Osteoarthritis

Presented by
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Osteoarthritis (OA)
the most common form of arthritis and is a major cause of pain and
disability in older people
It is characterised by focal loss of articular cartilage, subchondral
osteosclerosis, osteophyte formation at the joint margin and
remodelling of joint contour with enlargement of affected joints
Epidemiology
The prevalence rises progressively with age and it has been estimated
that 45% of all people develop knee OA and 25% hip OA at some point
.during life
There are major ethnic differences in susceptibility: the prevalence of
hip OA is lower in Africa, China, Japan and South Asia than in European
countries, while that of knee OA is higher
Pathophysiology
OA is a complex disorder, with both genetic and environmental
. components
Family-based studies have estimated that the heritability of OA ranges
from about 43% at the knee to between 60% and 65% at the hip and
.hand, respectively
In most cases, the inheritance is polygenic and mediated by several
.genetic variants of small effect
Structural abnormalities, such as slipped femoral epiphysis and
developmental dysplasia of the hip, are also associated with a high risk of OA,
.presumably due to abnormal load distribution across the joint
Biomechanical factors play an important role in OA related to certain
occupations, such as farmers (hip OA), miners (knee OA) and elite or
.professional athletes (knee and ankle OA)
It has been higher prevalence of knee OA in South and East Asia might
.be accounted for by squatting
There is also a high risk of knee OA in people who have had
destabilising injuries, such as cruciate ligament rupture, and those who
.have had meniscectomy
For most individuals, however, participation in recreational sport does
.not appear to increase the risk significantly
There is a strong association between obesity and OA, particularly of
the hip. knee. This is thought to be due partly to biomechanical factors,
but it has also been speculated that cytokines released from adipose
.tissue may play a role
Oestrogen appears important; lower rates of OA have been observed in
women who use hormone replacement therapy (HRT), while women
who receive aromatase inhibitor therapy for breast cancer often
.experience a flare in symptoms of OA
Degeneration of articular cartilage is the defining feature of OA. the
concentration of aggrecan in cartilage matrix falls and makes the
.cartilage vulnerable to load-bearing injury
 .large parts of the cartilage surface are damaged
OA is also accompanied by abnormalities in subchondral bone, which
becomes sclerotic and the site of subchondral cysts . Fibrocartilage is
produced at the joint margin, which undergoes endochondral
ossication to form osteophytes. Bone remodelling and cartilage
thinning slowly alter the shape of the OA joint, increasing its surface
area. It is almost as though there is a homeostatic mechanism
operative in
OA that causes enlargement of the failing joint to spread the
mechanical load over a greater surface area. Patients with OA also have
higher BMD values at sites distant from the joint and this is particularly
associated with osteophyte formation. This is in keeping with
observations made in epidemiological studies that show that patients
with OA are partially protected from developing osteoporosis and vice
versa. This is likely to be due to the fact that the genetic factors that
.predispose to osteoporosis might be protective for OA
The synovium in OA is often hyperplastic and may be the site of
inammatory change, but to a much lesser extent than in RA and
other inammatory arthropathies. Osteochondral bodies commonly
occur within the synovium, reecting chondroid metaplasia or
secondary uptake and growth of damaged cartilage fragments. The
outer capsule also thickens and contracts, usually retaining the stability
of the remodelling joint. The muscles surrounding affected joints
commonly show evidence of wasting and non-specic type II bre
.atrophy
 Clinical features
Osteoarthritis has a characteristic distribution, mainly targeting the hips,
knees, PIP and DIP joints of the hands, neck and lumbar spine (see Fig.
26.10). The main presenting symptoms are pain and functional restriction.
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.
Pain may also result from bursitis and enthesopathy secondary to altered
joint mechanics. Typical OA pain has the characteristics listed in Box 26.37.
For many people, functional restriction of the hands, knees or hips is an
equal, if not greater, problem than pain. The clinical ndings vary
.according to severity, but are principally those of joint damage
The correlation between the presence of structural change, as assessed
by imaging, and symptoms such as pain and disability varies markedly
according to site. It is stronger at the hip than at the knee and weak at
most small joints. This suggests that the risk factors for pain and
disability may differ from those for structural change. At the knee, for
example, reduced quadriceps muscle strength and adverse psychosocial
factors (anxiety, depression) correlate more strongly with pain and
disability than the degree of radiographic change. Radiological evidence
of OA is very common in middle-aged and older people, and the
disease may coexist with other conditions, so it is important to
.remember that pain in a patient with OA may be due to another cause
 Generalised nodal OA
Characteristics of this common form of OA are shown in Box 26.38.
