PAPER

CURRENT TREATMENT OF HIP OSTEOARTHRITIS

PEMBIMBING:
dr.Karina Besinga, Sp.OT
DISUSUN OLEH :
Ledy Artha Sihombing
(0861050159)

KEPANITERAAN KLINIK ILMU BEDAH RSU UKI

PERIODE 4 FEBRUARI 2013 30 MARET 2013
FAKULTAS KEDOKTERAN
UNIVERSITAS KRISTEN INDONESIA
JAKARTA
2013

FOREWORD

Praise to God who has given guidance so that the author can complete the paper about
"The Current Treatment Of Hip Osteoarthritis.
The paper is organized so that readers can add insight or expand existing knowledge about
the up-to-date treatment of hip soteoarthritis that the author presents

in this paper an

arrangement of a concise, easy to read and easy to understand.

The authors also wish to express many thanks to dr. Karina who has guided the author in
order to make authors of scientific papers in accordance with the provisions in force so that it
becomes a scientific paper is good and right.
Hopefully, this paper can be useful for readers and expanding horizons about osteoarthritis
treatment and do not forget also the author apologizes for any shortcomings here and there of the
paper's authors do.Please critique and suggestions.Thank you
March, 20, 2013

Author

TABLE OF CONTENTS
Foreword . I
Table Of Content 1
Chapter I
Preface 4
Chapter II
I.
Anatomy of the Hip 6
II. Physiology... 25
III. Definition 29
IV. Risk factor .. 29
V. Phatophysiology . 31
VI. Diagnosis 35
VII. Differential Diagnosis. 40
VIII. Treatment .. 41
IX. Prognosis 71
Chapter III
Conclusion 73
References 74

CHAPTER I
PREFACE
Osteoarthritis is the most common joint disorder in the United States and is the leading
cause of disability in the elderly, with nearly 200,000 total hip replacements performed annually.
3

Radiographic evidence of osteoarthritis of the hip is present in about 5% of the population over
the age of 65 years. However, not all patients with radiographic evidence of osteoarthritis have
symptoms. The inconsistent relationship between radiographic changes and symptoms may
account for discrepant findings in prevalence studies of osteoarthritis of the hip. The term
osteoarthritis is used to represent a heterogeneous group of joint disorders in patients
presenting with joint pain and stiffness. The pathogenesis of osteoarthritis is not completely
understood. Osteoarthritis most likely begins with degradation of the articular cartilage in a
localized, nonuniform manner. This process is followed by a subsequent thickening of the
subchondral bone, new bony outgrowths at joint margins (referred to as osteophytes), and mildto moderate synovial inflammation. The initiating events that lead to osteoarthritis are not clearly
established but are probably due to abnormal signals that alter the chondrocyte phenotype so that
it synthesizes proteins that degrade the Matrix and causes the joint to degenerate.
Osteoarthritis of the hip is categorized as primary (idiopathic) or secondary (systemic or
localized) disease. Risk factors for primary osteoarthritis of the hip include old age, high bone
mass, a genetic predisposition for the disease, Increased body mass index, participation in
weight-bearing sports (e.g., runningat an elite level), and occupationsthat require prolonged
standing, lifting, or moving of heavy objects. Secondary causes (systemic) include
hemochromatosis, hyperparathyroidism, hypothyroidism, acromegaly, hyperlaxity syndromes,
Pagets disease,gout, and chondrocalcinosis. Localized risk factors include joint injury,
developmental deformities (e.g., slipped capital femoral epiphysis), LeggCalvPerthes disease,
acetabular dysplasia, osteonecrosis, and rheumatoid or septic arthritis as a result of cartilage
damage. Polymorphisms and signaling pathways involved with the development and metabolism
of bone and cartilage have also been linked to the risk of osteoarthritis.
Clinical manifestations of osteoarthritis include altered proprioception, muscle weakness
and atrophy, pain, stiffness, and limitations in functional activities and social participation. With
progressive disease, malalignment and bone-on-bone joint pain may be present. Osteoarthritis
management

focuses

Pharmacotherapeutic

on

pain

options

relief

include

and

maximizing

acetaminophen,

function

and

anti-inflammatory

independence.
medications,

glucosamine, chondroitin sulfate, capsaicin and opiate derivatives. These medications target
inflammation and relieve pain. The integration of nonpharmacologic interventions such as
therapeutic exercise, manual therapy, splinting, bracing, orthotics and assistive devices are
4

recommended and provide a low-cost and minimal-risk option for patients to manage their
disease. There are many treatments which are used for treating the osteoarthritis of the hip, and it
needs the exact therapies for the the effective treatment. Therefore, For this paper we will
discuss more about the current treatment of osteoarthritis.

CHAPTER II
DISCUSSION
I. ANATOMY OF THE HIP

The hip joint is a ball-and-socket synovial joint: the ball is the femoral head, and the
socket is the acetabulum. The hip joint is the articulation of the pelvis with the femur, which
connects the axial skeleton with the lower extremity. The adult os coxae, or hip bone, is
formed by the fusion of the ilium, the ischium, and the pubis, which occurs by the end of the
teenage years. The 2 hip bones form the bony pelvis, along with the sacrum and the coccyx,
and are united anteriorly by the pubic symphysis. 11

Hip joints, anterior view.

Femur
The femur is the longest and heaviest bone in the human body. It consists of a superior or
proximal end, a shaft, and an inferior or distal end (see the image below).

Parts of femur.
The superior end of the bone is the articulating side of the femur to the acetabulum. The
upper femoral epiphysis closes by 16 years of age. 11
The trabecular bone configuration in the proximal femur obeys Wolff's Law, which states
that bony structures orient themselves in form and mass so as to best resist extrinsic forces. The
principal compressive group, the principal tensile group, the greater trochanteric group, the
secondary tensile group, the secondary compressive group, and, finally, Ward's triangle can be
found. 11
The superior end of the femur consists of a head, a neck, and greater and lesser trochanters.
The head of the femur is angled superomedially and slightly anteriorly when articulating with the
acetabulum. The head is attached to the femoral body or shaft by the neck of the femur. 11
The superior border of the neck begins just lateral to the femoral head and ends distally at
the greater trochanter. The inferior border of the neck begins lateral to the femoral head and
extends to the inferior trochanter. The superior border is shorter and thicker than the inferior
border. The anterior surface of the neck is rough in comparison to the smooth femoral head. The

necks posterior surface has a concave appearance. The head and neck are at an angle of 130 (
7) to the shaft. The angle is larger at birth and decreases with age. 11
The greater trochanter is a bony prominence on the anterolateral surface of the proximal
shaft of the femur, distal to the femoral neck. It serves as the insertion site for the gluteus medius
and gluteus minimus. The lesser trochanter is a bony prominence on the proximal medial aspect
of the femoral shaft, just distal to the femoral neck. It serves as the iliopsoas insertion site. 11
The intertrochanteric line is a raised area that extends from the greater to the lesser
trochanter anteriorly. This connection posteriorly is called the intertrochanteric crest, which
contains the calcar femorale, another anatomic location on the femoral neck. The calcar femorale
is a vertically oriented plate of dense cancellous bone from the posteromedial portion of the
femoral shaft radiating superiorly toward the greater trochanter. 11
Pelvis
At birth, each pelvic half consists of 3 separate primary bones: the ilium, the ischium, and the
pubis (see the images below). These bones are joined by hyaline cartilage.

Parts of pelvis.

Pelvis and acetabulum, with muscle attachment sites.

In infants and children, these large parts of the hip bones are incompletely ossified. At
puberty, the 3 primary bones are still separated by a Y-shaped triradiate cartilage centered in the
acetabulum. The primary bones begin to fuse at 15-17 years. Fusion is complete between 20-25
years of age. The fact that these bones were originally separate is fairly undetectable in adult
bones on imaging. Although the parts of the hip bone are fused in adulthood, they are still
referred to by their separate origins. 11
Ilium
The ilium is the largest part of the hip bone and makes up the superior part of the
acetabulum. The ala provides an insertion point for the gluteal muscles laterally and the iliacus
muscle medially. 11
Anteriorly, the ilium has an anterior superior iliac spine (ASIS); inferior to this is an
anterior inferior iliac spine. From the ASIS, anteriorly, the iliac crest comes around laterally and
continues posterior to the posterior superior iliac spine (PSIS). The PSIS marks the superior
point of the greater sciatic notch.

