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Osteoarthritis (OA) is the most common type of arthritis. Its high prevalence,
especially in the elderly, and the high rate of disability related to disease make it a leading
cause of disability in the elderly. Because of the aging of Western populations and because
obesity, a major risk factor, are increasing in prevalence, the occurrence of osteoarthritis is on
the rise. In the United States, osteoarthritis prevalence will increase from 66–100% by the
year 2020.1,2
Osteoarthritis (OA) is a chronic disorder of synovial joints in which there is
progressive softening and disintegration of articular cartilage accompanied by new growth of
cartilage and bone at the joint margins (osteophytes), cyst formation and sclerosis in the
subchondral bone, mild synovitis and capsular fibrosis. It differs from simple wear and tear in
that it is asymmetrically distributed, often localized to only one part of a joint and often
associated with abnormal loading rather than frictional wear. In its most common form, it is
unaccompanied by any systemic illness and, although there are sometimes local signs of
inflammation, it is not primarily an inflammatory disorder.1,2
It is also not a purely degenerative disorder, and the term ‘degenerative arthritis’ –
which is often used as a synonym for OA – is a misnomer. Osteoarthritis is a dynamic
phenomenon; it shows features of both destruction and repair. Cartilage softening and
disintegration are accompanied from the very outset by hyperactive new bone formation,
osteophytosis and remodelling. The final picture is determined by the relative vigour of these
opposing processes. In addition, there are various secondary factors which influence the
progress of the disorder: the appearance of calcium-containing crystals in the joint; ischaemic
changes (especially in elderly people) which result in areas of osteonecrosis in the
subchondral bone; the appearance of joint instability; and the effects of prolonged antiinflammatory medication. 1,2
OA affects certain joints, yet spares others . Commonly affected joints include the
cervical and lumbosacral spine, hip, knee, and first metatarsal phalangeal joint (MTP). In the
hands, the distal and proximal interphalangeal joints and the base of the thumb are often
affected. Usually spared are the wrist, elbow, and ankle. Our joints were designed in an

evolutionary sense, when humans were still brachiating apes. We thus develop OA in joints
that were ill designed for these tasks, i.e., joints involved in pincer grip in the hands and
lower extremity weight-bearing joints. Some joints, like the ankles, may be spared because
their articular cartilage may be uniquely resistant to loading stresses. 1,2
OA can be diagnosed based on structural abnormalities or on the symptoms these
abnormalities evoke. Based on cadaveric studies, structural changes of OA are nearly
universal by the elderly years. These include cartilage loss (seen as joint space loss on x-rays)
and osteophytes. Many persons with x-ray evidence of OA have no joint symptoms and,
while the prevalence of structural abnormalities is of interest in understanding disease
pathogenesis, what matters more from a clinical and public health perspective is the
prevalence of symptomatic OA. Symptoms, usually joint pain, determine disability, visits to
clinicians, and disease costs. 1,2
Symptomatic OA of the knee (pain on most days of a recent month in a knee plus xray evidence of OA in that knee) occurs in 12% of persons age ≥60 in the United States and
6% of all adults age ≥30. Symptomatic hip OA is roughly one-third as common as disease in
the knee. While radiographically evident hand OA and the appearance of bony enlargement in
affected hand joints are extremely common in older persons, most cases are often not
symptomatic. Even so, recent studies suggest that symptomatic hand OA occurs in 10% of
elderly individuals and often produces measurable physical functional limitation. 1,2
The prevalence of OA correlates strikingly with age. Regardless of how it is defined,
OA is uncommon in adults under age 40 and highly prevalent in those over age 60. It is also a
disease that, at least in middle- aged and elderly persons, is much more common in women
thanin men, and sex differences in prevalence increase with age. 1,2
Osteoarthritis (OA) is the most common form of arthritis and a leading cause of
chronic disability, in large part due to knee and/or hip involvement. The societal burden of
OA relates to its pervasive presence. For example, in the Rotterdam study, only 135 of 1040
persons 55 to 65 years of age were free of radiographic OA (definite osteophyte presence or
more severe) in the hands, knees, hips, or spine. Not all OA is symptomatic; still, the World
Health Organization estimates that OA is a cause of disability in at least 10% of the
population over age 60 years2and OA affects the lives of more than 20 million Americans.
Knee OA alone was as often associated with disability as were heart and chronic lung
disease.Current treatments for OA may improve symptoms but do not delay progression.
Progression of OA to advanced and disabling stages is the leading indication for joint
replacement. 3
The increase in the prevalence of symptomatic OA with age, coupled with the
inadequacy of symptom-relieving or disease-modifying treatment, contributes to its impact.
The number of persons in the U.S. with arthritis is anticipated to rise from 15% of the
population (40 million) in 1995 to 18% of the population (59 million) by 2020. 3 A better
understanding of the factors that contribute to disease and disability in OA is a high priority,
especially given the lack of disease-modifying treatment options. 3

