Scott Med J OnlineFirst, published on June 21, 2016 as doi:10.

1177/0036933015619588

Original Article
Scottish Medical Journal
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Knee osteoarthritis: a review ! The Author(s) 2016

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of management options DOI: 10.1177/0036933015619588
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SM Hussain1, DW Neilly2, S Baliga3, S Patil1 and RMD Meek1

Abstract
Osteoarthritis of the knee is a complex peripheral joint disorder with multiple risk factors. The molecular basis of
osteoarthritis has been generally accepted; however, the exact pathogenesis is still not known. Management of patients
with osteoarthritis involves a comprehensive history, thorough physical examination and appropriate radiological inves-
tigation. The relative slow progress in the disease allows a stepwise algorithmic approach in treatment. Non-surgical
treatment involves patient education, lifestyle modification and the use of orthotic devises. These can be achieved in the
community. Surgical options include joint sparing procedures such as arthroscopyando osteotomy or joint-replacing
procedures. Joint-replacing procedures can be isolated to a single compartment such as patellofemoral arthroplasty or
unicompartmental knee replacement or total knee arthroplasty. The key to a successful long-term outcome is optimal
patient selection, preoperative counselling and good surgical technique.

Keywords
Osteoarthritis, knee joint, total knee replacement, cartilage

Introduction
Osteoarthritis (OA) is a common form of degenerative
joint disease affecting the western population. The knee
is the principal peripheral joint affected resulting in pro-
gressive loss of function, pain and stiffness.1 It is esti-
mated that approximately a tenth of the population
aged over 50 years will be affected.2
Aetiology
OA is a complex disorder with multiple risk factors.
These include both generalised constitutional factors
(age, female sex, obesity, family history) and local
adverse mechanical factors (trauma, occupational and
recreational wear, malalignment, generalised laxity)3,4
(Figure 1).
There is a significant genetic component to the
prevalence of knee OA, but the exact gene responsible
is unknown. Classic twin studies have revealed that the
influence of genetic factors is between 39% and 65% in
radiographic OA of the hand and knee in women.5
Basic science
Articular cartilage is an avascular, alymphatic, aneural
connective tissue. With resilient wear resistance and
highly compressive stiffness, the articular cartilage
functions in providing low friction surface. Water
accounts for 65–80% of the wet weight. Ten per cent
of wet weight of cartilage is made up of collagen, which
provides tensile strength (Figure 2).
Type II collagen is the major fibrillar collagen, con-
stituting 90% to 95% of the total collagen and is spe-
cific to articular cartilage. It forms highly cross-linked
interconnected network of collagen fibrils. Type II col-
lagen is resistant to degradation by most proteases but
can be degraded by collagenases which has been impli-
cated in the pathogenesis of arthritis.
Types IX and XI collagen are other types of collagen
present in the articular cartilage. These are important in
the formation and function of cartilage, and genetic
aberrations can lead to various abnormalities. For
example, gene mutations in type XI collagen genes
can give rise to early onset OA.
1
Consultant Orthopaedic Surgeon, The Queen Elizabeth University
Hospital.1345 Govan Road. Govan G51 4TF Glasgow
2
Specialty Registrar, Trauma and Orthopaedics. Aberdeen Royal
Infirmary, Foresterhill Rd, Foresterhill, Aberdeen AB25 2ZN
3
Clinical Fellow, Department of Orthopaedics and Spinal Surgery, Royal
Stoke University Hospital. Newcastle Rd, Stoke-on-Trent ST4 6QG
Corresponding author:
S Baliga, Department of Orthopaedics, Aberdeen Royal Infirmary,
Aberdeen AB25 2ZN, UK.
Email: santoshbaliga@doctors.org.uk

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2 Scottish Medical Journal 0(0)

Figure 1. The aetiology of OA is a complex interplay between genetic and environmental factors. Disease can occur in excessively
loaded normal joints OT normal loading in structurally abnormal joints. Some genetic syndromes lead to joint malformations and
early-onset osteoarthritis.