The lateral surface of the ilium has 3 rough curved lines: the posterior, anterior, and inferior
gluteal lines. Medially, the ilium has an iliac fossa. Posteriorly, the medial aspect of the ilium has
an auricular surface. 11
Ischium
The ischium is the inferior aspect of the pelvis. The superior part of the body of the ischium
fuses with the pubis and ilium, forming the posteroinferior aspect of the acetabulum.
The ramus of the ischium joins the inferior ramus of the pubis to form a bar of bone called
the ischiopubic ramus, which constitutes the inferomedial boundary of the obturator foramen.
The posterior border of the ischium forms the lower margin of a deep indentation the greater
sciatic notch. The large triangular ischial spine at the inferior margin of this notch is a sharp
demarcation separating the greater sciatic notch from a smaller rounded inferior indentation
called the lesser sciatic notch.
The bony projection at the inferior end of the body of the ischium and its ramus is the
ischial tuberosity. 11
Pubis
The pubis makes up the anteromedial part of the hip bone and contributes the anterior part
of the acetabulum. The pubis has a flat body and 2 rami: superior and inferior.
Medially, the symphyseal surface of the body of the pubis articulates at the pubic
symphysis with the surface of the body of the contralateral pubis. The anterosuperior border of
the united bodies and symphysis forms the pubic crest. The pubic tubercles, small projections at
the lateral ends of this crest where the inguinal ligaments attach medially, are extremely
important landmarks of the inguinal regions. The posterosuperior aspect of the superior ramus of
the pubis is called the pectin pubis.
The obturator foramen is an oval opening formed by the rami of the pubis and the ischium.
The obturator canal houses the obturator nerve and vessels. 11
10

Acetabulum
As indicated above, the acetabulum is formed from parts of the ilium, ischium, and pubis.
The acetabulum is the cup-shaped socket on the lateral aspect of the pelvis, which articulates
with the head of the femur to form the hip joint.
The margin of the acetabulum is deficient inferiorly. An additional fibrocartilaginous
margin of the acetabulum is referred to as the acetabular labrum. The labrum functions to deepen
the acetabulum, thus holding the femoral head more securely. The lunate is the articular surface
of the acetabulum to the femoral head. The rough depression in the floor of the acetabulum is the
acetabular fossa, which is continuous with the acetabular notch.
The transverse acetabular ligament is located along the inferior aspect of the acetabulum; it
prevents the femoral head from moving inferiorly by deepening the acetabulum inferiorly.
Articular cartilage is the material that covers the ends of the bones of any joint. Articular
cartilage is about one-quarter of an inch thick in the large, weight-bearing joints like the hip.
Articular cartilage is white and shiny and has a rubbery consistency. It is slippery, which allows
the joint surfaces to slide against one another without causing any damage. The function of
articular cartilage is to absorb shock and provide an extremely smooth surface to make motion
easier. We have articular cartilage essentially everywhere that two bony surfaces move against
one another, or articulate.
In the hip, articular cartilage covers the end of the femur and the socket portion of the
acetabulum in the pelvis. The cartilage is especially thick in the back part of the socket, as this is
where most of the force occurs during walking and running. 11

11

Ligaments
The hip joint contains a strong fibrous capsule that attaches proximally to the acetabulum
and transverse acetabular ligament and distally to the neck of the femur anteriorly at the greater
trochanter (see the image below). Posteriorly, the fibrous capsule crosses to the neck 1-1.5 cm
proximal to the intertrochanteric crest.

Hip ligaments.

12

Most of the fibers go from the hip bone to the intertrochanteric line, but some deeper fibers
go around the neck, forming the orbicular zone, which holds the femoral neck in the acetabulum.
The anterior capsule of the hip is the strongest and thickest part.
This capsule is composed of 3 ligaments. The iliofemoral ligament, sometimes referred to
as the Y ligament of Bigelow, attaches to the anterior inferior iliac spine and the acetabular rim
proximally and takes an inferolateral direction to insert on the intertrochanteric line distally. It is
the strongest part of the capsule. The iliofemoral ligament prevents hyperextension of the hip
joint during standing by holding the femoral head within the acetabulum.
The ischiofemoral ligament reinforces the capsule posteriorly. It originates on the ischial
part of the acetabular rim and spirals superolaterally to the neck of the femur, medial to the
greater trochanter. This ligament, like the iliofemoral, also prevents hyperextension and holds the
femoral head within the acetabulum.
The pubofemoral ligament reinforces the capsule anteriorly and inferiorly. It begins from
the obturator crest of the pubic bone and passes inferolaterally to join the fibrous capsule of the
hip joint. This ligament prevents overabduction of the hip joint.
An iliopectineal bursa lies anteriorly over the gap in the ligaments, beneath the iliopsoas
tendon.
There are several additional structures of importance related to the fibrous capsule. Lining
the fibrous capsule is the synovial membrane. It covers the neck of the femur between the
attachment of the fibrous capsule and the edge of the articular cartilage of the head; it also covers
the nonarticular area of the acetabulum, providing a covering for the ligament of the femoral
head.
Retinacula, which contain blood vessels, are deep longitudinal fibers of the capsule that go
superiorly from the femoral neck and blend with the periosteum. The bursa is considered the
synovial extension beyond the free margin of the fibrous capsule onto the posterior aspect of the
femoral neck.

13

The ligament of the femoral head is weak. It attaches to the margins of the acetabular notch
and the transverse acetabular ligament; its narrow end attaches to the pit in the head of the femur.
Usually the ligament contains a small artery to the head of the femur.
A fat pad in the acetabular fossa is covered with synovial membrane. It fills the acetabular
area that is not filled by the femoral head. 11
The nerve supply to the hip joint is outlined in Table 1 and the images below.
Nerves of Hip Joint
Nerve
Genitofemoral
Obturator

Root

Sensory

Motor

level
L1-2
Proximal anteromedial None in hip and thigh
L2-4

thigh
Inferomedial thigh

Gracilis (anterior division)

Adductor longus (anterior division)

Adductor brevis (anterior/posterior

division)

Adductor magnus (posterior division)

Lateral femoral cutaneous L2-3

Femoral
L2-4

Lateral thigh
Anteromedial thigh
14

None
Psoas major

Sartorius

Articularis genus

Rectus femoris

Vastus lateralis

Vastus intermedius

Vastus medialis

Tibial

L4-S3

None in thigh

Biceps femoris (long head)

Semitendinosus
15

Semimembranosus

Common fibular (peroneal) L4-S2

Posterior femoral
S1-3

None in thigh
Posterior thigh

cutaneous nerve

Hip nerves, lateral view.

16

Biceps femoris (short head)

None

Hip nerves, anterior view.

Muscular Anatomy
The muscles of the hip joint are outlined in Table and the images below.
Muscles of Hip Joint
Muscle
Sartorius
Iliopsoas
Pectineus
Rectus femoris
Adductor magnus (anterior

Action
Hip flexion, external rotation
Hip flexion
Hip flexion
Hip flexion, leg extension
Hip flexion, adduction

Nerve
Femoral nerve
Femoral nerve
Femoral nerve
Femoral nerve
Obturator

part)
Adductor magnus (posterior

Thigh extension

Tibial

part)
Gracilis

Hip flexion, adduction, internal

Obturator

rotation
17

Tensor fascia lata

Adductor brevis
Adductor longus
Pectineus
Obturator externus
Gluteus maximus
Piriformis
Obturator internus
Gemellus superior
Gemellus inferior
Quadratus femoris
Gluteus medius
Gluteus minimus
Semimembranosus
Semitendinosus
Biceps femoris, long head
Biceps femoris, short head

Hip flexion, abduction

Hip adduction

Superior gluteal nerve

Obturator nerve (posterior

Hip adduction

division)
Obturator nerve (anterior

Hip adduction, flexion

Thigh external rotation

division)
Femoral
Obturator nerve posterior

Lateral rotation, extension

Lateral rotation
Lateral rotation
Lateral rotation
Lateral rotation
Lateral rotation
Hip abduction
Hip abduction
Thigh extension, leg flexion
Thigh extension, leg flexion
Thigh extension, leg flexion
Thigh extension, leg flexion

division
Inferior gluteal nerve
Nerve to piriformis
Nerve to obturator internus
Nerve to obturator internus
Nerve to quadratus femoris
Nerve to quadratus femoris
Superior gluteal nerve
Superior gluteal nerve
Tibial
Tibial
Tibial
Common fibular

Hip muscles, lateral view.

18

Hip muscles, anterior view.