Epidemiologic studies, in addition to incidence and prevalence data, have supplied
much of what is known about the natural history of OA and predisposing or protective
factors. In addition, epidemiologic investigation has provided information to aid the
performance and interpretation of clinical trials; such background information is critical in a
disease like OA, which is heterogeneous in its expression and variably progressive.3
Hyaline cartilage, the pearly gristle which covers the bone ends in every diarthrodeal
joint, is supremely adapted to transmit load and movement from one skeletal segment to
another. It increases the area of the articular surfaces and helps to improve their adaptability
and stability; it changes its shape under load and distributes compressive forces widely to the
subarticular bone; and, covered by a film of synovial fluid, it is more slippery than any manmade material, offering very little frictional resistance to movement and surface gliding. 5
This specialized connective tissue has a gel-like matrix consisting of a proteoglycan
ground substance in which are embedded an architecturally structured collagen network and a
relatively sparse scattering of specialized cells, the chondrocytes, which are responsible for
producing all the structural components of the tissue. It has a high water content (60–80 per
cent), most of which is exchangeable with the synovial fluid.5
Chondrocytes of adult hyaline cartilage have little capacity for cell division in vivo
and direct damage to the articular surface is poorly repaired, or repaired only with
fibrocartilage. The fact that the normal wear of daily joint activity does not result in
degradation of the articular surface is due to the highly effective lubricating mechanisms
bestowed by synovial fluid. In another sense, though, chondrocytes do undertake repair: in
the early stages of cartilage degradation, matrix molecular constituents will be replenished by
increased chondrocyte activity. The proteoglycans exist mainly in the form of aggrecan, a
large aggregating molecule with a protein core along which are arranged up to 100
chondroitin sulphate and keratan sulphate glycosaminoglycans (GAGs), rather like the
bristles on a bottlebrush. 5
Hundreds of aggrecan molecules are linked, in turn, to a long unbranched hyalurinate
chain (hyaluronan), to form an even larger molecule with a molecular weight of over 100
million daltons. These negatively charged macromolecules are responsible for the stiffness
and springiness of articular cartilage.The fibrillar component of articular cartilage is mainly
type II collagen. The collagen bundles are arranged in structured patterns, parallel to the
articular surface in the superficial zones and perpendicular to the surface in the deeper layers
where they anchor the articular cartilage to the subchondral bone. 5
The main functions of aggrecan are to absorb changes in load and mitigate
deformation, while the collagen network copes with tensile forces. There is considerable
interaction between the molecules of each component and between the molecules of the
different components of cartilage: if these links are degraded or broken, the cartilage will tend
to unravel. This happens to some degree with ageing, but much more so in pathological states
leading to osteoarthritis. 5

Proteoglycan has a strong affinity for water, resulting in the collagen network being
subjected to considerable tensile stresses. With loading, the cartilage deforms and water is
slowly squeezed onto the surface where it helps to form a lubricating film. When loading
ceases, the surface fluid seeps back into the cartilage up to the point where the swelling
pressure in the cartilage is balanced by the tensile force of the collagen network. As long as
the network holds and the proteoglycans remain intact, cartilage retains its compressibility
and elasticity. If the collagen network is degraded or disrupted, the matrix becomes water
logged and soft; this, in turn, is followed by loss of proteoglycans, cellular damage and
splitting (‘fibrillation’) of the articular cartilage. Trouble mounts up further as the damaged
chondrocytes begin to release matrix-degrading enzymes. 5

Diagram showing the components of a synovial joint
The soft tissues enclosing the joint consist of a fibrous capsule with tough
condensations on its surface – the ligaments – which, together with the overlying muscles,
help to provide stability. The ligaments running from one bone to another are inelastic and
have a fixed length. Not surprisingly, therefore, they are under different degrees of tension in
different positions of the joint. When the joint assumes a position where the ligaments are
fully taut, they provide maximum stability and may keep the joint ‘locked’ even without the
assistance of muscles; when less taut they permit a certain degree of laxity in the joint; and
when they are overstretched or torn the joint becomes unstable. 5
Non-pathological ligamentous laxity is a fairly common heritable trait which is
employed to astonishing (and sometimes bizarre) effect by acrobatic performers; stability is
maintained by highly developed muscle power and the articular cartilage is not necessarily
damaged. Inflamed or injured joints that need splinting should always be held in the position
where the ligaments are fully taut; if the ligaments are allowed to fibrose and shorten in the

