Introduction

Osteoarthritis is a condition that results from the loss of cartilage at synovial joints, and is often accompanied by degeneration of the underlying bone.
Radiologically there are:
  • osteophytes
  • Joint space narrowing

Epidemiology

  • most common type of arthritis
  • 80% people >60 will have some radiographic features
    • Only ¼ of these (20% of total population >65) is symptomatic
  • rare to present below the age of 55
  • OA of the hip is less common in black Africans and Chinese populations than in Caucasians
  • radiologic signs are more common than symptoms
  • More commonly affects women (M:F – 1:3)
  • The leading cause of disability in those over 55

Aetiology

  • there is a genetic component. Most commonly disease with interphalangeal involvement (nodal OA), and primary generalised OA are the inherited types
  • Genes that encode for ‘collagen type II’ are thought to be involved. Several have been identified, but it is thought that many genes are involved.
  • Previous trauma of a joint increases the risk of having OA in this joint.
  • Obesity
  • Hypermobility of joints predisposes you to OA
  • Osteoporosis REDUCES the risk of OA
  • Occupation – e.g. involving manual labour. Miners get OA of the hip, knee and shoulder, cotton workers – in the hand, and farmers – in the hip, sports people – often get OA in the lower limb.

Pathology

  • focal destruction of articular cartilage. Inflammation is usually not involved.
  • There is massive variability in the bone changes. In some individuals there may be no underlying bone change, but in others there can be massive new bone formation at the chondral margins.
  • Bone underneath cartilage is referred to as subchondral bone.

What is cartilage

It is 75% water, and the rest is mainly collagen (type II), mixed in with chondrocytes, fibroblasts and proteoglycans. Cartilage is smooth and can absorb impact. It is constantly damaged in normal use, but this is repaired by chondrocytes. This damage and repair is a balanced process in normal function. Chondrocytes are found throughout the cartilage itself – and along with fibroblasts, are the only cells found in cartilage.
  • Cartilage itself has no blood supply, and no nervous supply.Nutrients diffuse into the cartilage from the synovial fluid, and from the nearest blood supply – in the bone marrow.
  • So where does the pain come from in OA?! The reasons are pretty complex, but it is probably mainly due to irritation of the bone surface after the cartilage has worn away.
  • The precursor cells of chondrocytes also differentiate into osteoblasts.
  • The structure of collagen means water molecules are held in place by electrostatic forces between sidechains of the collagen. This gives cartilage its ability to absorb impact. Throughout the day, the collagen becomes dehydrated, and we lose height, due to the intervertebral discs becoming thinner. During the night when we are laid flat, the collagen rehydrates.
In OA, this balance between damage and repair is lost. There is chondrocytes proliferation, and excess cartilage is produced, however, it is oedematous. This leads to focal erosions forming. This leads to rapid destruction of the cartilage, for which, the chondrocytes cannot compensate, and later in the progression of the disease the chondrocytes die, through apoptosis.  
Adjacent areas of cartilage try to take over the role of repair, but this is inadequate.
Eventually, the synthesis of new matrix stops completely. The surface becomes fistulated and fibrillated.
  • Fibrillations are small ridges in the articular cartilage surface.
Now the bone has lost its protection, it is exposed to extra stressors. The two bones of a joint may rub directly against eachother.  There may be microfractures, and cyst formation.
The bone attempts to re-grow itself, but this process can be too great, and it results in the formation of osteophytes.
 
The disease is progressive. This can be gradual, or stepwise. In some very rare cases, radiological improvement has been seen. This could be the basis for future treatments.

Clinical features

Can affect most joints, and there are lots of different patterns. Disability results when knee and hip joints are affected.
  • joint pain and stiffness
    • Initially, the pain is intermittent, and often described as an ache. Typically it is provoked by movement of the affected joint, and relieved by resting the joint, but in later disease, there may also be pain at rest. It may be severe enough to wake the patient at night.
    • Stiffness is typically worse after long periods of inactivity – e.g. first thing in the morning. However – it typically only lasts a few minutes – as opposed to the long periods of morning joint stiffness seen in RA.
  • joint gelling – stiffness and pain of the joint after a period of immobility
  • Joint instability
  • Loss of function as a result of the above
  • Synovitis can also occur
    • This is inflammation of the synovial membrane – the membrane which forms the border of the joint capsule.
    • Causes joint swelling, as synovial fluid volume increases
    • Also lumps (nodes) may be palpable
    • Painful, especially on joint movement
    • More common in RA than OA. Can also occur in other joint disorders (e.g. gout).
    • Treatment depends on the cause, but when associated with OA, may just be treated with NSAID’s