Figure 2. Cartilage like all types of connective tissue has two main constituents – cells (chondrocytes) and extracellular matrix
(ECM). The chondrocytes are responsible for the manufacturing and maintenance of the ECM. The ECM is made of water, collagen and
proteoglycans.

pathogenesis. The end result of the osteoarthritic pro-

Molecular basis of OA
Although the causes of OA are not entirely understood,
biochemical changes in the subchondral bone, articular
cartilage and synovial membrane are important in its
cess is generally well accepted.
However, there is much debate on the pathogenesis
of this disease. Howell6 discussed three main views: one
view describes failure of cartilage due to the ageing

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Hussain et al.
process, a traumatic event or an originally defective
matrix; the second view attributes OA to net loss of
cartilage matrix due to failure of chondrocyte balancing
synthesis and degradation; and the third hypothesis
implicating extracartilagnious factors such as vascular
changes, bony remodeling, microfractures and synovial
changes as primary initiators with cartilage damage as a
secondary affect.
In OA, there is increased degradation of type II col-
lagen fibrils. Collagenases only cleave within the type II
collagen triple helix and not within types IX or XI col-
lagen, which is most likely, degraded by proteolysis.7
Aggrecans diminish in parallel to the severity of OA, as
there is a net loss of matrix due to the inability of chon-
drocytes to compensate for loss of proteoglycan. This
increased loss is due to the action of matrix metallopro-
tease (MMP) and aggrecanases. Although new aggre-
can is synthesised to help with cartilage repair in the
early stages of OA, it is lost to synovial fluid at later
stages.8 The composition of newly synthesised aggrecan
may be different to the original, particularly in the con-
tent of keratan sulfate and chondroitin sulfate.9 All
these changes hamper the ability of cartilage repair.
As a result of this altered extracellular matrix network,
the water content increases. These in turn decrease the
modulus of elasticity.
The formation and accumulation of advanced glyca-
tion end products (AGEs) is one of the molecular events
that has been suggested to be responsible for predispos-
ing to the development of cartilage damage in OA.10
There is increasing interest in defining the role of
inflammation in OA, which is often associated with
low-grade synovitis.11 Symptoms and progression of car-
tilage degeneration have been associated with syno-
vitis.12,13 Studies have demonstrated that chondrocytes,
osteoblasts and inflamed synovium all produce and con-
tribute to various proinflammatory cytokines.14–17 The
proinflammatory cytokine IL-1b has been implicated as
the most important factor responsible for the catabolic
process in OA. Other proinflammatory cytokines such as
TNF-a, IL-6, IL-8 have all been shown to contribute to
the cartilage degradation process in OA.14,18,19
Diagnosis
The diagnosis of knee OA can be made by history and
clinical examination and confirmed by radiography. A
precise diagnosis also helps to rule out other causes of
knee pain, such as pain referred from the hip or back
amongst others.
History
The cardinal symptoms of knee OA tend to be pain,
stiffness, reduced range of movement (ROM), crepitus
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3
and swelling. Pain during early disease process is usu-
ally described as a dull intermittent ache, localised to
one compartment. Typically worsened with activity and
is relieved with rest. With progression of the disease,
pain becomes continuous and diffuse, when all the
compartments are involved, even resulting in rest and
night pain.
The exact source of pain in OA is not well under-
stood, and it is deemed biopsychosocial in nature by
Dieppe and Lohmander20 Pain present with prolonged
sitting and stair climbing is suggestive of patellofemoral
involvement. This can be associated with mechanical
symptoms such as locking (from meniscal abnormality,
loose osteochondral fragment or significant articular
surface abnormality).
Ligamentous instability and arthrosis may coexist.
However, this should be differentiated from pain and
quadriceps inhibition resulting in a ‘giving away’
sensation.
Clinical examination
Physical examination should incorporate body habitus
and gait pattern. Patient should be examined standing
and supine looking for effusion, tenderness ROM and
ligament instability.
Gait should be assessed both in anteroposterior as
well as mediolateral plane. The presence of an antalgic
gait with knee flexion may suggest presence of a flexion
deformity. Also evidence of either medial or lateral
thrust should be noted.
Limb alignment or deformity can be visualised on
standing. Varus deformity is suggestive of medial com-
partment involvement, whilst valgus malalignment is
suggestive of lateral compartment disease. These are
indicative of longstanding disease process (Figure 3).
ROM both active and passive should be noted.
Special tests include assessment of the integrity of col-
lateral using varus/valgus stress test and also the assess-
ment of cruciates. Examination of the hip and spine
should be carried out to rule out referred pain.
Investigation
As per European League Against Rheumatism
(EULAR) recommendations, plain radiography is still
the gold standard for assessing the knee with clinical
evidence of OA.21 The views include weight-bearing
anteroposterior view (AP), non-weight bearing true
45-degree flexion lateral view and skyline patella view.22
In advanced disease the AP view demonstrates loss/
reduction of joint space, osteophytosis, subchondral
sclerosis and cysts (Figure 4). In the earlier stages of
the disease, there may be subtle changes, which will not
be evident in the standard weight-bearing AP view.
4 Scottish Medical Journal 0(0)

Figure 3. Normal knee alignment; this is usually 3–7 of valgus (centre). Varus malalignment as seen most commonly in knee OA
(left). Genu valgum is more often associated with rheumatoid arthritis (right).