‘relaxed’ position it may take months (or be impossible) to regain full passive movement
afterwards. 5
The interior surface of the capsule is lined by a thin membrane, the synovium, which
is richly supplied with blood vessels, lymphatics and nerves. It provides a nonadherent
covering for the articular surfaces and it produces synovial fluid, a viscous plasma dialysate
laced with hyaluronan. This fluid nourishes the avascular articular cartilage, plays an
important part in reducing friction during movement and has slight adhesive properties which
assist in maintaining joint stability. 5
In normal life the volume of synovial fluid in anyparticular joint remains fairly
constant, regardless of movement. When a joint is injured fluid increases (as in any bruised or
oedematous connective tissue) and this appears as a joint effusion. Synovium is also the
target tissue in joint infections and autoimmune disorders such as rheumatoid arthritis. 5
The coefficient of friction in the normal joint is extremely low – one reason why,
barring trauma or disease, there is little difference in the amount of wear on articular surfaces
between young adults and old people. This extraordinary slipperiness of cartilage surfaces is
produced by a highly efficient combination of lubricating systems. 5
Boundary layer lubrication at the bearing surfaces is mediated by a large, water
soluble glycoprotein fraction, lubricin, in the viscous synovial fluid. A single layer of
molecules attaches to each articular surface and these glide upon each other in a manner that
has been likened to surfaces rolling on miniscule ballbearings. This is most effective at points
of direct contact. 5
Fluid film lubrication is provided by the hydrodynamic mechanism described earlier
(see under Articular cartilage). During movement and loading fluid is squeezed out of the
proteoglycan-rich cartilage and forms a thin ‘cushion’ where contact is uneven, then seeps
back into the cartilage when loading ceases. Lubrication between synovial folds is provided
by hyalurinate molecules in the synovial fluid. 5
The most obvious thing about OA is that it increases in frequency with age. This does
not mean that OA is simply an expression of senescence. Cartilage does‘age’, showing
diminished cellularity, reduced proteoglycan concentration, loss of elasticity and a decrease
in breaking strength with advancing years. These factors may well predispose to OA, but it is
significant that the progressive changes which are associated with clinical and radiological
deterioration are restricted to certain joints, and to specific areas of those joints, while other
areas show little or no progression with age . 1,2,3,6
Primary changes in cartilage matrix might (theoretically) weaken its structure and
thus predispose to cartilage breakdown; crystal deposition disease and ochronosis are wellknown examples.‘Inheritance’ has for many years been thought to play a role in the

development of OA. A number of studies have demonstrated a significant increase in the
prevalence of generalized OA in first-degree relatives of patients with OA as compared with
controls and others have published similar observations for OA of the hip.1,2
However, one should bear in mind that OA of large joints is often attributable to
anatomical variations, e.g. acetabular dysplasia and other forms of epiphyseal dysplasia, and
it is these that are inherited rather than any tendency to develop OA as a primary abnormality.
At the molecular level, genetic defects in type II collagen have been demonstrated in some
cases, but it is unlikely that this is a major aetiological factor in the majority of cases.
Articular cartilage may be damaged by trauma or previous inflammatory disorders. Enzymes
released by synovial cells and leucocytes can cause leaching of proteoglycans from the
matrix, and synovial-derived interleukin-1 (IL-1) may suppress proteoglycan synthesis. This
could explain the appearance of ‘secondary’OA in patients with rheumatoid diseases; whether
similar processes operate in ‘primary’ (‘idiopathic’) OA is unknown.1,6
In most cases the precipitating cause of OA is increased mechanical stress in some
part of the articular surface. This may be due to increased load (e.g. in deformities that affect
the lever system around a joint) or to a reduction of the articular contact area (e.g. with joint
incongruity or instability). Both factors operate in varus deformity of the knee and in
acetabular dysplasia – common precursors of OA. Changes in the subchondral bone may also
increase stress concentration in the overlying cartilage, either by altering the shape of the
articular surface or by an increase in bone density (e.g. following fracture healing) which
reduces the shock-absorbing effect of the supporting cancellous bone. From the foregoing
outline it should be apparent that the division of osteoarthritis into ‘primary’ (when there is
no obvious antecedent factor) and ‘secondary’ (when it follows a demonstrable abnormality)
is somewhat artificial. This is borne out in clinical practice: patients with ‘secondary’ OA of
the knee following meniscectomy have been found also to have a higher than usual incidence
of ‘primary’ OA in other joints. Perhaps primary, generalized factors (genetic, metabolic or
endocrine) alter the physical properties of cartilage and thereby determine who is likely to
develop OA, while secondary factors such as anatomical defects or trauma specify when and
where it will occur. OA is, ultimately, more process than disease, occurring in any condition
which causes a disparity between the mechanical stress to which articular cartilage is exposed
and the ability of the cartilage to withstand that stress.1,23,6
The initial stages of OA have been studied in animal models with induced joint
instability and may not be representative of all types of OA. The earliest changes, while the
cartilage is still morphologically intact, are an increase in water content of the cartilage and
easier extractability of the matrix proteoglycans; similar findings in human cartilage have
been ascribed to failure of the internal collagen network that normally restrains the matrix
gel. At a slightly later stage there is loss of proteoglycans and defects appear in the cartilage.
As the cartilage becomes less stiff, secondary damage to chondrocytes may cause release of
cell enzymes and further matrix breakdown. Cartilage deformation may also add to the stress
on the collagen network, thus amplifying the changes in a cycle that leads to tissue

