REFERAT

OSTEOARTHRITIS

Diajukan guna memenuhi tugas Kepaniteraan Senior di Bagian Ilmu Bedah Fakultas Kedokteran
Universitas Diponegoro

Disusun oleh :
Sulung Ade Pratama
22010118220161

Pembimbing :
dr. Kamal Adib, Sp.OT, M.Kes

KEPANITERAAN SENIOR ILMU BEDAH

FAKULTAS KEDOKTERAN UNIVERSITAS DIPONEGORO
RUMAH SAKIT UMUM DAERAH BATANG
2019
 HALAMAN PENGESAHAN

Nama : Sulung Ade Pratama

NIM : 22010118220161
Judul Referat : Osteoarthritis
Pembimbing : dr. Kamal Adib, Sp.OT, M.Kes

Diajukan guna memenuhi tugas Kepaniteraan Senior di Bagian Ilmu Bedah Fakultas Kedokteran
Universitas Diponegoro

Batang, 25 Maret 2019

Pembimbing

dr. Kamal Adib, Sp.OT, M.Kes

A. Definition1

According to OARSI , osteoarthritis is a disorder involving movable joints characterized by

cell stress and extracellular matrix degradation initiated by micro- and macro-injury that
activates maladaptive repair responses including pro-inflammatory pathways of innate immunity.
The disease manifests first as a molecular derangement (abnormal joint tissue metabolism)
followed by anatomic, and/or physiologic derangements (characterized by cartilage degradation,
bone remodeling, osteophyte formation, joint inflammation and loss of normal joint function),
that can culminate in illness.
According to NICE guideline, osteoarthritis is characterized pathologically by localized loss
of cartilage, remodeling of adjacent bone and associated inflammation. A variety of traumas may
trigger the need for a joint to repair itself. Osteoarthritis includes a slow but efficient repair
process that often compensates for the initial trauma, resulting in a structurally altered but
symptom-free joint. In some people, because of either overwhelming trauma or compromised
repair, the process cannot compensate, resulting in eventual presentation with symptomatic
osteoarthritis; this might be thought of as ‘joint failure’. This explains the extreme variability in
clinical presentation and outcome that can be observed between people, and also at different
joints in the same person
According to Centers for Disease Control, osteoarthritis is a disease characterized by
degeneration of cartilage and its underlying bone within a joint as well as bony overgrowth. The
breakdown of these tissues eventually leads to pain and joint stiffness. The joints most
commonly affected are the knees, hips, and those in the hands and spine. The specific causes of
osteoarthritis are unknown, but are believed to be a result of both mechanical and molecular
events in the affected joint. Disease onset is gradual and usually begins after the age of 40.

B. Joint

Joints occur where two or more discrete bones meet each other in the body. These joints can
be fixed or can allow movement between the bones. There are three main types: fibrous joints,
cartilaginous joints and synovial joints.

Fibrous joints join bone or cartilage by fibrous tissue and allow very little movement, such as
in the sutures of the skull. Primary cartilaginous joints are between bone and hyaline cartilage. In
secondary cartilaginous joints the two bone ends are covered in a thin layer of hyaline cartilage
and these two ends are joined by interposed fibrous cartilage. An example of this is the
symphysis pubis. The spine consists of a series of fibrocartilaginous joints as each vertebra is
joined to its neighbour by an intervertebral disc consisting of fibrocartilage filled with gel. Even
in cartilaginous joints that allow very little movement the joint can fail, particularly if subjected
to heavy loads such as the acromioclavicular joint in weightlifters. Damage to the fibrocartilage
can sometimes be accompanied by osteophyte formation. This can bethought of as a variant of
OA. However, OA is usually defined as a condition of synovial joints.