Figure 4. Weight-bearing X-rays of knee showing features of OA. These include joint space narrowing, osteophytes and subchondral
sclerosi.

A weight-bearing 45-degree flexion posteroanterior
view23 may demonstrate subtle loss of joint space espe-
cially in the lateral compartment suggestive of early
OA. This view reveals the femoral notch clearly and
associated changes such as spiking of the tibial spine
and narrowing of notch. In addition, changes follow-
ing menisectomy such as peripheral osteophyte
formation, flattening of femoral condyle can also be
appreciated.
Magnetic resonance imaging is indicated in symp-
tomatic patients with minimal radiographic findings
or when there are clinical features suggestive of a
meniscal lesion. A degenerative meniscal lesion may
coexist with OA, but symptoms may not correlate

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Hussain et al.
Figure 5. An off-loader brace is useful to re-align a correctable
deformity. It results in pain relief when active. However, to be
effective correct sizing and fitting are essential.
well. Using delayed, gadolinium-enhanced magnetic
resonance imaging of cartilage (dGEMRIC) the glyco-
saminoglycan content of the cartilage can also be visua-
lized and early OA24 changes can be diagnosed. Other
causes of knee pain such as ostochondral fracture,
chondral defects, osteonecrosis, etc. can identified.
Radioisotope scanning is helpful when patients pre-
sent with arthritis like symptoms but have normal
radiographs. Abnormal uptake around the joint may
suggest periarticular lesion (Patellofemoral OA).25
Treatment
The relative slow progression of the disease allows for
stepwise algorithmic approach in management.
Following systematic review of research evidence and
expert consensus, the EULAR task force for OA devel-
oped evidence-based recommendations for the treat-
ment of knee OA. Options include both non-surgical
and surgical strategies.
Non-surgical
The aim of non-surgical option is patient education,
pain control, delay the progression disease and to
improve function.
Life style modification. Exercises involving high-impact
activity such as running on hard surfaces and jumping
should be avoided, instead low-impact activities such as
swimming, cycling should be encouraged. In patients
with evidence of patellofemoral OA, activities such as
stair climbing and squatting should be limited.
The obese patient should be advised and encouraged
to lose weight; obesity has been shown to be risk factor
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5
for developing symptomatic OA in a large cohort
study.26
Orthoses and footwear
The aim of an orthosis is to reduce pain and improve
function. The ideal candidate for an orthosis is a
patient with passively correctable unicompartmental
arthritis. A brace may function by improving the bio-
mechanical axis of the deformity thereby unloading the
compartment or by improving the perception of
instability (Figure 5). A recent Cochrane review has
demonstrated that there is improvement in pain and
function following the use of orthoses.25
Physiotherapy. There is good quality evidence that
muscle strengthening and an aerobic exercise program
is beneficial in the management of OA.28,29 Range-of-
motion exercises help to prevent the development of
contractures. Periarticular muscle strengthening exer-
cises tend to stabilise the knee and improve symptoms.
Pharmacotherapy. Non-steroidal anti-inflammatory
drugs (NSAIDS) are prescribed when the patient pre-
sents with exacerbation of pain and a swollen knee.
These agents act by blocking the proinflammatory
agents such as prostaglandins and leuktines by revers-
ibly blocking the cylooxygenase and lipooxygenese
pathway. Selective COX2 inhibitors have an anti-
inflammatory effect but are nephrotoxic. Due to its
cardiovascular toxicity the COX2 inhibitor,
Refecoxib, was withdrawn from the market in
October 2004.
Intra-articular corticosteroids are indicated when
there is exacerbation of symptoms despite using
NSAIDS. A systematic review has shown that intra-
articular corticosteroids are efficacious in controlling
pain in OA, but the effect lasts approximately one
week.30
Injectable hyluronate therapy has theoretical advan-
tage in OA as a result of its viscoelastic, analgesic, anti-
inflammatory and chondroprotective properties.31 A
Cochrane review revealed up to 5–13 weeks improve-
ment in pain and function post injection following the
use of Hyluron group of products.32
Surgical management
This can be broadly classified as joint preserving and
joint-replacing procedure (see Table 1).
Arthroscopy. Arthroscopic debridement of the knee, for
OA is controversial. Despite this, it is one of the
common procedures performed.33 Randomised con-
trolled trails have revealed that the symptomatic relief
6 Scottish Medical Journal 0(0)

Table 1. A summary of the surgical options in the management of symptomatic knee arthritis.