Articular cartilage has an important role in distributing and dissipating the forces
associated with joint loading. When it loses its integrity these forces are increasingly
concentrated in the subchondral bone. The result: focal trabecular degeneration and cyst
formation, as well as increased vascularity and reactive sclerosis in the zone of maximal
loading. What cartilage remains is still capable of regeneration, repair and remodelling. As
the articular surfaces become increasingly malapposed and the joint unstable, cartilage at the
edges of the joint reverts to the more youthful activities of growth and endochondral
ossification, giving rise to the bony excrescences, or osteophytes, that so clearly distinguish
osteoarthritis (once called ‘hypertrophic arthritis’) from ‘atrophic’disorders such as
rheumatoid disease.1,2
Joint dysplasia Disorders such as congenital acetabular dysplasia and Perthes’ disease
presage a greater than normal risk of OA in later life. It is not always easy to spot minor
degrees of dysplasia and careful studies may have to be undertaken if these are not to be
Trauma Fractures involving the articular surface are obvious precursors of secondary
OA, so too lesser injuries which result in joint instability. What is less certain is whether
malunion of a long-bone fracture predisposes to OA by causing segmental overload in a joint
above or below the healed fracture (for example, in the knee or ankle after a tibial fracture).
Contrary to popular belief, research has shown that moderate angular deformities of the tibia
(up to 15 degrees) are not associated with an increased risk of OA (Merchant and Dietz,
1989). This applies to mid-shaft fractures; malunion close to a joint may well predispose to
secondary OA.1,2,3,6

Occupation There is good evidence of an association between OA and certain
occupations which cause repetitive stress, for example OA of the knees in workers engaged in
knee-bending activities (Felson, 1991), OA in the upper limbs in people working with heavy
vibrating tools (Schumacher et al., 1972) and OA of the hands in cotton mill workers
(Lawrence, 1961). More controversial is the relationship of OA to sporting activity. Boxers
are certainly prone to developing OA of the hands but this may be due to trauma. The same
applies to footballers with OA of the knees and baseball pitchers with OA of the shoulder.
More convincing evidence of a causative relationship comes from recent studies which have
shown a significant increase in the risk of hip and knee OA in athletes (Harris et al., 1994;
Kulkala et al., 1994).1,2
Bone density It has long been known that women with femoral neck fractures seldom
have OA of the hip. This negative association between OA and osteoporosis is reflected in
more recent studies which have demonstrated a significant increase in bone mineral density
in people with OA compared to those without (Hannan et al., 1992; Hart et al., 1994).
However, this may not be simple cause and effect: bone density is determined by a variety of
genetic, hormonal and metabolic factors which may also influence cartilage metabolism
independently of any effect due to bone density. 1,2
Obesity The simple idea that obesity causes increased joint loading and therefore
predisposes to OA may be correct – at least in part. The association is closer in women than
in men and therefore (as with bone density) it may reflect other endocrine or metabolic
factors in the pathogenesis of OA.1,2,3,6
Family history Women whose mothers had generalized OA are more likely to develop
the same condition. The particular trait responsible for this is not known.1
Osteoarthritis (OA) is a condition that represents a pathological imbalance of
degradative and reparative processes involving the whole joint and its component parts, with
secondary inflammatory changes, particularly in the synovium, but also in the articular
cartilage itself . Idiopathic primary OA may involve one particular joint, or it may be
generalized or involve multiple joints in erosive inflammatory forms. The presentation of this
pathological condition in joints may be a consequence of the biomechanics within the joint
which reveal otherwise masked systemic genetically determined changes. The mechanical
pressures within the joint may therefore reveal weaknesses in tissue maintenance that are
more widespread than previously considered.3
Most forms of OA fall into two categories, depending on the predominant
background: those that are primary, and often idiopathic, with abnormalities of joint
biomaterial and biomechanically faulty joint structure that may result from a recognizable
mutation, and those that are secondary and result from superimposed risk factors affecting
distribution and severity of loading forces acting on specific joints, such as joint injury.3

Peripheral joints (single vs. multiple joints)
Interphalangeal joints (nodal) (e.g., distal
interphalangeal, proximal interphalangeal)
carpometacarpal, first metacarpophalangeal)
Large joints (e.g., hip, knee)
Apophyseal joints
Intervertebral joints
Erosive inflammatory osteoarthritis
Generalized osteoarthritis
Chondromalacia patellae
Diffuse idiopathic skeletal hyperostosis
(DISH, ankylosing hyperostosis

Chronic (occupational, sports, obesity)
Local (fracture, avascular necrosis, infection)
Diffuse (rheumatoid arthritis, hypermobility
syndrome, hemorrhagic diatheses)
Ochronosis (alkaptonuria)
Wilson disease
Kashin-Beck disease
Diabetes mellitus
Calcium pyrophosphate dihydrate
Calcium apatite
(e.g., tabes dorsalis, diabetes mellitus, intraarticular steroid overuse)
with skeletal dysplasias such as multiple
epiphyseal dysplasia, spondyloepiphyseal
Long-leg arthropathy