Synovial joints (see Figure 1) have evolved in order to allow movement between bones. The
adjoining bone ends are covered by extremely smooth hyaline cartilage (see Figure 2). This
junction is enclosed within a joint capsule containing synovial fluid which bathes and lubricates
the hyaline cartilage. The capsule is lined by a synovial membrane that contains cells called
synoviocytes. These produce lubricant and hyaluronic acid which is responsible for viscosity of
the synovial fluid. They also produce cytokines and growth factors and remove unwanted waste
products, such as metabolites, from the synovial fluid. The capsule is reinforced by ligaments.
These are arranged in such a way as to provide stability throughout the range of movement of the
joint. Some synovial joints have intra-articular discs of fibrocartilage. The hip has a ridge of
fibrocartilage called the labrum which deepens the articulation, whilst in the knee the same tissue
has migrated further into the joint and has become the menisci. The menisci spread load through
the knee and improve congruence, thereby improving stability. They thus protect the hyaline
cartilage from both compressive and shear forces. Synovial joints move in a controlled way
because of the muscle forces that act across them. Muscles are attached to bone by tendons.
Ligaments attach to bones in a similar way. These areas of attachments by soft tissues to bone
are called entheses and are subject to tensile forces.
 Figure 1 Diagram showing the
components of a synovial joint

All of the structures that compose synovial joints can fail and lead to the final common
outcome of OA. Once one structure begins to fail, the surrounding structures are affected
adversely and then also fail. Normally the insult, whether biological or mechanical, affects a
number of structures simultaneously and the remaining structures secondarily. For example, a
traumatic knee injury could lead to a tear of the meniscus, fracture of subchondral bone,
disruption of the hyaline cartilage and stretching of entheses, all occurring simultaneously.

Figure 2 Normal articular cartilage

Subchondral bone supports the overlying hyaline cartilage. It is susceptible to fracture when
subjected to great compressive force or to avascular necrosis when subjected to shear forces.
Collapse of the subchondral bone leads to splitting of the overlying hyaline cartilage. Synovium
can become inflamed due to chemical irritants such as crystals, or infection; additionally, the
synovium is prone to inflammation resulting from systemic immune-related problems, as in
rheumatoid arthritis. Synovitis of any cause results in the release of inflammatory mediators such
as cytokines, and affects the production of hyaluronic acid, thereby altering the viscosity of the
synovial fluid. The cytokines in the synovial fluid affect the catabolic and anabolic activities of
the chondrocytes and osteocytes in the nearby cartilage and bone, as well as the capsule, leading
to alterations in the normal integrity of these tissues, rendering them more susceptible to
mechanical insults. The entheses are commonly stretched by injuries producing inflammation
and oedema in the adjacent bone; they are also susceptible to inflammation in the seronegative
spondarthropathies, such as ankylosing spondylitis. The menisci or the labrum are susceptible to
tearing under excessive shear forces. Once their function is compromised, the hyaline cartilage
can become exposed to abnormal load and can fail.

Failure of hyaline cartilage results in the subchondral bone being subjected to both increased
load and direct pressure from synovial fluid. The final common pathway of all of these
mechanisms is damage to hyaline cartilage, increased load on the underlying bone, cyst
formation due to penetration of the subchondral bone by synovial fluid under pressure, and new
bone formation on the joint margins (osteophytes), i.e. the development of osteoarthritis (OA).
OA, therefore, can occur as a result of any form of joint disease.
C. Prevalence and distribution
Most of the available data on the prevalence of OA comes from the developed Western
world, and most of it is based on a radiographic definition of the condition, rather than a
pathological or clinical one. The joint sites most commonly involved are the knees, hips,
hands, feet and spine. OA affects focal areas within joints: early in the disease only a
localized area is affected, although later on it may spread to affect the whole joint. The sites
most commonly affected in the knee are the anteromedial compartment of the tibiofemoral
joint, and the lateral facet of the patellofemoral joint, in the hip it is the superolateral aspect
that is most often damaged, and in the hands and feet it is the terminal (distal) interphalangeal
joints, as well as the first MTP and thumb base that are most often involved.
Increasing age is a strong risk factor, and there are differences in prevalence and
distribution in men and women. Figure 3 illustrates the overall prevalence in Western men
and women of hip, knee and hand OA. Some racial/ethnic differences exist in the prevalence
and distribution of OA. For example, superolateral hip OA, which is very common in
Caucasians, is relatively uncommon in people of Chinese origin. As explained later, this may
be due to subtle differences in skeletal shape.