Joint preserving Joint replacing

Symptomatic treatment Unicompartmental

Arthroscopy Total knee arthroplasty
Joint surface restoring procedures
Cartilage
Autologous chondrocyte transplantation (ACT)
Autologous osteochondral transplantation (OCT)
Bone microfracture, drilling and aberration arthroplasty
Joint alignment procedure
Osteotomy
- Proximal tibial osteotomy
- Distal femoral osteotomy

obtained is attributable to placebo effects.34,35 However,

in a selected group of patients, arthroscopy did provide
beneficial effects. The factors which predicted better out-
comes are younger age, mechanical symptoms such as
locking, medial joint line tenderness, mild to moderate
radiographic evidence of OA and presence of unstable
degenerative tear of the meniscus.36–38

Osteotomy. The goal of an osteotomy is to transfer the

mechanical axis from the pathologic area to the normal
compartment. In a normal knee, the mechanical axis tra-
vels from the centre of the hip through the centre of knee
to the centre of the ankle joint. In medial compartment
OA with resultant varus deformity, the mechanical axis
tends to move medially, this in turn leads to more stress
on the medial compartment38 (see Figure 6). Conversely,
in lateral compartment OA with a valgus deformity, the
mechanical axis runs more to the lateral compartment.
Proximal tibial osteotomy was popularised in
Coventry (UK) in 1962.39 Several types of osteotomies
have been described; these include opening wedge, clos-
ing wedge, oblique plane osteotomy and ball and socket
osteotomy. However, the opening and closed wedge
have been popularly used due to its technical ease.
Regardless of the type of osteotomy, the aims are simi-
lar to normalise the mechanical axis and off-load the
degenerate side.

Medial compartment arthritis. The absolute and relative

indications for high tibial osteotomy for varus deform-
ity are given in Table 2.40 Over the past few years’
studies have shown favorable outcomes with high
tibial osteotomy. Coventry et al.41 revealed that
approximately 61% of patients had less pain and
65% had better function at 10 years. Omori et al., fol-
lowing closing wedge osteotomy in 37 patients reported
71% good to excellent function at 17 years.42 Literature
has revealed that for a successful outcome, patient
selection is paramount. Obesity and advancing age
Figure 6. The mechanical axis of the lower limb is a line between
the centres of the hip and ankle joints. Normally, this line crosses
the centre of the knee joint (left). However, this is disrupted in
medial compartment OA and the resultant genu vara (right).
have been reported to be detrimental for long-term out-
come.41,43 A Cochrane review in 2007 concluded that
valgising high tibial ostotomy for varus deformity did
improve pain and function.44