Vasculature
he arteries of the hip are outlined in Table 3 and the image below.
Arteries of Hip Joint
Artery
Obturator
Femoral

Branches
Anterior and posterior branches
In femoral triangle, runs in medial thigh between vastus medialis and adductor
longus, in adductor canal, through adductor hiatus, then becomes popliteal artery
behind knee

Superficial circumflex iliac

Superficial epigastric

19

Superficial external pudendal

Deep external pudendal

Deep femoral artery

Descending genicular artery

Articular branch

Saphenous branch

Deep femoral

Medial circumflex femoral: major supply to femoral neck

artery

Lateral circumflex femoral: also supplies femoral neck

20

Ascending branch

Transverse branch

Descending branch

Perforators/muscular branches

Artery
Obturator

Course
Runs through ligament of femoral head

Artery of
ligament teres

Deep femoral

Branches from femoral artery in femoral triangle

artery

21

Between pectineus and iliopsoas to posterior femoral neck

Medial
circumflex
femoral
Runs on quadratus femoris deep to sartorius and rectus femoris to greater trochanter
anteriorly
Ascending
branch
Extracapsular branches of anastomosis

Descending
branch

Intracapsular branches: run along neck, enter bone at base of femoral head

Lateral

Extends laterally

circumflex
femoral
Ascending

Under rectus femoris

branch
Cervical
branches
Retinacular
arteries
Transverse
22

branch
Descending
branch

II.

PHYSIOLOGY
Lubrication of Joints
Lubrication reduces frictional resistance between bearing surfaces by keeping them
apart. Friction and the resulting wear of two unlubricated surfaces sliding on each other are
23

due to the interaction or contact between the opposing surfaces. In many mechanical
bearings lubricated by oil, the relative continuous motion of the surfaces produces a wedge
of lubricant that keeps the surfaces apart. This phenomenon is defined as hydrodynamic
lubrication and requires uninterrupted motion in the same direction to maintain the integrity
of the wedge. Because joints oscillate and change direction of motion, pure hydrodynamic
lubrication is not the mechanism by which synovial fluid functions as a lubricant.
Many theories based on extensive investigation of the physical properties and abilities
of synovial fluid to act as a lubricant have been presented to explain the mechanisms of
joint lubrication. It appears that the low frictional resistance to joint motion is due to a
combination of mechanisms. Each mechanism complements the other and depends on the
tissues involved and the load imparted to the joint. Resistance to joint motion comes from
the stretching of surrounding soft tissues (ligaments, tendons, muscle) and frictional
resistance of the joint parts that must slide across each other (cartilage, synovium, tendons
in sheaths). Surfaces that contact each other during joint motion and therefore give rise to
frictional resistance have been defined as (1) a soft tissue interface-synovium on synovium
or synovium on cartilage-and (2) a cartilage-on-cartilage type. Lubrication of synovial
surfaces by synovial fluid requires hyaluronate and is due to a boundary phenomenon.
Boundary lubrication occurs when each bearing surface is coated or impregnated with a
thin layer of lubricant that keeps the sliding surfaces apart, allowing ease of motion with a
low coefficient of friction between the sliding surfaces. Hyaluronate sticks to the synovial
surfaces. The lubricating properties of synovial fluid in a soft tissue system are directly
related to the concentration and molecular weight of the hyaluronate, which is also
determined by viscosity. However, it is not the viscosity of synovial fluid that is responsible
for lubrication of this system but the stickiness or boundary phenomena exhibited by the
fluid. Viscous solutions containing no hyaluronate do not lubricate a soft tissue system
nearly as well as solutions containing hyaluronate of equal or even lower viscosity.
The lubricating properties of synovial fluid on articular cartilage were originally
attributed to its viscosity, which in turn is due to the presence of hyaluronate or mucin.
However, viscosity or the resistance of a fluid to shearing forces is not the same as
lubricating effectiveness. Digestion of synovial fluid hyaluronate by hyaluronidase, which
24

totally destroys the viscous nature of the fluid, does not decrease the lubricating properties
of synovial fluid on articular cartilage when compared with a nonviscous buffer. This is in
contrast to the finding that proteolytic digestion of synovial fluid decreases its lubricating
abilities. A glycoprotein has been isolated from synovial fluid. and removal of this fraction
from the fluid deprives it of its lubricating properties.
The mechanisms of cartilage-on-cartilage lubrication have been attributed to
boundary effects and the presence of a fluid film. The boundary effect of synovial fluid in a
cartilage-on-cartilage system is similar to that in a soft tissue system in that synovial fluid
readily adheres to the cartilage surfaces, helping to keep them apart and decreasing
frictional forces. Unlike the soft tissue system, however, the boundary effect of synovial
fluid is not due to the hyaluronate but to the lubricating glycoprotein fraction Of synovial
fluid. It is this fraction that sticks firmly to the articular cartilage surfaces. Although
hyaluronate does not directly decrease the coefficient of friction in a cartilage-on-cartilage
system, it may enhance the longevity of the lubricating ability of the protein fraction and
act as a spreading factor. Articular cartilage is quite resistant to shear forces but very
sensitive to impact loading. Boundary lubrication of articular cartilage is extremely
effective in preventing wear due to motion but loses its protective abilities under high
loads. Therefore, other lubricating mechanisms must be at work. Fluid-film lubrication is a
class of mechanisms of lubrication in which a film of fluid separates the opposing sliding
surfaces. Squeeze-film lubrication is a form of lubrication in which the approaching
surfaces generate pressure in the lubricant as they squeeze it out of the area of impending
contact. The resulting pressure keeps the surfaces apart, and the lubricant film that forms in
the area of impending contact is referred to as the squeeze film. Electromicroscopically,
articular cartilage is shown to have depressions and irregularities on its surface. In the early
phases of loading these depressions may trap fluid. With increasing load, the articular
cartilage surface may deform and the irregularities disappear. The surface deformation and
intrinsic elasticity of articular cartilage will tend to make the space of impending cartilage
contact narrower at its margin than at its center. More fluid will be trapped in the center of
the contact area where it may help to form a squeeze film. This mechanism of lubricant

25

trapping has been called "boosted" lubrication. However, there is disagreement regarding
the validity of a "boosted" component in the squeeze-film type of fluid-film lubrication.
In summary, synovial joints contain two systems that require lubrication: a soft tissue
system and a cartilage-on-cartilage system. Lubrication of the soft tissue system is of the
boundary type, requiring the hyaluronate of the synovial fluid to stick to the sliding
surfaces of the system, thus keeping them apart. In contrast, the cartilage-on-cartilage
system is independent of hyaluronate and dependent on a glycoprotein fraction of synovial
fluid. At low loads the lubricating action of the glycoprotein is of the boundary type. At
high loads the cartilage surfaces are kept apart by fluid film composed of fluid and
interstitial fluid wept from the articular cartilage itself. The elasticity of articular cartilage
may potentiate the fluid-film lubricating mechanisms at high loads.
Normal synovial fluid is clear, pale yellow, viscid, and does not clot. Studies of
mammalian synovial fluid have found considerable similarities among species, although
notable differences do exist. The majority of investigative work determining the
composition of synovial fluid has been performed on bovine synovial fluid mainly because
large quantities of it are available.
Synovial fluid is believed to have two main functions: to aid in the nutrition of
articular cartilage by acting as a transport medium for nutritional substances, such as
glucose, and to aid in the mechanical function of joints by lubrication of the articulating
surfaces. Articular cartilage has no blood, nerve, or lymphatic supply. Glucose for articular
cartilage chondrocyte energy is transported from the periarticular vasculature to the
cartilage by the synovial fluid. Under fasting conditions, the glucose concentration of
synovial fluid is usually approximately equal to that of blood. A decreased amount of
synovial fluid glucose may be associated with articular diseases, particularly septic and
immune-mediated arthritis.
Vascular permeability and synovial membrane permeability are altered by
inflammation, which accounts for protein content changes in diseased synovial fluid.
Immunoglobulins, immune complexes, and complement are produced by cells
26

accumulating in the inflamed synovial membrane and periarticular lymph nodes and find
their way to the synovial fluid.
Normal synovial fluid complement levels in humans are approximately 10% of the
serum values. In the inflamed joint synovial fluid complement levels will vary. The longterm patterns of variation have some prognostic value in human rheumatoid arthritis
patients.
III. DEFINITION
OA (osteoarthritis) is joint failure, a disease in which all structures of the joint have
undergone pathologic change, often in concert. The pathologic sine qua non of disease is
hyaline articular cartilage loss, present in a focal and, initially, nonuniform manner. This is
accompanied by increasing thickness and sclerosis of the subchondral bony plate, by
outgrowth of osteophytes at the joint margin, by stretching of the articular capsule, by mild
synovitis in many affected joints, and by weakness of muscles bridging the joint. In knees,
meniscal degeneration is part of the disease. There are numerous pathways that lead to joint
failure, but the initial step is often joint injury in the setting of a failure of protective
mechanisms.