Figure 3 Incidence of symptomatic osteoarthritis

(OA) of the hand, knee and hip as a function of age

D. Aetiology and risk factors

OA has no single cause; rather, it is due to a variable combination of several risk factors
affecting different individuals and different joint sites, which explains its heterogeneity. OA
arises as a result of a mixture of both systemic predisposition and local biomechanical risk
factors, as shown in Figure 4, and Box 1 shows the major risk factors currently known.
a) Genetic Predisposition
From twin studies and other data, it has been estimated that about 40% of the
predisposition to OA may be genetic. However, there is no ‘OA gene’; rather, several
different sites within the genome each confer a small increased risk. Many of the sites
associated with this increased risk relate to genes important for skeletal development,
adding to other evidence that suggests that bone size and shape are important
determinants of the likelihood of getting OA.

Figure 4 Systemic predisposition and

local biomechanical risk factors in OA
b) Age
OA is strongly associated with increasing age. But this is not because age-related changes in
joints are similar to those of OA – there are major differences in the ‘pathology’ of ageing
joints from those of OA, and it has been suggested that we would need to live for over 200
years before the age-related changes in the joints alone (such as thinning of the cartilage) would
cause OA. The association with age may have more to do with joint stability and muscles than
joints. As we age, our cartilage gets thinner and our muscles get weaker, and the stability of
major joints such as the knee may be affected in subtle but important ways by these changes.
Some studies have suggested that muscle weakness precedes the development of knee OA.
c) Gender

As shown in Figure 3, there are differences in prevalence of OA between men and women. The
reasons for this are not clear. Changes related to the female menopause appear to be particularly
important, as knee OA prevalence in women rises sharply after the menopause, and
inflammatory OA of the hands often starts during the menopause.

d) Diet and Obesity

Obesity is a strong risk factor, particularly for knee OA. It is also a risk factor for increased
incidence of hand OA, suggesting that it may have some systemic influence, perhaps through
changes in obesity-related biochemical factors such as leptin levels. In addition, there have been
a number of studies to suggest that some vitamin deficiencies may be important in the
development of OA, including vitamins C, D and K.

e) Abnormal Joint Shape and Size

Joint shape is an important risk factor, particularly for hip OA. Hip dysplasia predisposes you to
hip OA in later life, and more subtle abnormalities of the size or shape of the head of the femur
or acetabulum (such as the shape changes that cause femoroacetabular impingement – FAI),
may be responsible for much of the common-or-garden hip OA seen. The differences in shape
of hips in Chinese from that in Caucasians may explain the low prevalence of hip OA in
Chinese people. It is possible that joint size and shape are also important in knee OA.
f) Previous Injury

Injuries that affect the shape or stability of a joint predispose to OA. This is most apparent in
joints which have a low prevalence of ‘common-or-garden’ OA such as the wrist or ankle – OA
at these sites is usually due to a previous significant injury. At the knee joint, meniscal and
ligament injuries, particularly ACL rupture, are important predisposing factors for OA.

g) Neuromuscular Problems

Severe neurological problems of specific types can lead to the important variant of OA called
‘Charcot’s joints’. Lesser forms of neurological change, including weak muscles, and loss of
proprioception, may be important in ‘common-or-garden’ OA. In addition, joint laxity seems to
predispose to OA. Conversely, spasticity results in very tight joints accompanied by abnormal
joint loading leading to joint damage and secondary osteoarthritis. OA of the hip is particularly
common in persons suffering from spastic cerebral palsy.

h) Joint Loading, Occupation and Obesity

The extent to which normal or excessive joint use, including exercise, are risk factors for
OA, or alternatively protective to the condition, is a contentious issue, and we do not yet
understand exactly what aspects of joint loading matter most to joint health. However, certain
specific occupations involving repetitive ‘overuse’ of joints can predispose to OA, resulting in
special forms of the condition such as ‘picca-thumpers thumb’ (OA at the base of the thumb in
people who spent their working days shifting printing blocks around with their thumbs).