Signs

  • Joint line tenderness
  • Limited range of movements
  • Joint crepitus on movement
  • Bony swelling
  • Joint effusion with may or may not include inflammation
  • Muscle wasting
  • Limitation of range of movement
  • There may also be occasional joint effusions
  • Audible joint crepitus
  • Nodes
    • Heberden’s nodes – seen at the DIP joints
      • To help remember this you can remember ‘Outer Hebrides’ – to remember that Heberden’s Nodes are distal
    • Bouchard’s Nodes – seen at the PIP joints
  • Squaring of the hand – this refers to a deformity of the CMC joint of the thumb. The joint appears more prominent than in a normal hand, thus making the base of the hand appear ‘squared’.

Classifications of OA

OA can be classified by cause, or presentation.

Cause

Primary
i.e. idiopathic – there is no underlying cause. Genetic factors likely to be involved.
Secondary
Likely to be the result of another underlying disease process or event. E.g.:

Presentation

Nodal OA
  • Joints of the hand affected. Usually one joint at a time, over a period of several years
  • DIP’s more than PIP’s
    • If PIP’s are affected, it may mimic rheumatoid arthritis. The patient may even be positive for rheumatoid factor – but this is not diagnostic, and is of no significance.
  • Commonly presents around the time of the menopause in women
  • Usually bilateral
  • Often occurs in painful episodes – there may be joint swelling and some inflammation (although – a typical of feature of OA – despite inflammation – CRP and ESR are usually normal!)
  • Functionally, patients do not usually have any problems, although if there is severe involvement of the DIP’s, there may be reduced grip strength.
  • The inflammation will gradually reduce over time (months to years), and it often leaves behind stiffness deformity. Deformity is usually in the form of painless bony nodules
    • Heberden’s nodes – found at DIP
    • Bouchard’s nodes – found at PIP
      • These nodes are the result of osteophyte formation
  • On x-ray
    • Joint space narrowing
    • Nodes at essentially large osteophytes

Other types of Hand OA

  • Often OA of the carpometocarpal joints and metocarpophalangeal joints co-exists with nodal OA. This may be painful at first, but pain declines overtime, as the joint stiffens.
  • Unlikely to serious affect function
  • May cause a squared hand, due to fixed adduction of the thumb.
  • Polyarticular hand OA – is associated with ↑risk of OA at other sites
  • in all types of hand OA:
    • symptoms are episodic, and may settle after time
    • rarely disabling
    • family history

Hip OA

  • Affects 7-25% of Caucasians. Less common in black Africans.
  • There are two main types:
    • Superior pole OA – joint space narrowing, sclerosis of both head of femur and acetabulum. More common in men, often presents unilaterally, but can spread to become bilateral
      • Pain is usually felt in the groin – typically on exercise. May also radiate to the buttocks, anterior thigh, knee and even lower leg – this is why it is important to examine the joints above in your orthopaedic examination!
      • Another typical presentation is the patient is unable to reach down to tie their shoelaces/cut their toenails/put on their socks. As the disease progresses, pain in the knee becomes more common. Pain may also disturb sleep in later disease.
    • Medial cartilage loss – less common. Usually in women. Associated with hand OA. Rapidly disabling. Bilateral
    • Other clinical features
      • Pain on internal rotation – early disease
      • Pain on external rotation – late disease
      • Limb shortening
      • Quads and gluteal wasting and weakness
      • Reduced range of movement in all directions. Rotation movements are usually the most painful.
      • Fixed flexion deformity
      • Tenderness is rare

Knee OA

  • Present in 40% of over 75’s
  • More common in women
  • Strongly associated with obesity
  • Usually bilateral
  • Strongly associated with polyarticular OA of the hand in elderly women
  • Medial compartment more often affected. Leads to varus deformity.
  • Risk factors:
    • Previous trauma
    • Meniscal and ligament damage
  • Symptoms:
    • Knee pain
    • Pain on walking – particularly upstairs
    • Antalgic gaita limb adopted to avoid pain. Will have short stance phase on one side usually.
    • Difficulty getting out of chairs
    • Joint line tenderness
    • Joint line bony swelling
    • Crepitus
    • Quads wasting
    • Varus deformity (valgus possibly but rare)
    • Fixed flexion deformities