Some patients are asymptomatic whereas others develop pain, stiffness
and swelling of one or more PIP and DIP joints of the hands from the
age of about 40 years onwards. Gradually, these develop posterolateral
swellings on each side of the extensor tendon, which slowly enlarge
and harden to become Heberden’s (DIP) and Bouchard’s (PIP) nodes
(Fig. 26.17). Typically, 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 a result of osteophyte
formation and often show characteristic lateral deviation, reecting the
asymmetric focal cartilage loss of OA (Fig. 26.18). Involvement of the rst
carpometacarpal (CMC) joint 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 also at increased
.risk of OA at other sites, especially the knee
 Knee OA
At the knee, OA principally targets the patello-femoral and medial
tibiofemoral compartments, but eventually spreads to affect the whole of
thejoint (Fig. 26.19). It may be isolated or occur as part of generalised
nodal OA. Most patients have bilateral and symmetrical involvement. In
men, trauma is often 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 difcult. Local examination ndings may include
a jerky, asymmetric (antalgic) gait with less time weight-bearing on the
painful side  a varus (Fig. 26.20) or, less commonly, valgus and/or a
xed exion deformity  joint-line and/or periarticular tenderness
(secondary anserine bursitis and medial ligament enthesopathy (see
Box 26.25), causing tenderness of the upper medial tibia)
weakness and wasting of the quadriceps muscle  restricted exion
.and extension with crepitus  bony swelling around the joint line
CPP crystal deposition in association with OA is common at the knee.
This may result in a more overt inammatory component (stiffness,
effusions) and super-added acute attacks of synovitis (acute CPP crystal
arthritis), which may be associated with more rapid radiographic and
.clinical progression
 Hip OA
Hip OA most commonly targets the superior aspect of the joint (Fig. 26.21). It 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 con- ned to women. It is
often bilateral at presentation and can be associated with generalised 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
difculties are the same as for knee OA; in addition, restricted hip abduction in
:women may cause pain during sexual intercourse. Examination may reveal
  an antalgic gait  weakness and wasting of quadriceps and gluteal •
muscles
pain and restriction of internal rotation with the hip exed – 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  xed exion, external rotation
deformity of the hip  ipsilateral leg shortening with severe joint
attrition and superior femoral migration. Obesity is associated with
.more rapid progression of hip OA
 Spine OA
The cervical and lumbar spine are the sites most often targeted by OA,
where it is referred to as cervical spondylosis and lumbar spondylosis,
respectively (Fig. 26.22). 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
Rarely, 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, specic causes of OA need to be considered in people with
early-onset disease affecting several joints, especially those not
normally targeted by OA, in which case rare causes need to be
.considered (Box 26.39)
 Kashin–Beck disease is a rare form of OA that occurs in children, •
typically between the ages of 7 and 13, in some regions of China. The
cause is unknown, but suggested predisposing factors are selenium
deciency and contamination of cereals with mycotoxin-producing
.fungi
Erosive OA This term is used to describe an unusual group of patients
with hand OA who have a more prolonged symptom phase, more overt
inammation, 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 joints should be performed and often will show one or
more of the typical features of OA (see Fig. 26.16 and Figs. 26.18–26.22). In addition
to providing diagnostic information, X-rays are of value in assessing the severity of
structural change, which is helpful if joint replacement surgery is being considered.
Non-weight-bearing postero-anterior views of the pelvis are adequate for assessing
hip OA. Patients with suspected knee OA should have standing anteroposterior X-
rays taken to assess tibio-femoral cartilage loss and a exed skyline view to assess
patello-femoral involvement. Spine OA can often be diagnosed on a 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, though
inammatory OA can be associated with a mild acute phase response. Synovial
.uid aspirated from an affected joint is viscous, with a low cell count
Unexplained early-onset OA requires additional investigation, guided by
the suspected underlying condition. X-rays may show typical features of
dysplasia or osteonecrosis, widening of joint spaces in acromegaly,
multiple cysts, chondrocalcinosis and MCP joint involvement in
.haemochromatosis or disorganised architecture in neuropathic joints
 Management
Treatment follows the general principles outlined earlier this chapter.