The fact that obesity is particularly important for knee OA indicates that a part of the risk is
likely to be due to loading factors, as well as any systemic influence.

i) Bone Mineral Density

Long ago it was noted that people who came to hip replacement because of fractures caused by
osteoporosis were unlikely to have hip OA. Subsequent studies have confirmed that, at both the
knee and the hip, high bone mineral density is a risk factor for OA, and low bone mineral
density is protective. It is not understood how these relationships operate, and it is unclear to
 what extent this is a systemic factor, or whether it is about local loading of cartilage and
subchondral bone.

E. Pathology

The key pathological features of OA are shown in Table 1, which also documents their
radiographic correlates. Historically, pathologists and academics interested in OA have
concentrated on the changes seen in articular hyaline cartilage, more than the changes in other
joint tissues. The cartilage changes include: early softening and swelling or articular cartilage,
with an increase in its water content; intermediate fragmentation and fissuring of the cartilage
surface; and late erosion down to the underlying bone (see Figure 5). This pathology is very well
described, and several classification and scoring systems are available.

The Outerbridge classification is most commonly used by orthopaedic surgeons. It originally

described changes to the articular surface of the patella, but it is now used in all synovial joints,
particularly as arthroscopy is now common and allows direct visualization of many joints.
Figure 5 Osteoarthritis – histology (a) Destructive changes (loss of articular cartilage and cyst
formation) are most marked where stress is greatest; reparative changes are represented by
sclerosis around the cysts and new bone formation (osteophytes) in less stressed areas. (b) In this
high-power view, the articular cartilage show loss of metachromasia and deep clefts in the surface
(fibrillation). Attempts at repair results in (c) subarticular sclerosis and buds of fibrocartilage
mushrooming where the articular surface is destroyed (d).

Grade 1 Softening and swelling of the cartilage

Grade 2 Fragmentation and fissuring of the cartilage in an area less than ½ inch in diameter

Grade 3 Fragmentation and fissuring of the cartilage in an area more than ½ inch indiameter

Grade 4 Exposure of underlying bone.

The cartilage changes are accompanied by extensive changes in the tidemark between bone and
cartilage, with vascular invasion and extension of the calcified zone, as well as thickening of the
subchondral bone. At the margins of the joint, periosteal cells proliferate and change their
phenotype to form bone (osteophytes). In addition, there is usually some synovial inflammation,
which may result in joint effusions, as well as thickening and fibrosis of the joint capsule, which
may be extensive. In advanced cases the damage to the subchondral bone can lead to the
formationof cysts, and loss of bone volume. All of these changes vary in extent in different
individuals, and there are also some differences according to joint site, with, for example,
unusual pathological features such as hyaluronan cyst formation being a feature of some hand
OA.

The radiograph is a blunt instrument for revealing these pathological changes, but it is the only
routinely available tool to detect them, and as long as the changes in the joint are severe enough,
they result in characteristic joint space narrowing, osteophyte formation and subchondral bone
sclerosis, which are pathognomonic of OA. As with the pathological changes, there are a number
of different scoring systems available to assess the severity of radiographic changes. The one
used most commonly is the Kellgren and Lawrence scoring system, which divides OA X-ray
changes into five categories:

0 Normal No features of OA

1 Doubtful Minimal osteophyte, doubtful significance

2 Minor Definite osteophyte, no loss of joint space

3 Moderate Some diminution of joint space

4 Severe Advanced joint space loss and sclerosis of bone

F. Pathogenesis

As already explained, the OA process is initiated by a mixture of systemic predisposing

factors interacting with local mechanical influences that affect the site and severity of the OA
changes, but the changes themselves are chemically mediated.

There are many different hypotheses about how the process is mediated. As with OA
pathology, research on OA pathogenesis has been dominated by work on articular cartilage rather
than other tissues, although it is now seen as a disorder of the whole synovial joint organ.