Primary generalised OA

aka nodal generalised OA
  • Less common than nodal OA, but often co-exists with it
  • More common in women
  • Strong familial association
  • Onset is often sudden and severe
  • Associated with immune complex deposition – may have an autoimmune cause.
  • Affects:
    • Knees
    • Hip
    • Intervertebral joints
    • Hands

Erosive OA

  • Rare
  • Affects DIP’s and PIP’s in a similar presentation to nodal OA
  • Functional outcome is poor (unlike nodal OA)
  • Can develop in RA – some believe it is not truly OA

Crystal Associated OA

aka crystal arthropathy, crystal arthritis.
  • Usually the result of calcium pyrophosphate deposition in the cartilage. This phenomenon is known as chondrocalcinosis.
  • Chondrocalcinosis is usually asymptomatic, and frequency increases with age
  • Usually affects the knees and wrists
  • Causes a chronic arthropathy, sometimes referred to as pseudo-OA. Usually marked cyst formation and oseteophytes of x-ray. Also, calcification of the cartilage is often seen.
  • May be rapid onset and disabling. Most commonly seen in elderly women.
  • Associated with pseudo-gout.

Secondary OA

  • 50% of patients who have an open knee menisectomy will get OA within 21 years
  • After hip dislocation fracture, average time to get OA is 7 years

Course of the disease

Joint pain and stiffness joint destruction joint replacement
The disease typically progresses slowly, although some patients can remain stable for years. Even with early intervention, up to 65% of patients will show deterioration 15 years after diagnosis.

Investigations

  • X-ray – often signs may be visible on x-ray, before symptoms of pain and stiffness develop. X-rays are usually AP. Often, the correlation between radiographic features and symptoms is poor, although in larger joints, it is more reliable than smaller ones. X-rays are not very useful to distinguish types of arthritis if the history is inconclusive. To assess joint space narrowing, you need to take a weight bearing x-ray! On the left is a normal knee radiograph, on the right, a knee with OA.
  • Blood tests – there aren’t really any useful tests. ESR and CRP will be negative. Rheumatoid factor and antinuclear antibodies are also usually negative, but if positive, are unhelpful. May be useful to exclude other differentials.
  • MRI – can show bone and cartilage changes. Not widely used for OA at the moment, but may be able to detect early cartilage changes in the future.
  • Arthroscopy – is good for looking at early changes of the cartilage (e.g. fissuring, surface erosion).

Treatment

  • Treat the symptoms! – don’t treat the radiological findings.
    • Depression often co-exists.this, along with quadriceps wasting, is the main predictor of pain.
  • Education of the patient about the disease mechanisms and prognosis can reduce pain, and aid compliance

Physiotherapy and exercise

Initial treatment should be around ‘self-help’, such as exercise and life-style changes.
Physio and exercise are particularly important in lower limb OA, especially so for the knee. Increasing quadriceps strength helps knee stability.
  • Physiotherapists should be used to teach patients how to exercise, and not relied upon for regular care.
  • Thick, soft soled shoes can make a lot of difference to some patients.
Hydrotherapy may be useful in lower limb OA. Massage and heat & ice packs are often useful.
NSAID’s are debateable – many patients take them, but the proven benefit is marginal, if any. Have been associated with avascular necrosis and destructive arthropathy.
  • You should add some sort of gastro protection (e.g. omeprazole), or use a selective COX2 NSAID, to reduce the risk of gastritis.
  • Be wary of NSAID’s in patients with cardiovascular risk factors – which will be a lot of patients in this age range!
Weight reduction is helpful in those with BMI >28
In patella-femoral OA, performing a patellar tap can relieve symptoms!

Alternative treatments

TENS and acupuncture have been shown to be beneficial to some patients.
Pain relief
Is important to help function.
  • First – try paracetomol. Up to 4g daily. If uncontrolled:
  • Second – add codeine
  • Third – if still not well controlled, consider NSAID’s – but only give in short doses.
Steroids
Despite the fact that OA is usually not inflammatory, local injections of steroids during severe exacerbations are often helpful. Do not do this more than twice a year. This is particularly useful when there is joint effusion.
Other treatments
  • Hyaluronate – some recommend this for those unresponsive to intra-articular steroid injections. It is also administered by intra-articular injection. Other question the benefit
  • Glucosamine and chondroitin – these agents appeared in early trials as though they may alter the long term outcome of the disease, but have subsequent trials have been ineffective.