27

IV. RISK FACTOR

The causes of primary OA probably are multifactorial: altered biomechanics, cytokine
abnormalities, and genetic factors may combine to initiate a cascade of changes that become
self-perpetuating as damage accumulates. The main risk factor for OA is age; more than 80%
of persons older than 75 years are affected. However, OA is not a natural consequence of
aging. 4
Family studies indicate that the heritable component of risk of OA may be 50% to
65%.5 Candidate genes have been identified as, among others, those coding for type II
collagen (Drug information on collagen), the vitamin D receptor, and the estrogen receptor.6
OA is twice as likely to develop in women as in men, especially after menopause. The
finding of functional estrogen receptors on chondrocytes suggests that estrogen deficiency
may mediate this association.7 In fact, hormone replacement therapy has been linked with
decreased rates of OA in women. 4

28

Secondary OA, which is less common than primary OA, may involve joints not frequently
affected by primary OA. The causes of secondary OA include metabolic, mechanical, and
inflammatory processes. 4
V. PHATOPHYSIOLOGY
Joint Protective Mechanisms And Their Failure
Joint protectors include: joint capsule and ligaments, muscle, sensory afferents, and
underlying bone. Joint capsule and ligaments serve as joint protectors by providing a limit
to excursion, thereby fixing the range of joint motion.10
Synovial fluid reduces friction between articulating cartilage surfaces, thereby serving
as a major protector against friction-induced cartilage wear. This lubrication function
depends on the molecule lubricin, a mucinous glycoprotein secreted by synovial fibroblasts
whose concentration diminishes after joint injury and in the face of synovial inflammation.
The ligaments, along with overlying skin and tendons, contain mechanoreceptor
sensory afferent nerves. These mechanoreceptors fire at different frequencies throughout a
joint's range of motion, providing feedback by way of the spinal cord to muscles and
tendons. As a consequence, these muscles and tendons can assume the right tension at
appropriate points in joint excursion to act as optimal joint protectors, anticipating joint
loading.
Muscles and tendons that bridge the joint are key joint protectors. Their cocontractions at the appropriate time in joint movement provide the appropriate power and
acceleration for the limb to accomplish its tasks. Focal stress across the joint is minimized
by muscle contraction that decelerates the joint before impact and assures that when joint
impact arrives, it is distributed broadly across the joint surface.
The bone underneath the cartilage may also provide a shock-absorbing function, as it
may give way subtly to an oncoming impulse load.

29

Failure of these joint protectors increases the risk of joint injury and OA. For
example, in animals, OA develops rapidly when a sensory nerve to the joint is sectioned
and joint injury induced. Similarly, in humans, Charcot arthropathy, which is a severe and
rapidly progressive OA, develops when minor joint injury occurs in the presence of
posterior column peripheral neuropathy. Another example of joint protector failure is
rupture of ligaments, a well-known cause of the early development of OA. 10
Cartilage And Its Role In Joint Failure
In addition to being a primary target tissue for disease, cartilage also functions as a
joint protector. A thin rim of tissue at the ends of two opposing bones, cartilage is
lubricated by synovial fluid to provides an almost frictionless surface across which these
two bones move. The compressible stiffness of cartilage compared to bone provides the
joint with impact-absorbing capacity. Both the smooth frictionless surface and the
compressive stiffness of cartilage serve as protective mechanisms preventing joint injury. 10
Since the earliest changes of OA may occur in cartilage and abnormalities there can
accelerate disease development, understanding the structure and physiology of cartilage is
critical to an appreciation of disease pathogenesis. The two major macromolecules in
cartilage are type 2 collagen, which provides cartilage its tensile strength, and aggrecan, a
proteoglycan macromolecule linked with hyaluronic acid, which consists of highly
negatively charged glycosaminoglycans. In normal cartilage, type 2 collagen is woven
tightly, constraining the aggrecan molecules in the interstices between collagen strands,
forcing these highly negatively charged molecules into close proximity with one another.
The aggrecan molecule, through electrostatic repulsion of its negative charges, gives
cartilage its compressive stiffness. Chondrocytes, the cells within this avascular tissue,
synthesize all elements of the matrix. In addition, they produce enzymes that break down
the matrix and cytokines and growth factors, which in turn provide autocrine/paracrine
feedback that modulates synthesis of matrix molecules (Fig. 326-3). Cartilage matrix
synthesis and catabolism are in a dynamic equilibrium influenced by the cytokine and
growth factor environment and by mechanical stress. While chondrocytes synthesize
numerous enzymes, especially matrix metalloproteinases (MMP), there are only a few that
30

are critical in regulating cartilage breakdown. Type 2 cartilage is degraded primarily by

MMP-13 (collagenase 3), with other collagenases playing a minor role. Aggrecan
degradation is complex but appears to be a consequence, in part, of activation of
aggrecanase 1 (ADAMTS-4) and perhaps of MMPs. Both collagenase and aggrecanase act
primarily in the territorial matrix surrounding chondrocytes; however, as the osteoarthritic
process develops, their activities and effects spread throughout the matrix, especially in the
superficial layers of cartilage. 10
The synovium and chondrocytes synthesize numerous growth factors and cytokines.
Chief among them is interleukin (IL) 1, which exerts transcriptional effects on
chondrocytes, stimulating production of proteinases and suppressing cartilage matrix
synthesis. In animal models of OA, IL-1 blockade prevents cartilage loss. Tumor necrosis
factor (TNF) may play a similar role to that of IL-1. These cytokines also induce
chondrocytes to synthesize prostaglandin E2, nitric oxide, and bone morphogenic protein 2
(BMP-2), which together have complex effects on matrix synthesis and degradation. Nitric
oxide inhibits aggrecan synthesis and enhances proteinase activity, whereas BMP-2 is a
potent stimulator of anabolic activity. At early stages in the matrix response to injury and in
the healthy response to loading, the net effect of cytokine stimulation may be matrix
turnover but, ultimately, excess IL-1 triggers a process of matrix degradation. Enzymes in
the matrix are held in check by activation inhibitors, including tissue inhibitor of
metalloproteinase (TIMP). Growth factors are also part of this complex network, with
insulin-like growth factor type 1 and transforming growth factor playing prominent roles in
stimulating anabolism by chondrocytes. 10

31

While healthy cartilage is metabolically sluggish, with slow matrix turnover and a
net balance of synthesis and degradation, cartilage in early OA or after an injury is highly
metabolically active. In the latter situation, stimulated chondrocytes synthesize enzymes
and new matrix molecules, with those enzymes becoming activated in the matrix, causing
release of degraded aggrecan and type 2 collagen into cartilage and into the synovial
fluid. OA cartilage is characterized by gradual depletion of aggrecan, an unfurling of the
tightly woven collagen matrix, and loss of type 2 collagen. With these changes comes
increasing vulnerability of cartilage, which no longer has compressive stiffness. 10 14

32

VI. DIAGNOSIS
Medical History and Physical Examination .
The pain that is associated with osteoarthritis of the hip is usually related to activity.
Patients typically report a gradual onset of hip pain, which increases with joint use and is
relieved, although incompletely, with rest. As the disease becomes more severe, morning
stiffness and pain (lasting up to 30 minutes) and pain at rest or at night are common.
However, hip pain at night may instead reflect inflammatory arthritis, infection, tumors, or
crystal diseases.
Physical examination should rule out other causes of hip pain. An assessment of the
range of motion of the knee joint and lower lumbar spine will help determine whether hip
33

pain is referred from these other joint areas. The strongest clinical indicator of osteoarthritis
of the hip is pain, exacerbated by internal or external rotation of the hip while the knee is in
full extension. Trochanteric bursitis and damage to the sciatic nerve can cause pain similar to
that of osteoarthritis of the hip but may be distinguished by the presence of associated
tenderness over the greater trochanter (for trochanteric bursitis) and pain in the posterior hip
or buttocks (for sciaticnerve damage associated with lumbar radiculopathy) Anterior or
inguinal pain and tenderness generally indicate trueinvolvement of the hip joint. In about
20% of patients with osteoarthritis of the hip, the condition is bilateral; both hip joints should
be examined.
The Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) is a
validated instrument for the assessment of pain, stiffness, and physical function in patients
with osteoarthritis of the knee or hip. Although this index is a useful research tool for
evaluating clinically relevant changes in health status after treatment, it is not routinely used
in clinical practice.
The diagnosis of hip OA can be made with a reasonable level of certainty on the basis
of the history and physical examination. Joint space narrowing along with other radiographic
features including osteophytes and subchondral sclerosis on plain lm radiographs is
considered the denitive diagnosis.3