A lot of current work revolves around the generation of local cytokines and proteolytic
enzymes within the joint, and cell signalling pathways that link chondrocyte activity to changes in
the subchondral bone, synovium and capsule. The main emphasis of much OA research remains
on trying to understand how sparsely distributed cells in cartilage (chondrocytes) maintain the
integrity of the articular cartilage in normal joints, and the anabolic and catabolic processes that
result in OA. The early changes in cartilage appear to result from collagenase enzymes disrupting
the integrity of the type II collagen matrix which encloses the hydrophilic proteoglycans, leading
to swelling and softening; subsequently, more proteolysis and damage to proteoglycans, as well
as collagen, results in the fissuring and loss of volume. It is less clear how the changes at the
tidemark and in subchondral bone are mediated, where increased calcification and angiogenesis
are switched on, and trabecular thickening is seen, perhaps in part as a result of subchondral
micro-fractures of trabeculae.

One of the problems encountered by those studying OA is to detect it in its earliest stages,
before the pathology is severe enough to become apparent on an X-ray or be clinically relevant.
Animal models of the condition help here, and there has been interest in what comes first –
changes in the cartilage, bone, synovium or other parts of the joint? The evidence, not
surprisingly, is that they occur together and are linked and, contrary to earlier ideas, it is apparent
that changes in the bone and soft tissues can occur in the earliest stages of the process in humans.
However, the OA process and the homeostasis of the normal synovial joint are yet to be well
understood.

G. Symptoms and signs

. But, as already noted and shown in Figure 6, there is a poor correlation between the
radiographic evidence of OA in joints, and the prevalence of the clinical symptoms such as
pain.
The most common symptoms and clinical signs reported by/seen in people with clinical OA
are documented in Box 2.

Figure 6 The relationship between

osteoarthritic

symptoms and radiological features of

osteoarthritis
Most people with clinical OA report discomfort or pain in or around the joints affected, but
their pain experiences vary hugely, both over time, between individuals, and, as outlined
further below, according to the joints affected. It is very common for patients to have trouble
describing their pain. They often refer to the sensation as a deep-seated discomfort similar to a
toothache emanating from within the joint. Reported experiences vary from: a dull ache after
exercise; through to the more common moderate, activity-related pain; to excruciating,
continuous pain and pain at night. Severe pain that wakes the patient nightly is a particularly
debilitating symptom of severe arthritis and leads to sleep deprivation. Many people report
that no two days are the same, the pain experience being variable and seemingly inexplicable.
We do not know why OA sometimes causes pain. There are no nocioceptive receptors in
the cartilage, which is the major tissue affected pathologically, but nocioceptive pathways do
occur in subchondral bone, in periosteum and in the synovium and capsule of the joint. It
would appear likely that some of the variation in the pain experience is related to differences
in where the nocioceptive drive is coming from in different people/joints; there is good
evidence for bone being a major source of pain in advanced knee OA, but in other
sites/severity, it may be different (see Figure 7)
 Figure 7 The pathogenesis of pain
in osteoarthritis

In addition to there being a nocioceptive drive to cause pain, pain amplification systems, both
locally in the joint and within the central nervous system, can contribute to the pain experience in
chronic OA. Once pain has become chronic, amplification pathways can be activated locally and
at both spinal and cortical levels, leading to chronic and more widespread pain, which is difficult
to treat, particularly if accompanied by mood changes. Anxiety and depression both affect the
perception of pain and its response to interventions.

Other Symptoms

Stiffness, or gelling of the joint after inactivity, is a classical feature of OA, resulting in people
having difficulty getting moving after resting. This is particularly common in the early morning
after first awakening. The cause is not known. Less well-appreciated symptoms of OA include
fatigue, sleep disturbance caused by pain and anxiety/depression. Each of these is very common,
and can have a big impact on individuals, and, as discussed below, may need management
separately from any attempt to deal with joint damage or pain.