Joint replacement

Used widely in severe disease. Only really used for hip and knee joints. very good outcomes in those whose disease is not well controlled with physical and pharmacological intervention. Also can greatly reduce functional deficits. The risk of complications is equal in both (about 1%). For the vast majority of patients pain is greatly reduced, and function greatly increased, after joint replacement.
  • Don’t let the young age of a patient put you off
  • In those unfit for general anaesthesia, they can be performed under spinal agents.
  • Contraindications:
    • Ongoing sepsis / leg ulcer
    • Peripheral vascular disease
Hip replacement
  • 90% of cases will be pain free after recovery
  • Vast majority of cases have large functional improvement
  • 75% of patients will not need a second hip replacement.
    • The lifespan of a hip replacement is typically 10-20 years, although some patient have been known to have them for 30+. 90% of prosthesis will survive >15 years.
    • The second replacement (revision surgery)carries greater procedural risk, and often the outcome is not as satisfactory as the first.
    • Younger patients may have a metal on metal replacement – as these may have a long lifespan. These type of replacements tend to involve more of a resurfacing of the articular surface, than the large replacements seen with other types of surgery.
  • Total hip replacement – ARTHROPLASTY – this is the most common form of joint replacement. About 50 000 are performed each year in the UK.
    • Usually a metal ‘ball’ in a plastic ‘socket’, to reduce the friction co-efficient.
    • Can be cemented, or uncemented. In the UK, nearly all are ‘cemented’. In the uncemented version, the prosthesis is held in place as a result of the elastic quality of bone, and a very tight fitting prosthetic joint!
  • Partial hip replacement – the acetabulum may be left in place, and only the head of femur is replaced.
  • Recovery
    • Mobilise the patient ASAP. This prevents long-term stiffness and aids a full range of movement
    • Average recovery time is 6/7 months, before full activities can be resumed
    • Recovery can be painful, but usually pain is well controlled with medication. After a full recovery there should be little pain
  • Risks
  • DVT – Risk minimised with stockings, pumps to aid bloodflow. You must inform the patient that there is a risk of death – but balance this by describing what you will do to reduce the risk, and reassure that it is rare (death from DVT is <0.1%, total risk of death is about 1%)
  • Infection (2% – 1% deep infection, 1% superficial infection)
    • Bacteria are able to adhere to the prosthesis. This is dangerous, as they can then protect themselves from oral AB’s with a biofilm, making the infection impossible to treat in this way. The prosthesis has to be removed whilst the patient recovers; meaning 2 operations and no functioning hip joint, before they can start again!
    • The risk is greatly reduced with prophylactic antibiotics. Also reduced with MRSA screening, laminal air-flow theatre. Don’t ever perform if there is an ongoing infection!
    • Prophylactic AB used – commonly cephalosporins – e.g. cefazolin (first generation), or cefuroxime (
  • Altered leg length – Patient will probably still have better function and less pain than without the op though!
  • Dislocation – Risk is about 2%
Consent
  • You must inform the patient that there is a risk of death – but balance this by describing what you will do to reduce the risk, and reassure that it is rare (roughly 1%)
  • Remember – OA isn’t life threatening – but surgery can be! Although the risk is tiny, and OA can be very disabling.
  • When disclosing risks – remember to lay out the alternatives – in this case – pretty much carry on as you are!
  • Who can take consent –best practice if it is the surgeon who will carry out the procedure – but it doesn’t have to be. Has to be somebody who is properly qualified, competent, and understands and is able to explain the procedure.
Knee Surgery
  • Tibial osteotomy – an alternative to knee replacement in suitable patients (young, physically active). In an osteotomy, bones are cut, shaped and re-aligned, to allow better functioning of the joint. This can prolong the need for knee replacement by up to 10 years.
    • It is particularly useful when there is varus/valgus deformity.
    • Recovery process is often longer and more difficult than knee replacement
  • Knee replacement – full recovery often seen within about 4 months. Pain relief is great, but range of movement may not be improved.
  • Hip and knee OA is the same leg – the hip is usually replaced first.

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