Patients usually present after middle age. Joint involvement follows several different
patterns: symptoms centre either on one or two of the weightbearing joints (hip or knee), on
the interphalangeal joints (especially in women) or on any joint that has suffered a previous
affliction (e.g. congenital dysplasia, osteonecrosis or intra-articular fracture). A family history
is common in patients with polyarticular OA.1
Pain is the usual presenting symptom. It is often quite widespread, or it may be
referred to a distant site – for example, pain in the knee from OA of the hip. It starts
insidiously and increases slowly over months or years. It is aggravated by exertion and
relieved by rest, although with time relief is less and less complete. In the late stage the
patient may have pain in bed at night. There are several possible causes of pain: mild synovial
inflammation, capsular fibrosis with pain on stretching the shrunken tissue; muscular fatigue;
and, perhaps most important of all, bone pressure due to vascular congestion and intraosseous

Stiffness is common; characteristically it occurs after periods of inactivity, but with
time it becomes constant and progressive.1,2,3
Swelling may be intermittent (suggesting an effusion) or continuous (with capsular
thickening or large osteophytes). 1,2,3
Deformity may result from capsular contracture or joint instability, but be aware that
the deformity may actually have preceded and contributed to the onset of OA. 1,2,3
Loss of function, though not the most dramatic, is often the most distressing symptom.
A limp, difficulty in climbing stairs, restriction of walking distance, or progressive inability to
perform everyday tasks or enjoy recreation may eventually drive the patient to seek help. 1,
Typically, the symptoms of OA follow an intermittent course, with periods of
remission sometimes lasting for months. 1,2,3

Joint swelling may be the first thing one notices in peripheral joints (especially the
fingers, wrists, knees and toes). This may be due to an effusion, but hard (‘knobbly’) ridges
around the margins of the distal interphalangeal, the first metatarsophalangeal or knee joints
can be just as obvious. 1,2,3
Tell-tale scars denote previous abnormalities, and muscle wasting suggests
longstanding dysfunction. 1,2,3
Deformity is easily spotted in exposed joints (the knee or the large-toe
metatarsophalangeal joint), but deformity of the hip can be masked by postural adjustments
of the pelvis and spine.1
Local tenderness is common, and in superficial joints fluid, synovial thickening or
osteophytes may be felt.1
Limited movement in some directions but not others is usually a feature, and is
sometimes associated with pain at the extremes of motion. 1,2,3
Crepitus may be felt over the joint (most obvious in the knee) during passive
movements. 1,2,3
Instability is common in the late stages of articular destruction, but it may be detected
much earlier by special testing. Instability can be due to loss of cartilage and bone,
asymmetrical capsular contracture and/or muscle weakness. 1,2,3
Other joints should always be examined; they may show signs of a more generalized
disorder. It is also helpful to know whether problems in other joints add to the difficulties in
the one complained of (e.g. a stiff lumbar spine or an unstable knee making it more difficult
to cope with restricted movement in an osteoarthritic hip). 1,2,3
Function in everyday activities must be assessed. X-ray appearances do not always
correlate with either the degree of pain or the patient’s actual functional capacity. Can the
patient with an arthritic knee walk up and down stairs, or rise easily from a chair? Does he or
she limp? Or use a walking stick?1,3

The components of a comprehensive physical examination are outlined in . Body
habitus and gait are observed. Antalgia, medial or lateral thrusts, and other dynamic
compensatory gait patterns (quadriceps avoidance, out-toeing) are determined. Clinically,
static limb alignment and deformity serve as a rough index of the duration and severity of the
disease process. In long-standing primary OA or secondary OA after trauma or
meniscectomy, genuvarum suggests medial compartment involvement and genu valgum
suggests lateral compartment involvement. With long-standing deformity, patients may
exhibit pseudolaxity due to stretching of the collateral ligaments on the contralateral side of
the affected compartment. 1,3
Range of motion with side-to-side comparison is assessed in the supine and prone
positions. Patients may commonly present with a mild flexion contracture (i.e., <10°) and
lack full flexion (i.e., by >20°). Larger losses of motion are unusual in active individuals.
Patients may complain of swelling or perceive stiffness due to swelling. Patellofemoral or
joint line crepitus is a common finding. 1,3
Patellofemoral evaluation includes patellar tilt, lateral and medial patellar glide, and
patellar facet tenderness as described in the section on anterior knee pain and patellofemoral
disorders. Stability in the coronal plane (i.e., varus or valgus at 0° and 30° of flexion) and
sagittal (anteroposterior) plane is determined. Positive results of the Lachman and pivot shift
tests may indicate chronic anterior cruciate ligament insufficiency. Similarly, loss of the
normal 5 to 10 mm of anteromedial tibial step-off relative to the medial femoral condyle or
the presence of a tibial “sag sign” with the hip and knee held in 90° of flexion in the
supine position may be indicative of chronic posterior cruciate ligament insufficiency. 1,3
Evaluation for joint line tenderness and swelling, and provocative meniscal tests such
as the McMurray test are performed. The McMurray test is performed with the patient in the
supine position with the hip and knee flexed to 90° while the axially loaded foot is
maneuvered from a position of abduction and external rotation to one of adduction and
internal rotation to elicit a painful ,pop or click in the affected compartment. The hip, back,
and neurovascular status are evaluated for additional pathologic changes including losses in
motion, with the need for radiographic imaging of these regions if a concomitant pathologic
process is suspected. 1,3
An accurate history and a thorough examination must precede special tests that are to
confirm the diagnosis of OA. Currently there is no single reliable diagnostic test; thus a
stepwise approach is employed. In straightforward symptomatic cases, plain radiography is
often all that is necessary to confirm the diagnosis. If the process is thought to be linked to
crystal deposition disease or secondary to an inflammatory arthropathy, a full workup
including urate levels, full blood count, erthyrocyte sedimentation rate, C-reactive protein,
rheumatoidfactor, and autoantibody screen may be indicated. 1,3