34

LABORATORY TESTS
No blood tests are routinely obtained in the workup for a patient with chronic hip pain
unless the medical history and physical examination suggest inflammatory arthritis. Extraction
and examination of synovial fluid from the hip joint is not routine and requires guidance by
means of either ultrasonography or fluoroscopy. If the procedure is performed for suspected inf
lammatory arthritis, a white-cell count below 1000 per cubic millimeter in the synovial fluid is
consistent with osteoarthritis, whereas higher white-cell counts (above 2000 per cubic
millimeter) suggest inflammatory arthritis. The presence of crystals in thesynovial fluid supports
a diagnosis of gout or pseudogout.
Pelvic radiography that is performed while the patient is standing is used to confirm the
diagnosis of osteoarthritis, particularly if hip pain is moderate to severe, related to activity, or
present at night. Although these findings are all consistent with osteoarthritis, they may indicate
other conditions, including inflammatory arthritis and cancer. Moderate loss of joint space (i.e.,
an articular width of less than 2 mm),osteophyte formation, and sclerosis at the joint margins are
consistent with osteoarthritis of the hip. 3

35

AP radiographs of (A) a normal hip and three forms of abnormalities associated with mild slipped capital femoral
epiphyses called (B) flattening, (C) the bump, and (D) the hook. Reproduced with permission from Harris
WH. Etiology of osteoarthritis of the hip. Clin Orthop Relat Res.

Magnetic resonance imaging can reveal early changes in cartilage and bone that are
consistent with osteoarthritis but is not indicated for patients with chronic hip pain unless
evaluation raises suspicion regarding a worrisome cause. 3
The following clinical criteria are typically present in individuals who have radiographic
ndings consistent with hip OA. Reports of moderate pain in the lateral or anterior hip with
weight bearing. This pain may progress to the anterior thigh or knee region Adults, greater than
50 years of age. Limited passive hip joint ROM in at least 2 of its 6 directions (exion,
extension, abduction, adduction, internal rotation, and external rotation) Morning stiffness, which
improves in less than 1 hour Clinical criteria for the classication of patients with hip pain
associated with OA were developed through a multicenter study by the American College of
Rheumatology. 3
One hundred fourteen patients, with a mean age of 64 years and 87 controls with a mean
age of 57 years, were included in the study. Patients were classied as having hip OA if they (1)
reported experiencing hip pain,and (2) presented with either one of the following clusters of
clinical ndings: 3
-

Hip internal rotation less than 15, along with

Hip exion less than or equal to 115
Age greater than 50 years

Hip internal rotation greater than or equal to 15, along with

Pain with hip internal rotation
Duration of morning stiffness of the hip less than or equal to 60 minutes
Age greater than 50 years 3

Or,

When patients were classied using these clinical criteria compared to a radiographic
reference standard of joint space narrowing and osteophytes, the following diagnostic accuracy
statistics were reported: sensitivity, 86%; specicity, 75%.
Hip OA is classied as primary in the absence of any obvious underlying joint abnormality,
or secondary if degeneration occurs as a result of a pre-existing abnormal joint Problem. Some
suggest that all hip OA is secondary to some pre-existing problem (eg, dysplasia). The clinical
36

and/or radiological criteria presented above are usually sufcient to diagnose a patient with OA
of the hip and the associated ICF impairment-based category of hip pain (b2816 Pain in joints)
and mobility decits (b7100 Mobility of a single joint). 3
IMAGING STUDIES
Imaging studies, specically plain lm radiographs, are conrmatory for moderate to
severe hip joint OA; however, radiographs are less useful in demonstrating early osteoarthritic
joint changes. Joint space narrowing detected on radiographs may be a relatively late stage
phenomenon of OA. Joint space narrowing has been advocated as the best indicator and best
predictor of arthritic change in patients with hip OA, with joint space narrowing occurring more
superiolateralthan superiomedial. The normal hip joint space is 3 to 5 mm. A reduction of
greater than or equal to 0.5 mm represents a clinically relevant and signicant reduction in joint
space width. Hip joint OA is considered moder- ate when joint space is less than 2.5 mm and
severe when joint space is less than 1.5 mm. The development of newer imaging techniques,
such as gadolinium enhanced magnetic resonance imaging, has been suggested as a method to
detect deciencies in cartilage structure that may represent early arthritic changes in young
patients. 16
In addition to joint space narrowing, other criteria, including osteophytic spurs and
subchondral sclerosis, also are used to identify patients with hip OA. The Kellgren/Lawrence
scale has been used to classify degenerative ndings associated with hip OA. The scale consists
of 4 grades: grade 1, no radiographic evidence of OA; grade 2, doubtful narrowing of joint space
and possible (minute) osteophytes; grade 3, moderate denite osteophytes, denite moderate
narrowing of joint space; grade 4, large osteophytes, severe joint space narrowing, subchondral
sclerosis, and denite deformity of bone contour. A potential caveat when using the Kellgren/
Lawrence scale is spurs or osteophytes are emphasized and not all patients with hip OA have
osteophytes. 16
VII. DIFFERENTIAL DIAGNOSIS
37

The following differential diagnoses should be considered in an individual with signs or

symptoms suggestive of hip OA:
-

Bursitis or tendinitis
Chondral damage or loose bodies
Femoral neck or pubic ramus stress fracture
Labral tear
Muscle strain
Neoplasm
Osteonecrosis of the femoral head
Pagets disease
Piriformis syndrome
Psoriatic arthritis
Rheumatoid arthritis
Sacroiliac joint dysfunction
Septic hip arthritis
Referred pain as a result of an L2-3 radiculopathy 16
The following physical examination measures may be helpful in the differential

diagnostic process when differentiating hip pain from other sources of pain:
-

The Scour test for labral tears

FABER (Patricks) test for labral tears
Fitzgeralds test for labral tears
Flexion-adduction internal rotation tests for labral tears
Sacroiliac joint provocation tests for sacroiliac joint pain
Femoral nerve stretch test for L2-3 radiculopathy
Clinicians should consider diagnostic classications other than osteoarthritis of the hip

when the patients history, reported activity limitations, or im-pairments of body function and
structure are not consistent with those presented in the diagnosis/classication section of this
guideline, or, when the patients symptoms are not diminishing with interventions aimed at
normalization of the patients impairments of body function. 16
VIII.

TREATMENT
Osteoarthritis (OA) is the most common type of arthritis and the major cause of
chronic musculoskeletal pain and mobility disability in elderly populations worldwide.
Knee and hip pain are the major causes of difculty in walking and climbing stairs in
38

the elderly in Europe and the USA and as many as 40% of people over the age of 65 in
the community in the United Kingdom suffer symptoms associated with knee or hip OA.
Treatment of OA of the knee and hip is directed towards:

Reducing joint pain and stiffness.

Maintaining and improving joint mobility.

Reducing physical disability and handicap.

Improving health-related quality of life.

Limiting the progression of joint damage.

Educating patients about the nature of the disorder and its management.
More than 50 modalities of non-pharmacological, pharmacological and surgical

therapy for knee and hip OA are described in the medical literature. Over the years a
number of National and Regional Guidelines

have

been

developed

to

assist

physicians, allied health professionals and patients in their choice of therapy for the
management of knee and hip OA, but internationally agreed and universally applicable
guidelines for the management of these global disorders have been lacking.
In September 2005 the Osteoarthritis Research Inter- national (OARSI)
appointed an international, multidisciplin- ary committee of experts with a remit to
produce up to date, evidence-based, globally relevant, consensus recom- mendations
for the management of knee and/or hip OA in 2007. The rst part of the work of this
committee was to un- dertake a critical appraisal of all existing evidence-based and
consensus guidelines for the treatment of knee and/or hip OA and a systematic review
of the recent research evidence. The results of this critical appraisal and systematic
review
were published recently. This second part of the report con- tains the current OARSI
evidence-based, expert consensus recommendations for the treatment of knee and/or hip
OA.

39

40

Pharmacological Therapy
Pharmacologic modalities.
The approach to pharmacologic therapy for the patient with hip OA is similar to that for
the patient with knee OA except that no recommendations were made for intraarticular
hyaluronates, duloxetine, or topical NSAIDs because of the lack of data fromRCTs on either
benet or safety at the time of the TEP meeting in December 2008. Again, opioid analgesics are
strongly recommended only for patients with symptomatic hip OA who have not had an adequate
response to both nonpharmacologic and pharmacologic modalities and are either unwilling to
undergo or are not candidates for total joint arthroplasty. 9

Pharmacologic recommendations for the initial management of hip oa*

We conditionally recommend that patients with hip OA should use one of the following:
-

Acetaminophen

Oral NSAIDs

Tramadol

Intraarticular corticosteroid injections

We conditionally recommend that patients with hip OA should not use the following:
-

Chondroitin sulfate

Glucosamine

We have no recommendation regarding the use of the following:

-

Topical NSAIDs

Intraarticular hyaluronate injections

Duloxetine

Opioid analgesics
41

* No strong recommendations were made for the initial pharmacologic management of hip
osteoarthritis (OA). For patients who have an inadequate response to initial pharmacologic
management, please see the Results for alternative strategies. NSAIDs _ nonsteroidal
antiinammatory drugs.