Measures that are pertinent in older people are summarised in Box
26.40 Education It is important to explain the nature of the condition
fully, outlining the role of relevant risk factors such as obesity, heredity
and trauma. The patient should be informed that established structural
changes are permanent and that, although a cure is not possible, pain
and function can often be improved. The prognosis should also be
discussed, mentioning that it is generally good for nodal hand OA and
.better for knee than hip OA
 Lifestyle advice Weight loss has a substantial benecial effect on •
symptoms if the patient is obese and is probably one of the most
effective treatments available for OA of the lower limbs. Strengthening
and aerobic exercises also have benecial effects in OA and should be
advised, preferably with reinforcement by a physiotherapist. Quadriceps
strengthening exercises are particularly benecial in knee OA. Shock-
absorbing footwear, pacing of activities, use of a walking stick for painful
knee or hip OA, and provision of built-up shoes to equalise leg lengths
can all improve symptoms. Non-pharmacological therapy Acupuncture
and transcutaneous electrical nerve stimulation (TENS) can be effective
in knee OA. Local physical therapies, such as heat or cold, can sometimes
.give temporary relief
Pharmacological therapy If symptoms do not respond to non-
pharmacological measures, paracetamol should be tried. Addition of a topical
NSAID and then capsaicin for knee and hand OA can also be helpful. Oral
NSAIDs should be considered in patients who remain symptomatic. These
drugs are significantly more effective than paracetamol and can be
successfully combined with paracetamol or compound analgesics if the pain
is severe. Strong opiates may occasionally be required. Antineuropathic
drugs, such as amitriptyline, gabapentin and pregabalin, are sometimes used
in patients with symptoms that are difcult to control, but the evidence
base for their use is poor. Neutralising antibodies to nerve growth factor have
been developed and are an effective treatment for pain in OA, but they are
.not yet licensed for routine clinical use
Intra-articular injections Intra-articular glucocorticoid injections are
effective in the treatment of knee OA and are also used for symptomatic
relief in the treatment of OA at the rst CMC joint. The duration of effect
is usually short, but trials of serial glucocorticoid injections every 3 months
in knee OA have shown efcacy for up to 1 year. Intra-articular injections
of hyaluronic acid can help to an extent in knee OA, but the treatment is
expensive and the effect short-lived. In the UK they have not been
considered to be costeffective by NICE. Neutraceuticals Chondroitin
sulphate and glucosamine sulphate have been used alone and in
combination for the treatment of knee OA. There is evidence from
randomised controlled trials that these agents can improve knee pain to a
.small extent (3%–5%) compared with placebo
Surgery Surgery should be considered for patients with OA whose
symptoms and functional impairment impact signicantly on their quality
of life despite optimal medical therapy and lifestyle advice. Total joint
replacement surgery is by far the most common surgical procedure for
patients with OA. It can transform the quality of life for people with severe
knee or hip OA and is indicated when there is signicant structural
damage on X-ray. Although surgery should not be undertaken at an early
stage during the development of OA, it is important to consider it before
functional limitation has become advanced since this may compromise
outcome. Patient-specic factors, such as age, gender, smoking and
presence of obesity, should not be barriers to referral for joint
.replacement
 Only a small proportion of patients with OA progress to the extent •
that total joint replacement is required, but OA is by far the most
frequent indication for this. Over 95% of joint replacements continue
to function well into the second decade after surgery and most
provide life-long, painfree function. Up to 20% of patients are not
satised with the outcome, however, and a few experience little or
no improvement in pain. Other surgical procedures are performed
much less frequently. Resurfacing of the femoral head can be
considered for younger patients with hip OA
as an alternative to total joint replacement. Tibial osteotomy )age < 60(
represents an alternative to total joint replacement in younger patients
with knee OA and can be effective at improving pain by altering
alignment of the lower leg. Cartilage repair is sometimes performed to
treat focal cartilage defects resulting from joint injury