Signs

On examination the joints affected may appear swollen, there may be evidence of wasting and
weakness of surrounding muscles (as in quadriceps muscle wasting at the knee, or the
Trendelenburg sign at the hip which signifies weakness of hip abductors) and, in advanced OA,
joint deformity. Palpation may reveal bony swelling at the margin of the joint, signs of mild
inflammation, such as heat over the joint line, and an effusion. On movement there is usually a
reduced range, with pain at the end of the range, and crepitus may be felt as the joint is moved; in
advanced disease instability may be detected. As emphasized in this chapter, the challenge for
the clinician is to ascertain whether the symptoms and signs are the result of OA or of some other
articular or periarticular problem

Symptoms and signs on Knee osteoarthritis

Occurs most commonly in the medial tibiofemoral joint but can occur in all three
compartments and is often tricompartmental. Isolated patellofemoral OA is probably due to
altered biomechanics of the extensor mechanism. Pain is felt globally over the knee and the
proximal tibia. In isolated patellofemoral OA the pain is felt anteriorly over the knee and is often
worst when ascending or descending stairs as the patella is compressed against the femur. As in
the hip, the pain is a deep-seated aching sensation related to exercise. Rest pain and night pain
develop in the later stages of the disease. Patients sometimes report audible crepitus (crackling or
grating sounds) coming from the knee as well as symptoms of instability (a feeling that the knee
is going to give way). They may notice gradual deformity of the knee, in particular varus
deformity, but less commonly valgus deformity. Fixed flexion deformity means that the knees
cannot lock in full extension and thus patients cannot stand comfortably for prolonged periods
due to muscle fatigue. Loss of flexion beyond 90 degrees makes standing from a sitting position
difficult as patients cannot move their centre of gravity anterior to their mid-coronal plane.
Swelling and stiffness are common features.

Examination reveals an antalgic gait, wasting of quadriceps muscles, joint effusion, joint
deformity, and crepitus palpable and sometimes audible on movement. The joint deformity may
be passively correctable. Deformity is towards the compartment most severely affected, usually
varus deformity with predominantly medial compartment OA. There is sometimes tenderness
along the joint line and palpable osteophytes that can be tender.

H. Differential diagnosis, investigation and assessment

The major problem is the common assumption that any joint symptoms in an older person are due
to OA, compounded by the fact that they are very likely to have radiographic changes of OA,
even if that is not the cause of their symptoms.
Joint pain may:
• be referred from above (e.g. hip OA causing knee pain)
• be due to a periarticular problems
• come from the joint itself
• be due to central nervous system pain sensitization (as in ‘fibromyalgia’)
• result from a complex mixture of the above.
In people with OA we think that there is often a complex mixture of several mechanisms
underlying their symptoms, with nocioceptive drives coming from both the joint and the
periarticular tissues, and a degree of pain sensitization complicating the picture.
Clinical examination may help to differentiate between these different types of pain
problem: areas of localized tenderness may reflect articular or periarticular pathology (but
beware, referred tenderness can occur), and the presence of widespread pain or allodynia (severe
skin sensitivity) may indicate pain sensitization. If movement of the joint reproduces the patient’s
common symptoms, this suggests that joint pathology is the problem, but it is not easy to find
out why a joint is painful, or whether OA pathology is the cause.
Routine investigations do not help. All blood tests are generally normal in OA (although
there might be a small rise in CRP levels), but tests for evidence of systemic inflammation (such
as the ESR or CRP) may be useful in differentiating OA from inflammatory forms of joint
disease. As explained, the plain radiograph is simply an historical record of preceding joint
changes, and it is not possible to use other imaging techniques such as MRI or scintigraphy to
detect pathophysiology in routine care.
Assessment
Pain, the main symptom of OA, is a subjective experience which cannot easily be measured or
assessed. Similarly, it is not easy to ascertain the severity of the functional problems that any
individual patient may be experiencing. So the assessment of severity and of the likelihood of a
good response to interventions such as surgery is difficult in routine clinical practice. One is
largely reliant on what the patient says, supplemented by the observation of gait, any difficulties
the patient has undressing, dressing or getting onto or off the examination couch and clinical
examination.
For research purposes a number of instruments are available to assess the severity and
impact of OA. Patient self-assessment questionnaires such as the ‘WOMAC’, Oxford hip, knee
and shoulder scores, Hip Dysfunction and Osteoarthritis Outcome Score ‘HOOS’ (for hips), Knee
Dysfunction and Osteoarthritis Outcome Score ‘KOOS’ (for knees) and the Australian–Canadian
Hand Osteoarthritis Index ‘AUSCAN’ (for hands) are often used. In addition, semi-objective tests
of function, such as walking speed, can be measured to assess disability, and special imaging
techniques such as MRI may be used to assess the degree of joint damage. However, plain
radiographs are so characteristic as to make other imaging studies unnecessary. The four cardinal
signs are osteophyte formation, joint space narrowing, sclerosis of the underlying bone, and
subchondral bone cysts. Again for research purposes it is important to try to understand whether
the disease process is active or not, and what tissues are undergoing change.
Academics have invested heavily in the development of biochemical markers of the OA
process, such as blood or urinary levels of degradation products of cartilage, as well as functional
imaging techniques (fMRI) in order to try to understand more about the disease, its
responsiveness to different therapies, and its activity, but no clear consensus on what measures
are most useful has yet emerged.
I. Management