1. Glucosamine sulfate and chondroitin sulfate

Glucosamine is one of the most commonly used complementary or alternative medicine
products in North America. Typically derived from the ground shells of shellfish or from
processed grains, glucosamine has proponents who claim it restores glycosaminoglycans in
arthritic joints and reduces pain and inflammation. Evidence for the proposed mechanism is
insufficient in vivo, but some studies have reported benefits from glucosamine in terms of
pain relief and even radiographic progression.Evidence for a positive effect is controversial,
however, with several studies showing no benefit over placebo. The Osteoarthritis Research
Society International (OARSI) guidelines state that treatment with glucosamine and/or
chondroitin sulphate may provide symptomatic benefit in patients with knee OA, but if no
response is apparent within 6 months treatment should be discontinued.Other guidelines,
such as those for the American Academy of Orthopaedic Surgeons, make a recommendation
that physicians not prescribe glucosamine. Both sets of guidelines are based on level I
evidence. This disparity in recommendations is considered to be due to the heterogeneity of
existing studies, of allocation concealment. Little or no benefit has been observed when
concealment is adequate. Evidence regarding chon droitin sulfate is similarly inconsistent.
There is marked heterogeneity of outcomes between trials, and again higher-quality studies
with adequate concealment have been unable to show significant benefit Overall, the
evidence

and

recommendations

remain

inconsistent

for

both

glucosamine

and

chondroitin.We do not recommend prescription of these supplements as their benefit remains

unproven, but the risk of their use seems limited to mild stomach upset and the cost of the
pills.A trial of treatment for 6 months would not be unreasonable if a patient expresses great
interest in such products. Future independent high-quality studies are required to further
clarify the efficacy of both agents. 5 7 17
42

2. Acetaminophin
Several studies have shown acetaminophen to be superior to placebo and
equivalent to nonsteroidal anti-inflammatory agents (NSAIDs) for the short-term
management of OA pain. At present, acetaminophen (up to 4,000 mg/daily) is the
recommended initial analgesic of choice for symptomatic OA. ( ACR GuidelinesGuidelines for Medical Management of OA of the knee) However, many patients
eventually require NSAIDs or more potent analgesics to control pain.
Acetaminophen is a common first-line analgesic for treatment of hip and knee
osteoarthritis. OARSI found the use of acetaminophen to be a core rec- ommendation in
16 of 16 guidelines evaluated. Compared with placebo, statistically significant effects
on pain relief have been demonstrated with- out statistically significant risk of tox- icity.
OARSI guidelines recommend up to 4 g per day as an effective first- line therapy in
patients with mild to moderate pain from OA. Current European League Against
Rheuma- tism (EULAR) recommendations for hip and knee OA suggest that acetaminophen at these doses should be the first choice for mild to moderate pain, and if
successful, should be used as the preferred long-term oral anal- gesic. For most
patients the differ- ence in pain relief between acetamin- ophen and NSAIDs is not
clinically significant. 5 7
Higher doses of acetaminophen or even prolonged use at recommended doses are
not without risk. Although not common in the studies referenced by the guidelines above,
acetaminophen overdose can result in hepatoxicity and severe sequelae. Patients should
be counseled and monitored regard- ing their daily dosage. In the absence of an
adequate response, or in the pres- ence of severe pain or inflammation (or both),
alternative therapy should be considered. Combining acetamin- ophen with another
medication (e.g., ibuprofen) at lower doses of each can also be effective. NSAIDs or
nonsteroidal anti-inflam- matory drugs are among the most commonly used
analgesics in the world and are often used as first-line medications for joint pain. One
UK telephone survey in 2003 reported that 50% of respondents with osteoarthri- tis were
43

taking NSAIDs. 5 7
There is good level I evidence for the analgesic effect of NSAIDs in OA, and
meta-analyses of short-term, placebo-controlled randomized trials have shown an effect size
between 0.23 and 0.32 in terms of reduction in pain.2 NSAIDs, however, are associated
with more adverse effects than acet- aminophen. 2,3 Gastrointestinal (GI) discomfort
occurs more frequently and, more importantly, serious com- plications such as peptic
ulcers, perfo- rations, and bleeds are more likely to occur. Pooled relative risk compared to
placebo is estimated at 270%. Risk also increases with age, concurrent use of other
medications, and duration of therapy. In patients at greater GI risk, there is level I evidence
that NSAIDs should be used in combination with a proton pump inhibitor or misoprostol
for gastroprotection, or that the use of a COX-2 selective agent should be con- sidered.
Gastroprotection is recom- mended in all eight of the guidelines where NSAIDs are
considered for the management of hip or knee OA.2 COX-2 inhibitors are recommended
in all 11 of the guidelines where they are considered.2 H2-receptor antago- nists do not
have similar protective qualities, and the GI benefit associat- ed with COX-2 agents is lost
with con- current low-dose daily acetylsalicylic acid. Cardiovascular (CV) risk is anoth- er
concern. After rofecoxib was with- drawn from the market due to in- creased risk of
thrombotic events, a number of studies were done to inves- tigate the CV safety of other
NSAIDs. Celecoxib and valdecoxib do not appear to have the same risks, and overall
CV risk with COX-2 inhibitors has not been found significantly high- er than with
nonselective NSAIDs.Serious vascular events occur at ap- proximately 1% per year on
COX-2 inhibitors versus 0.9% on traditional NSAIDs.
CV risk is greater in patients with a history of ischemic heart disease or stroke, or in
patients with risk factors for heart disease such as hypertension, hyperlipidemia, diabetes,
smoking, or peripheral arterial disease.2 Caution should be exercised when prescribing all
NSAIDs in these patients. Renal toxicity is also a concern in selected patients. In patients
with con- gestive heart failure, pre-existing renal insufficiency, or transplanted kidneys,
the use of NSAIDs can lead to acute renal failure. Care should be taken to screen for
clinical or labora- tory evidence of existing diminished creatinine clearance and considera44

tion should be given to follow-up lab analysis after treatment is begun. Renal clearance
decreases significant- ly with age.
In patients with symptomatic hip or knee OA, NSAIDs should be used at the lowest
effective dose and their long-term use should be avoided if possible.2,3 In patients at greater
GI risk, either a COX-2 selective agent or a nonselective NSAID in combination with a
gastroprotective agent should be considered.2,3 All NSAIDs should be used with caution in
patients with CV risk factors.2 Physicians should continue to choose an NSAID on the basis
of the agents overall safety profile and the patients individual risk factors. 5 7 17
3. Opioids
Weak opioids have increasingly been used recently for the treatment of refractory
pain in patients with hip or knee OA. A number of systematic reviews and meta-analyses
of opioids for chronic non-cancer pain, musculoskeletal pain, and OA have provided
evidence of efficacy and acceptable safety in short-term trials.2 Analysis of 18
randomized placebo- controlled trials of 3244 OA patients showed a moderate effect size
for reduction in pain intensity (0.25).2 However, there was substantial heterogeneity
between studies. This was not obviously related to the preparation used or the quality of
the RCTs.2 A systematic review regarding acetaminophen and codeine combinations
indicated a small analgesic benefit over acetaminophen alone (approximately 5%), but
adverse effects were more frequent.2 Another meta-analysis of opioids for chronic noncancer pain, including OA, dem onstrated that only strong opioids were significantly
more effective in relieving pain than acetaminophen or NSAIDs.2 Benefits associated
with the use of opioids, however, are limited by frequent side effects such as nausea
(30%), constipation (23%), dizziness (20%), somnolence (18%), and vomiting (13%).2
One-quarter of patients treated with opioids withdrew from studies. This compared with
7% of placebo-treated patients. There have been no long-term trials of the use of opioids
for OA, and ongoing concerns remain about the risks of dependence. Recovery from
arthroplasty surgery is more difficult for patients on chronic opioid therapy, and their
optimal outcome may be compromised. We feel that strong opioid analgesics should be
reserved for patients in exceptional circumstances with severe pain who are not
candidates for other therapy. Short courses of weak opioids like codeine or tramadol and
45

acetaminophen combinations can be used for brief exacerbations of pain if tolerated.2

