have OA on X-ray.
• Aged 65, 90% have OA but only 5-10% symptomatic.
Other rheumatic diseases (inflammation of the synovial membrane) are more
disabling.
–
Rheumatoid arthritis ~ 1% (peak onset 45-55)
–
Reactive arthritis ~ 1% (peak onset 25-35)
Diagnosis of Osteoarthritis
It is characterised by joint pain, especially distal inter-phalangeal joints, carpometacarpal joint, hips or knees. It can cause knees to be:
 Valgus: outward angulation of the distal bone i.e. tibia is turned outward in
relation to the femur, resulting in a knock-kneed appearance.
 Varus: inward angulation of a distal bone i.e. the tibia is turned inward in relation
to the femur.
Symptoms
 Pain experienced worsens upon using the joint affected.
 Swelling that may be present is usually hard (as it is caused by proliferation of
bone and cartilage around the joint margins).
 Effusion (fluid leak into the joint) due to secondary synovitis is common. It
mostly affects large joints.
 There is stiffness…
– Morning stiffness – in OA it lasts for less than an hour (remember in
RA it lasts for more than an hour).
– Evening stiffness which mostly occurs after use of the joints (for
example exercise, or continuous use during the day (such as at work)
and relaxation in the evening (at home) may lead to joint stiffness).
 There is also joint deformity due to cartilage loss.
The risk of development can be increased by past history of injury or surgery, playing
traumatic sports, hip dysplasias and family history.
Examinations
Upon general examination, look for patients weight and fat proportion. The joints
should then be examined by looking, feeling and moving.
Hands
• LOOK.
– Redness
– Pattern of joint involvement
– Heberden’s and Bouchard’s nodes
– Squaring of hand (CMC)
– Joint deformities (varus or valgus)
• FEEL.
– bony swelling
• MOVE
– Crepitus: (cracking or grinding sound as bones rub)
Particularly CMC joint
Knee
• LOOK
– Quads wasting
– Valgus or varus deformity
– Gait
• FEEL
– Joint effusion
– Bony swelling
• MOVE
– Crepitus
– Reduced range of movement
– Lateral instability
Neck
• LOOK
– Kyphosis or scoliosis
• FEEL
– local tenderness
• MOVE
– Reduced range of movement
• Neurological examination of the arms is important as many of the nerves that
control arm movements run through the root of the neck and so the risk of
compressing these nerves in spinal OA.
Hip
•
•
•
LOOK
– usually nothing visible
– Gait
Feel
– Tenderness over the joint (mid-point inguinal ligament)
Move
– Reduced range of movement (particularly rotation in flexion)
The differential diagnosis for osteoarthritis:
• Presence of:
– Heberden’s nodes
– Squaring of the hand and CMC crepitus
– Quad wasting, bony swelling and crepitus of the knee. Sometimes
valgus or varus deformity.
– Pain on movement of the hip
• Absence of (compared to RA or reactive arthritis)
– Warm joints
– Soft tissue swelling
– Large effusions
Investigations
• Blood
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–
• X-ray
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ESR and CRP normal
ANA (antinuclear antibodies) and Rheumatoid factor are negative
Joint space narrowed
Periarticular sclerosis
Osteophytes
(Subchondral cysts may be seen)
Treatment
• Reassurance – they do not have rheumatoid arthritis
• Lose weight to aid weight bearing joits
• Physiotherapy
– To increase muscle tone
– Quads exercises in quad wasting
• Analgesics, NSAIDs (COX-2 inhibitors)
• Intra-articular steroids to reduce inflammation and swelling
• Support devices and footwear
• Surgery