Plain radiography may be unremarkable in the early stages, but joints exhibiting
classic disease demonstrate characteristic features, as noted by Kellgren and Lawrence, who
encouraged the classification of OA solelyon radiologic grounds . Alternative grading
systems have evolved since the 1950s, but physicians and surgeons still regard the
radiographic presence of osteophytes, loss of joint space, subchondral sclerosis, and cyst
formation, combined with a suggestive history,as diagnostic of OA. 1,6

Magnetic resonance imaging (MRI) is playing an increasingly important role in the
diagnosisof early OA. In addition to quantifying the extent of the disease, MRI is useful in
discriminating between OA and non-OA pain in or around joints that cannot be clinically
differentiated. For example, the pain of transient osteoporosis in the distal femur/proximal
tibia or hip presents like OA of the knee and hip and cannot usually be seen on plain
radiographs. Patients with that type of pain do not benefit from arthroscopy or intraarticular
joint injection.1,2,3,6
Bone scans are of limited value in the diagnosis of OA. Their use tends to be
restricted to the elimination of more sinister pathologies, such as primary or secondary
malignancy and osteomyelitis. Diagnostic hip injection using a mixture of a local anesthetic
and steroid and done under fluoroscopic guidance is commonly performed in patients who
complain of nonclassic hip pain or have concurrent back pain. If the patient reports a
significant improvement following the injection, the pathology probably has originated in the

Severe tricompartmental osteoarthritis. A, Lateral, B, Frontal, and C, Merchant view radiographs of
the left knee reveal joint space obliteration in the medial femoral tibial, lateral femoral tibial, and
patellofemoral compartments; varus angulation and lateral subluxation of the tibia; and osteophyte

Arthroscopy of osteoarthritic joints is a useful diagnostic and increasingly therapeutic
aid to the surgeon. Most major joints that are affected by the disease are now within anatomic
reach of modern arthroscopic equipment. Chondral changes are graded according to the
modified Outerbridge classification . The original description referred only to radiographic
changes of chondromalacia patellae. The modified classifications represent similar grading
scales, but rely on arthroscopic observations. They describe the spectrum of change from
chondral softening on probing to grade 4 changes, representing OA.1,3

A number of conditions may mimic OA, some presenting as a monarthritis and some
as a polyarthritis affecting the finger joint.1,3
Avascular necrosis ‘Idiopathic’ osteonecrosis causes joint pain and local effusion.
Early on the diagnosis is made by MRI. Later x-ray appearances are usually pathognomonic;