When prescribing these, precautions should be taken: patients should be counseled about
their use and potential for dependence. Nonpharmacological therapies should continue
and surgical treatments should be considered. It is highly recommended that strong
narcotics such as morphine, oxycodone, and hydromorphone not be prescribed for
osteoarthritis. Instead, patients should be referred for surgical treatment. 5 7 17
4. Non-steroidal Anti-inflammatory Agents (NSAIDs)
NSAIDs have been an important treatment for the symptoms of OA for a very long
time. The mechanism by which NSAIDs exert their anti-inflammatory and analgesic effects
is via inhibition of the prostaglandin-generating enzyme, cyclooxygenase (COX) . In addition
to their inflammatory potential, prostaglandins also contribute to important homeostatic
functions, such as maintenance of the gastric lining, renal blood flow, and platelet
aggregation. Reduction of prostaglandin levels in these organs can result in the wellrecognized side effects of traditional non-selective NSAIDs (ibuprofen, naprosyn,
indomethacin) that is, gastric ulceration, renal insufficiency, and prolonged bleeding time.
The elderly are at higher risk for these side effects. Other risk factors for NSAID-induced GI
bleed include prior peptic ulcer disease and concomitant steroid use. Potential renal toxicities
of NSAIDs include azotemia, proteinura, and renal failure requiring hospitalization.
Hematologic and cognitive abnormalities have also been reported with several NSAIDs.
Therefore, in elderly patients, and those with a documented history of NSAID-induced
ulcers, traditional non-selective NSAIDs should be used with caution, usually in lower dose
and in conjunction with a proton pump inhibitor. Renal function should be monitored in the
elderly. In addition, prophylactic treatment to reduce risk of gastrointestinal ulceration,
perforation and bleeding is recommended in patients > 60 years of age with: prior history of
peptic ulcer disease; anticipated duration of therapy of > 3 months; moderate to high dose of
NSAIDs; and, concurrent corticosteroids. The development of selective cyclooxygenase-2
(COX-2) inhibitors offers a strategy for the management of pain and inflammation that is
likely to be less toxic to the GI tract. 5 7 17
COX-2 Inhibitors
46

Cyclooxygenase-2 (COX-2) inhibitors are a class of NSAIDs) that recently received

Food and Drug Administration (FDA) approval. These specific COX-2 inhibitors are
effective for the pain and inflammation of OA. Their theoretical advantage, however, is that
they will cause significantly less toxicity than conventional NSAIDs, particularly in the GI
tract. NSAIDs exert their anti-inflammatory effect primarily by inhibiting an enzyme called
cyclooxygenase (COX), also known as prostaglandin (PG) synthase. COX catalyzes the
conversion of the substrate molecule, arachidonic acid, to prostanoids. 5 17

Prostanoids consist of prostaglandins E, D and F2a, prostacyclin and thromboxane. The

major inflammatory vasoactive prostanoids are PGE2 and prostacyclin. Thromboxane is critical
for platelet clotting, while PGD2 is involved in allergic reactions and PGF2a in uterine
contraction. 5
Use of non-steroidal anti-inflammatory drugs
Statement

Category of

NSAIDs are effective drugs in relieving pain and immobility associated with

evidence
A*

osteoarthritis. COX-2 selective agents are equally effective.

NSAIDs and COX-2 inhibitors vary in their potential gastrointestinal, liver and

A*

cardio-renal toxicity. This risk varies between individual treatments within both
groups and is increased with dose and duration of treatment
COX-2 selective agents are associated with a significantly lower gastrointestinal
47

A*

toxicity (PUBs and dyspepsia) compared to non-selective NSAIDs. Coprescribing of aspirin reduces this advantage.
PPI should always be considered with a non-selective NSAID and with a COX-2

agent in higher GI risk patients.

*A-Directly based on evidence from a meta-analysis of randomised controlled trials or from at least one randomised
controlled trials.
C Directly based on evidence from non-experimental descriptive studies, such as comparative studies, correlation
studies and case control studies or extrapolated from meta-analysis of randomised controlled trials, or extrapolated
from at least one randomised controlled trial.

5. Topical Agents
Adjunctive treatments or alternatives to oral analgesics in knee OA.2 Ameta-analysis of
13 RCTs, including 1983 patients with hand and knee OA, showed topical NSAIDs to be
superior to placebo in terms of analgesia, relief of stiffness, and function, with a reduced
relative risk of adverse GI events compared with oral forms. In one large case control study
topical NSAIDs were reported to have no more GI side effects than placebo. Topical NSAIDs
are less effective than oral NSAIDs in the first week of treatment, but efficacy is apparent
within 2 weeks, with pain relief effect.
Topical analgesic therapies include topical capsaicin and methyl salicylate creams.
There is an FDA approved topical NSAID for the treatment of OA, diclofenac gel, which can
be particularly useful for patients who are intolerant to the gastrointestinal side effects of
NSAIDs.Topical NSAIDs can be effective.
Topical capsaicin creams contain a lipophilic alkaloid extracted from chili peppers that
activates and sensitizes peripheral pain and heat receptors by binding and activating specific
cation channels. Application to the skin causes a burning sensation initially but can lead to
effective analgesia that prevails over the sensation of burning. The efficacy of capsaicin is
supported by a meta-analysis of RCTs of its use in the treatment of chronic painful
conditions, including a single placebo-controlled trial in 70 patients with knee OA and two
RCTs in patients with hand OA. The mean reduction in pain was 33% after 4 weeks of
therapy.2 Treatment is safe, but local burning, stinging, or erythema troubles 40% of patients.
48

The burning sensation also prevents adequate blinding with this agent, which may influence
conclusions based on the available data. Despite these shortcomings, topical capsaicin can be
a useful alternative or adjunctive treatment in selected patients.2 A typical dose is 0.025%
cream four times a day.17
6. Intraarticular Therapies
The judicious use of intra-articular glucocorticoid injections is appropriate for OA
patients who cannot tolerate, or whose pain is not well controlled by, oral analgesic and antiinflammatory agents. Periarticular injections may effectively treat bursitis or tendonitis that
can accompany OA. The need for four or more intra-articular injections suggests the need for
orthopedic intervention. Intraarticular injection of hyaluronate preparations has been
demonstrated in several small clinical trials to reduce pain in OA of the knee. These
injections are given in a series of 3 or 5 weekly injections (depending on the specific
preparation) and may reduce pain for up to 6 months in some patients.
Intra-articular injection of the hip generally requires fluoroscopic or ultrasound
guidance to ensure accurate placement. Multiple descriptions exist for intra-articular
injection of the knee joint. The patient should be supine and relaxed. It is easiest to inject the
knee in full extension. All injections should be performed in a sterile manner. Its helpful to
palpate surface landmarks prior to antiseptic cleansing and draping. A 25-gauge 11/2 inch
needle should be used. One study found the lateral mid-patellar ap proach to have the greatest
accuracy.5 More common, and our method of choice, is to use the soft point at the superior
lateral pole of the patella between the patella and the femur, with the needle inserted into the
uprapatellar pouch at that level. Entry should be deliberate and smooth. Joint effusion can
make the process much easier, while factors such as joint degeneration, diminished range of
motion, and obesity can make insertion more difficult.If the needle meets an obstruction, pull
back slightly and adjust the trajectory. Aspiration of joint fluid can be used for confirmation
of accurate placement. During injection, patient complaints of increased pain should be
considered an indication of possible extra-articular placement. The fluid should flow
smoothly and cause little or no discomfort. If infiltration is difficult, reposition and reattempt
injection as necessary. 17
49