Many different interventions are available for the treatment of people with OA, and there
are a plethora of guidelines available. Interventions are generally divided into symptomatic
therapies and disease-modifying therapies. As yet, there are no drugs with proven ability to
modify the disease process, although claims have been made for many different agents. Disease
modification can occur in response to mechanical interventions, such as joint distraction and
osteotomy. All other interventions are symptomatic.

The main symptoms of OA (pain, stiffness, fatigue, and anxiety/depression) are very
susceptible to so-called ‘placebo’ and ‘nocebo’ effects. Placebo is generally thought of as a sham
or dummy intervention, and we know that sham surgery can work well in OA, but what placebo
research teaches us is that symptoms of conditions such as OA are highly responsive to the whole
context in which any therapy is administered. If patients and clinicians feel safe and trusting of
each other, and if the clinician is able to validate the patient’s experiences (i.e. the patient feels
fully understood), then outcomes will be good, whatever the intervention. And the opposite is also
true.
Symptomatic Therapy

Figure 8 illustrates the basic principles of the symptomatic management of OA. As noted, there
are several evidence-based, published guidelines on the management of OA. This discussion is
based on the UK National Institute for Health and Care Excellence (NICE) 2014 guideline
CG177: Osteoarthritis: Care and Management, which recommends that clinicians follow the
steps described below.

Figure 8 The pyramid of treatment

for symptomatic osteoarthritis

Step 1 Take a holistic approach and encourage self-management. This means assessing the
impact of the OA on the individual’s quality of life, function, mood, relationships and activities,
thinking about their context and any comorbidities (including depression) and thinking about the
potential risks and benefits of any intervention. Self-management strategies include considering
alterations of diet (particularly to lose weight), alteration in activities, changing footwear, taking
a more positive approach to the condition and exercising more.
Step 2 Introduce the ‘core treatments’ appropriate for most people with OA. These include the
provision of information about the condition and its management, helping people to increase
their exercise level and to do specific exercises to strengthen muscles around affected joints,
footwear advice, and help with weight loss for those who are obese.

Step 3 Introduce specific non-surgical interventions. These may be pharmacological or non-

pharmacological. The non-pharmacological interventions of proven value include supervised
courses of physical therapy, the use of aids and devices to reduce instability of to help with
functional problems, walking aids such as sticks or crutches, some electrotherapy techniques,
such as TENS machines for pain control, and some manipulations, particularly in the case of hip
OA with a reduced range of motion of the hip.

Pharmacological options include the use of regular or on-demand paracetamol, and topical
NSAIDs, which are considered to be the first choices for pain. More recent evidence has
suggested that paracetamol is no better than placebo, but both have been demonstrated to reduce
pain. If they are insufficient, NSAIDs, COX-2 inhibitors and opioid analgesics can be
considered. Intra-articular local anaesthetic and corticosteroid injections can be considered as an
adjunct to other treatments, but hyaluronan injections are not recommended because of lack of
evidence. The very widely used ‘nutriceuticals’ such as glucosamine and chondroitin are not
recommended because of lack of the lack of robust evidence to support their use.

Step 4 Consider surgical options. There are many different surgical options available. Surgery is
broadly divided into joint realignment, joint fusion, joint excision and joint replacement
(arthroplasty), which may be total or partial (such as unicompartmental knee replacement). Joint
debridement such as arthroscopic knee debridement has largely been discredited by randomized
controlled trials of sham surgery versus debridement, which showed no treatment benefit.