however, once bone destruction occurs the x-ray changes can be mistaken for those of OA.
The cardinal distinguishing feature is that in osteonecrosis the ‘joint space’ (articular
cartilage) is preserved in the face of progressive bone collapse and deformity, whereas in OA
articular cartilage loss precedes bone destruction.1,3
Inflammatory arthropathies Rheumatoid arthritis, ankylosing spondylitis and Reiter’s
disease may start in one or two large joints. The history is short and there are local signs of
inflammation. X-rays show a predominantly atrophic or erosive arthritis. Sooner or later other
joints are affected and systemic features appear.1,3
Polyarthritis of the fingers Polyarticular OA may be confused with other disorders
which affect the finger joints (see Fig. 5.10). Close observation shows several distinguishing
features. Nodal OA affects predominantly the distal joints, rheumatoid arthritis the proximal
joints. Psoriatic arthritis is a purely destructive arthropathy and there are no interphalangeal
Tophaceous gout may cause knobbly fingers, but the knobs are tophi, not osteophytes.
X-rays will show the difference.1
Diffuse idiopathic skeletal hyperostosis (DISH) This is a fairly common disorder of
middle-aged people, characterized by bone proliferation at the ligament and tendon insertions
around peripheral joints and the intervertebral discs (Resnick et al., 1975). On x-ray
examination the large bony spurs are easily mistaken for osteophytes. DISH and OA often
appear together, but DISH is not OA: the bone spurs are symmetrically distributed, especially
along the pelvic apophyses and throughout the vertebral column. When DISH occurs by itself
it is usually asymptomatic.1,3
Multiple diagnosis Osteoarthritis is so common after middle age that it is often found
in patients with other conditions that cause pain in or around a joint. Before jumping to the
conclusion that the symptoms are due to the OA features seen on x-ray, be sure to exclude
peri-articular disorders as well as more distant abnormalities giving rise to referred pain.1,3
The goals of the treatment of OA are to alleviate pain and minimize loss of physical
function. To the extent that pain and loss of function are consequences of inflammation, of
weakness across the joint, and of laxity and instability, the treatment of OA involves
addressing each of these impairments. Comprehensive therapy consists of a multimodality
approach including nonpharmacologic and pharmacologic elements. Patients with mild and
intermittent symptoms may need only reassurance or nonpharmacologic treatments. Patients
with ongoing, disabling pain are likely to need both nonpharmaco- and pharmacotherapy.2,3
Treatments for knee OA have been more completely evaluated than those for hip and
hand OA or for disease in other joints. Thus, while the principles of treatment are identical for
OA in all joints, we shall focus below on the treatment of knee OA, noting specific
recommendations for disease in other joints, especially when they differ from those for
disease in the knee.1,2


Since OA is a mechanically driven disease, the mainstay of treatment involves
altering loading across the painful joint and improving the function of joint protectors, so
they can better distributeload across the joint. Ways of lessening focal load across the joint
include : 2
(1) avoiding activities that overload the joint, as evidenced by their causing pain;
(2) improving the strength and conditioning of muscles that bridge the joint, so as to optimize
their function; and
(3) unloading the joint, either by redistributing load within the joint with a brace or a splint or
by unloading the joint during weight bearing with a cane or a crutch.
There is, as yet, no drug that can modify the effects of OA. Treatment is, therefore,
symptomatic. The principles are: (1) maintain movement and muscle strength; (2) protect the
joint from ‘overload’; (3) relieve pain; and (4) modify daily activities.1
Physical therapy The mainstay of treatment in the early case is physical therapy,
which should be directed at maintaining joint mobility and improving muscle strength. The
programme can include aerobic exercise, but care should be taken to avoid activities which
increase impact loading. Other measures, such as massage and the application of warmth,
may reduce pain but improvement is short-lived and the treatment has to be repeated.1,2
Load reduction Protecting the joint from excessive load may slow down the rate of
cartilage loss. It is also effective in relieving pain. Common sense measures such as weight
reduction for obese patients, wearing shock-absorbing shoes, avoiding activities like climbing
stairs and using a walking stick are worthwhile.1,2

While nonpharmacologic approaches to therapy constitute its mainstay,
pharmacotherapy serves an important adjunctive role in OA treatment. Available drugs are
administered using oral, topical, and intraarticular routes. Acetaminophen, Nonsteroidal Antiinflammatory Drugs (NSAIDs), and COX-2 Inhibitors Acetaminophen (paracetamol) is the
initial analgesic of choice for patients with OA in knee, hip, or hands. For some patients, it is
adequate to control symptoms, in which case more toxic drugs such as NSAIDs can be
avoided. Doses up to 1 g 4 times daily can be used.2,3
NSAIDs are the most popular drugs to treat osteoarthritic pain. In clinical trials,
NSAIDs produce 30% greater improvement in pain than highdose acetaminophen.
Occasional patients treated with NSAIDs experience dramatic pain relief, whereas others
experience little improvement. Initially, NSAIDs should be taken on an “as needed” basis
because side effects are less frequent with low intermittent doses, which may be highly
efficacious. If occasional medication use is insufficiently effective, then daily treatment with
NSAIDs is indicated, with an anti-inflammatory dose selected . Patients should be reminded
to take low-dose aspirin and NSAIDs at different times to eliminate drug interactions.2,3
NSAIDs have substantial and frequent side effects, the most common of which is
upper gastrointestinal toxicity, including dyspepsia, nausea, bloating, gastrointestinal
bleeding, and ulcer disease. Some 30–40% of patients experience upper gastrointestinal (GI)
side effects so severe as to require discontinuation of medication. Strategies to avoid or
minimize the risk of nonsteroidal related GI side effects include:2,3

• Take medications after food.
• Avoid use of two NSAIDs.
• Use a relatively safe NSAID. In terms of GI toxicity, meta-analyses have suggested that
nonacetylated salicylates, ibuprofen and nabumetone, are among the safer NSAIDs; more
dangerous ones include piroxicam, ketorolac, and ketoprofen.
• For persons at high risk of GI bleeding and/or complications, prescribe a gastroprotective