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Hussain et al.
Table 2. Absolute and relative indications for high tibial osteotomy for varus deformity.
Indications
Age younger than 60 years
Pain and disability due to OA
OA confined to one compartment on a weight
bearing X-ray
Preoperative arc of flexion >90
Lateral compartment arthritis. OA of the lateral compart-
ment with valgus deformity is less common than medial
compartment OA. Mild valgus deformity has been trea-
ted with proximal tibial osteotomy. When the deform-
ity is severe with a superolateral slopping joint line a
distal femoral osteotomy (DFO) is indicated. The oste-
otomy on restoring the mechanical axis also alters
patellofemoral biomechanics by reducing the Q angle.45
The indications are similar to that for medial com-
partment OA. Contraindications include inflammatory
arthritis, severe patellofemoral OA, panarthrosis,
severe restriction of knee movement and ligamentous
instability.
Favourable outcomes have been reported following
DFO; in a series of 40 patients, Miniaci et al.46 have
reported 86% good to excellent results at 5.5 years.
Finkelstein et al. have shown 10-year survival rate of
64% following supracondylar DFO.47 Dejour et al.48 in
a comparative study between high tibial osteotomy and
DFO, recommended DFO as the procedure of choice
for younger patients with valgus deformity exceeding
14 .48 There is supportive evidence suggesting that the
osteotomy may delay the need of knee replacement for
5–10 years49,50 and that varising DFO can make TKR
technically easier.51
Arthroplasty
Unicompartmental knee arthroplasty. With improved
prosthetic design, surgical techniques, wear properties
of polyethylene and recent publications of better long-
term results, unicompartmental knee arthroplasty
(UKA) has undergone resurgence.52
The prerequisite for UKA are stable joint, correct-
able varus deformity, fixed flexion less than 10 and
minimal lateral compartment disease. The relative
merits of UKA over total knee are shorter surgical
time, less blood loss, quicker rehabilitation and better
range of movement.53,54 Moreover, the revision of
UKA to total knee replacement is reasonably straight
forward compared to revision of a TKR.55
Schai et al.56 reported 90% good or excellent
results in terms of pain and function in patients <60
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7
Contraindications
Absolute
Inflammatory arthritis
Lateral knee thrust during Gait Flexion contracture >10–15
Previous menisectomy in lateral compartment
Ligamentous instability
Severe patellofemoral OA Lateral tibiofemoral subluxation > 1 cm
Relative
Obesity
years with an average follow-up of 2–6 years.
Pennington et al.57 reported 93% survivorship at 11-
year follow-up.
Patellofemoral arthroplasty. Incidence of isolated patello-
femoral arthritis is 13.6 to 25% in women and 11 to
15.4% in men older than 55 years.58,59 The surgical
options used to treat this condition include arthro-
scopic debridement with or without lateral release,
unloading tibial tubercle osteotomy, patellofemoral
arthroplasty, total knee replacement and rarely patel-
lectomy.60–62 Even though total knee replacement gives
90% results, many of these patients are younger than
those suffering from tricompartmental arthritis.
Therefore, a less aggressive approach using patellofe-
moral arthroplasty may be appropriate.
Indications for patellofemoral arthroplasty include
middle-age patient with isolated patellofemoral OA
with significant pain and functional disability. The
contraindications include inflammatory arthritis, crys-
tal arthropathy, severe patellar maltracking, tibiofe-
moral arthritis and high activity.62 The short- to mid-
term follow-ups so far has been variable between 60
and 85% showing good to excellent results.63–65 The
most common problems encountered are patellar mal-
tracking, excessive polyethylene wear and progression
of arthritis in the other compartments.
Current designs have shown some promise with
strict patient selection. Lonner et al. have reported
96% good to excellent results with second-generation
implants. The five-year survivorship with revision
as endpoint is 95.8% for Avon patellofemoral
arthroplasty.66
Total knee replacement. Total knee replacement is
reserved as the final option for patients with arthritis.
Advances in the implant design, with better poly-
ethylene wear properties and appropriate patient selec-
tion, reproducible results of 96% have been achieved at
10 years.66,67
The timing of knee replacement is still debatable.
Gidwani et al., in a series of patients, have reported
that good results can be obtained when intervention is
8 Scottish Medical Journal 0(0)
carried out at earlier stages of radiological OA in a
symptomatic patient.68 There is no correlation between
radiological stages and symptoms.69 The overall com-
plication rate following primary TKR is 5% in patients.
This includes infection about 1.5% and symptomatic
deep vein thrombosis or pulmonary embolism is
between 1 and 3 %.70 This increases up to 26% follow-
ing revision knee replacement.
One of the main risk factors for early revision as per
the Swedish arthroplasty register is young age;71 hence,
orthopaedic surgeons are often reluctant to offer TKR
for young patients. Despite this, recent studies have
shown promising results in younger patients. Gill
et al., in their cohort of patients who were <55 years
when they underwent TKR, reported good or excellent
score in all knees using the knee society score.72
Similarly, Duffy et al.67 at minimum follow-up of 10
years reported survivorship of 96% at 10 years and
85% at 15 years. The average at the time of surgery
was 53 (range 29–55 years).
Conclusion
The knee is the commonest peripheral joint affected by
OA. Initial treatment should include non-operative
modalities in the form of patient education, exercises,
life-style modification and analgesics. Once these are
exhausted, a surgical option, which should be patient
specific, should be considered. Arthroplasty should be
used as the last option following appropriate patient
counseling.
Acknowledgements
The authors thank Paul Gray (Senior Physiotherapist
Woodend Ortheopaedic Unit) for providing and fitting the
offloader knee brace and Mr Iain Stevenson (Consultant
Orthopaedic Surgeon, Aberdeen Royal Infirmary) for provid-
ing pre- and post-knee X-rays.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of this
article.
Funding
The author(s) received no financial support for the research,
authorship, and/or publication of this article.
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