Surgery is usually confined to end-stage disease once pain has become refractory to other
treatment options. Hip and knee replacements are particularly successful treatments for advanced
OA, often resulting in complete resolution of pain and a dramatic improvement in function and
quality of life. However, a small but important minority of patients do not benefit from joint
replacement (between 5 and 15%, lack of response being more common for knee replacement
than hip replacement) and have persistent severe pain in the long-term post surgery despite no
evidence of technical issues with the surgery performed.

Principles Of Management

The natural history, presentation, impact and prognosis are different for each of the major joint
sites affected, and management needs to be based on prognosis and impact in particular, so here
we provide a brief outline of the principles of management of hip, knee and hand OA.

Hip OA This responds relatively well to physical therapy and walking aids. It is important to
assess leg length and think about corrective footwear, and shock-absorbing shoes can help.
Among the most useful interventions are the use of a stick in the contralateral hand to reduce
loading while walking, and physiotherapy aimed at increasing the range of motion and
improving muscle strength and pelvic stability. OA of the hip often progresses relatively rapidly,
so patients may have a story of a relatively long period of mild problems, such as exercise-
related aching in the groin, followed by the development of severe pain over a period of a few
weeks or months. If pain becomes very severe, interfering with activities and sleep, then hip
replacement is likely to be the best option. Spontaneous recovery from severe hip OA
occasionally occurs, particularly in those who stay active, but this cannot be predicted or relied
upon. The mainstays of treatment are weight loss, walking aids, physiotherapy and simple
analgesics combined with NSAIDs. When these treatment modalities no longer control
symptoms, total hip replacement is usually very effective.

Knee OA This often responds well to simple non-surgical interventions, and it often remains
relatively stable and mild for many years, during which people can adjust to it, and find ways of
making sure it interferes with life minimally. Knee OA is strongly related to obesity, and
relatively recent research has shown that even modest amounts of weight loss can result in
marked reduction in symptoms, so this should be prioritized. Keeping the quadriceps muscles
strong is important, as they are key to knee stability. Topical NSAIDs are useful, as are shoes or
appliances that reduce impact loading (shock absorbing) and/or adjustments to unload the most
affected compartments (usually the medial tibiofemoral compartment). Patella strapping is useful
for patellofemoral OA. Corticosteroid injections can result in good pain relief for relatively short
periods of time (a few weeks to months) and can, therefore, be of great value as an adjunct to a
course of physical therapy, or to help a patient manage a planned, important life event such as a
wedding. There are many surgical options if the condition becomes severe. These include
osteotomies of various types, and unicompartmental or total joint replacements. Arthroscopic
joint lavage is not recommended because of insufficient evidence for efficacy over and above its
very big placebo effect.

Hand OA Osteoarthritis in the hand often has a relatively good long-term prognosis, unless there
is severe thumb base disease. Management therefore usually involves strategies that reduce pain
without putting the patient at risk. Topical NSAIDs and capsaicin are of proven value for
interphalangeal joint disease. There are good surgical options for advanced thumb base OA. It is
important to re-emphasize the fact that most people with OA do not progress to a severe enough
state to warrant surgical intervention, and that the prognosis is generally relatively good.
Therefore, interventions should be kept as simple and as safe as possible. Most people with OA
are older adults, many of whom have comorbidities that can make pharmacological and surgical
interventions more hazardous than usual. In addition, as noted above, symptomatic OA responds
well to context (placebo) effects, meaning that it is crucially important to make sure that
whatever is being offered in terms of advice or intervention is offered in a positive manner, and
in a safe environment for the patient, in which he or she feels ‘heard’. As the song says, ‘It ain’t
what you do it’s the way that you do it.’
 Bibliography
1. Osteoarthritis Cartilage. Call for Standardized Definition of Osteoarthritis Stratification
for Clinical Trials and Clinical Use. 2016;23(8):1233–41.
2. Apley and Solomon’s system of orthopaedics and trauma. System of orthopaedics and
trauma. Tenth edition.