Major NSAID-related GI side effects can occur in patients who do not complain of
upper GI symptoms. In one study of patients hospitalized for GI bleeding, 81% had no
premonitory symptoms. There are other common side effects of NSAIDs, including the
tendency to develop edema, because of prostaglandin inhibition of afferent blood supply to
glomeruli in the kidneys and, for similar reasons, a predilection toward reversible renal
insufficiency. Blood pressure may increase modestly in some NSAID-treated patients.2,3
Alternative anti-inflammatory medications are cyclooxygenase-2 (COX- 2) inhibitors.
While their rate of GI side effects may be less than for conventional NSAIDs, their risk of
causing edema and renal insufficiency is similar. In addition, COX-2 inhibitors, especially at
high dose, increase the risk of myocardial infarction and of stroke. This is because selective
COX-2 inhibitors reduce prostaglandin I2 production by vascular endothelium, but do not
inhibit platelet thromboxane A2 production, leading to an increased risk of intravascular

Intraarticular Injections: Glucocorticoids and Hyaluronic Acid
Since synovial Inflammation is likely to be a major cause of pain in patients with OA,
local anti-inflammatory treatments administered intraarticularly may be effective in
ameliorating pain, at least temporarily. Glucocorticoid injections provide such efficacy, but
work better than placebo injections for only 1 or 2 weeks. This may be because the disease
remains mechanicallydriven and, when a person begins to use the joint, the loading factors
that induce pain return. Glucocorticoid injections are useful to get patients over acute flares
of pain and may be especially indicated if the patient has coexistent OA and crystal
deposition disease, especially from calcium pyrophosphate dihydrate crystals . There is no
evidence that repeated glucocorticoid injections into the joint are dangerous.2,3
Hyaluronic acid injections can be given for treatment of symptoms in knee and hip
OA, but there is controversy as to whether they have efficacy vs. placebo . Optimal therapy
for OA is often achieved by trial and error, with each patient having idiosyncratic responses
to specific treatments. When medical therapies have failed and the patient has an
unacceptable reduction in their quality of life and ongoing pain and disability, then at least for
knee and hip OA, total joint arthroplasty is indicated.2,3
Progressive joint destruction, with increasing pain, instability and deformity
(particularly of one of the weightbearing joints), usually requires reconstructive surgery.
Three types of operation have, at different times, held the field: realignment osteotomy,
arthroplasty and arthrodesis. 1,2
Realignment osteotomy Until the development of joint replacement surgery in the
1970s, realignment osteotomy was widely employed. Refinements in techniques, fixation
devices and instrumentation led to acceptable results from operations on the hip and knee,
ensuring that this approach has not been completely abandoned. High tibial osteotomy is still
considered to be a viable alternative to partial joint replacement for unicompartmental OA of
the knee, and intertrochanteric femoral osteotomy is sometimes preferred for young patients
with localized destructive OA of the hip. These operations should be done while the joint is
still stable and mobile and x-rays show that a major part of the articular surface (the
radiographic ‘joint space’) is preserved. Pain relief is often dramatic and is ascribed to (1)
vascular decompression of the subchondral bone, and (2) redistribution of loading forces
towards less damaged parts of the joint. After load redistribution, fibrocartilage may grow to
cover exposed bone.1,2,3
Joint replacement Joint replacement, in one form or another, is nowadays the
procedure of choice for OA in patients with intolerable symptoms, marked loss of function
and severe restriction of daily activities. For OA of the hip and knee in middle-aged and older
patients, total joint replacement by modern techniques promises improvement lasting for 15
years or longer. Similar operations for the shoulder, elbow and ankle are less successful but
techniques are improving year by year. However, joint replacement operations are highly
dependent on technical skills, implant design, appropriate instrumentation and postoperative

care – requirements that cannot always be met, or may not be cost-effective, in all parts of the
Arthrodesis Arthrodesis is still a reasonable choice if the stiffness is acceptable and
neighbouring joints are not likely to be prejudiced. This is most likely to apply to small joints
that are prone to OA, e.g. the carpal and tarsal joints and the large toe metatarsophalangeal

Capsular herniation ,osteoarthritis of the knee is sometimes associated with a marked
effusion and herniation of the posterior capsule (Baker’s cyst). Loose bodies Cartilage and
bone fragments may give rise to loose bodies, resulting in episodes of locking. Rotator cuff
dysfunction Osteoarthritis of the acromioclavicular joint may cause rotator cuff impingement,
tendinitis or cuff tears. Spinal stenosis Longstanding hypertrophic OA of the lumbar
apophyseal joints may give rise to acquired spinal stenosis. The abnormality is best
demonstrated by CT and MRI. Spondylolisthesis In patients over 60 years of age, destructive
OA of the apophyseal joints may result in severe segmental instability and spondylolisthesis
(socalled ‘degenerative’ spondylolisthesis, which almost always occurs at L4/5).1,3



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