Viscosupplementation
Hyaluronic acid (HA) or hyaluronan is a glycosaminoglycan constituent of synovial
fluid. Injection of HA preparations into the knee and hip is commonly used to treat
osteoarthritis, but there is considerable ongoing controversy about the treatments efficacy,
cost-effectiveness, and benefit-to-risk ratio.Numerous studies have examined the
effectiveness of various HA preparations and generally show positive effects, but there are
significant concerns in terms of trial quality, potential publication bias, and unclear clinical
significance. Pooled effects from poor-quality trials are as much as twice those obtained from
higher quality ones. In systematic reviews there is significant heterogeneity between studies
and evidence to suggest publication bias and overestimation of effect size. A Cochrane
review of 40 placebo controlled trials with five different hyaluronan products found
statistically significant improvements in pain on weight bearing when results were pooled,
but improvements were variable. Pain reduction from baseline at 5 to 13 weeks varied from
28% to 54% for pain and 9% to 32% for functional outcome scores.2 Data to suggest that the
higher molecular weight HA preparations were more effective than lower molecular weight
preparations were inconclusive.2 In a randomized comparison of three injections of high and
low molecular weight HA, there were significant improvements of approximately 40% in
pain and functional scores up to 6 months after treatment. However, in another
placebocontrolled trial comparing HA with corticosteroid or saline at 2 weekly intervals,
there were no significant differences between the groups.Discordant conclusions in
systematic reviews of HA have been found to be due to inclusion of different controlled
trials, differences in the outcome measures and time points selected for extraction, and
different statistical methods for data synthesis, which resulted in conflicting estimates of
therapeutic effect.No major safety issues were detected, but in placebo-controlled trials minor
adverse events such as transient pain at the injection site occurred slightly more frequently in
patients treated with intra articular hyaluronan than in those treated with intraarticular
corticosteroids. Because of the conflicting evidence from the literature and existing
guidelines, the use of intra-articular HA is not universally recommended.Relief may be
gained for patients with mild to moderate hip or knee OA symptoms, and results are
characterized by delayed onset but prolonged duration. The adequacy of clinical benefit
50

remains somewhat unclear and costs are not insignificantinjections typically range from
$130 to $230 per injection and 3 to 5 weekly injections are required. We tend not to
recommend these injections, particularly in patients with moderate to severe disease, but if
patients are given realistic expectations and have adequate resources, a trial of therapy is not
unreasonable,particularly for mild OA. 17
7. Corticosteroid therapy
Despite the unclear role of inflammation in the pathogenesis and progression of
osteoarthritis, 11 of 13 existing treatment guidelines recommend injection of
corticosteroids for OA at some stage of the disease. Multiple systematic reviews conclude
that it is effective for relieving pain at least in the short term (i.e., 1 to 2 weeks). The
efficacy is also supported by evidence from a Cochrane systematic review, which
examined data from 13 randomized placebo-controlled trials. The effect size for pain
relief is in the moderate range (0.25) at 2 and3 weeks after injection, with a lack of
evidence for pain relief by 4 weeks and 24 weeks after injection. Evidence for hip steroid
injection is more limited, and mixed in terms of results.Some randomized controlled trials
have demonstrated better outcomes in patients with synovial effusions or other clinical
signs of inflammation, but this has not been seen universally and it remains controversial
whether steroid injections should be restricted to these patients.2 The analgesic effect
may be due to additional mechanisms unrelated to the purely anti-inflammatory effect. In
terms of toxicity, potential side effects include post-injection flares of pain, crystal
synovitis, hemarthrosis, joint sepsis, articular cartilage atrophy, and steroid-induced
arthropathy. Side effects such as bruising and lipodystrophy are not uncommon but can
be minimized with careful technique. Overall, in 28 controlled trials of intra-articular
steroid injections in 1973 patients with OA of the knee, no serious adverse events were
reported as a consequence.2 In cases where inflammatory or infectious arthritis is
considered, aspiration and analysis of synovial fluid prior to injection should also be
considered. OARSI guidelines state that intraarticular injections with corticosteroid can
provide short-term symptomatic relief of knee OA, and should be considered, particularly
in cases of moderate to severe pain not responding to other analgesics and
51

nonpharmacologic modalities. Anecdotally we have found a small percentage of patients

to achieve long-term improvement. For the most part, however, improvements are shortlived for what is a chronic problem.7 Too few head to head comparisons exist to support
any particular choice of corticosteroid, and data are insufficient to state how frequently it
is safe to repeat injections. More than four times annually is generally not recommended.
One indication for these injections is if a patient needs to be active for a short period of
time while awaiting surgery, either because of work or family commitments. The
temporary relief, particularly if the patient is clearly informed about its temporary nature,
is often appreciated. 17
8. Antidepressants
Depression and osteoarthritis are both common and often coexist. Multiple studies
have demonstrated that psychosocial factors are equally or more important than diseasespecific factors in reports of pain intensity and disability in several conditions, including
joint pain. Awareness and treatment of depressive symptoms can result in significantly
less pain and improved quality of life. In one study of older adults with arthritis and
comorbid depression, treatment of depression extended beyond improved mood to
significant improvement in pain, function, and quality of life. 17

Non-pharmacological Management
Base case. An adult with symptomatic hip OA without cardiovascular comorbidities,
current or past up- 2012 ACR Recommendations for Management of Hand, Hip, and Knee OA
471 per GI problems, or chronic kidney disease presents to her primary care provider for
treatment. As few trials have been performed in patients with symptomatic hip OA, the TEP (
Technical Expert Panel ) considered that patients with hip OA should be treated in a similar
fashion to those with knee OA except for selected differences.
52

Nonpharmacologic modalities.
The TEP ( Technical Expert Panel ) strongly recommends that all patients with
symptomatic hip OA be enrolled in an exercise program commensurate with their ability to
perform these activities. The TEP expressed no preference for aquatic exercises as opposed to
land-based exercises based on benets or safety; the decision should be individualized and based
on patient preferences and the ability to perform exercises. The TEP strongly recommends that
all patients with symptomatic hip OA who are overweight be counseled regarding weight loss.
The TEP conditionally recommends that patients with hip OA should 1) participate in selfmanagement programs that may include psychosocial interventions, 2) use thermal agents and
manual therapy in combination with exercise supervised by a physical therapist, and 3) use
walking aids, if necessary. Interventions for which data are available only for knee OA and not
hip OA were not considered for patients with only hip OA (e.g., insoles, patellar taping,
acupuncture, transcutaneous electrical stimulation, tai chi).
1. Weight reduction
Two relevant SRs have been published since 2006. One reviewed studies of physical
therapy interventions which included weight reduction while the other focussed on studies
specically designed to look at outcomes in patients with knee OA as a result of therapeutic
weight reduction . There are now four published RCTs which have examined symptomatic
outcomes following weightreduction. However, the recommendation that patients with hip
OA should be encouraged to lose weight and maintain their weight at a lower level is still
only based on expert opinion unsupported by research evidence (LoE IV).
Weight reduction in obese patients has been shown to significantly relieve pain,
presumably by reducing biomechanical stress on weight bearing joints. Exercise has also
been shown to be safe and beneficial in the management of OA. It has been suggested that
joint loading and mobilization are essential for articular integrity. In addition, quadricep
weakness, which develops early in OA, may contribute independently to progressive articular
damage. Several studies in older adults with symptomatic knee OA have shown consistent
improvements in physical performance, pain and self-reported disability after 3 months of
53

aerobic or resistance exercise. Other studies have shown that resistive strengthening
improves gait, strength and overall function. Low-impact activities, including water-resistive
exercises or bicycle training, may enhance peripheral muscle tone and strength and
cardiovascular endurance, without causing excessive force across, or injury, to joints. Studies
of nursing home and community-dwelling elderly clearly demonstrate that one additional
important benefit of exercise is a reduction in the number of falls. 15
2. Excercise
Seven new SRs of exercise therapy in OA hip and knee haveb been undertaken in
the past 3 years . In addition to conrming the conclusion from the earlier MA that both
strengthening and aerobic exercise are associated with relief of pain in knee OA , one SR
found that exercise, particularly strengthening exercise, was also associated with
reduction in pain in hip OA , and another showed that water-based exercise resulted in
relief of pain , and improvement in function in both knee and hip OA. The reported costs
per QALY were very variable depending on the type of exercise, the comparator used, the
country where the study was undertaken and the perspective from which the EE was
undertaken . Within study direct comparisons suggest that class-based exercise may be
more economically efcient than home-based exercise, indirect comparisons between
studies suggest that water-based exercise may not necessarily be more cost-effective than
land based exercise. 15
Regular exercise is very important for successful control of osteoarthritis.
Strengthening and stretching exercises can help by:

Relieving pain and improving joint movement

Building up the muscles around the joint, making the joint more stable and resisting
further damage.
Specific exercises may be prescribed to improve strength and range of motion in

particular joints and muscles. Three types of exercise are used to treat osteoarthritis:
1. Stretching exercise
2. Isometric exercise
54

3. Aerobic (endurance) exercise

1. Stretching exercise.
Also called range-of-motion (ROM) exercise, it helps to maintain joint flexibility
and reach. It includes anything that puts a joint through its fullest range of motion (for
example, stretching the shoulder joint by holding the arms out at the sides and circling
them in a windmill fashion). Stretching exercise often is more easily performed if the
person takes a pain reliever or applies heat to the joint before starting to exercise.
2. Isometric exercise.
This is exercise in which muscles are tensed for a period without actually moving
them. It can be performed without actually bending a painful joint. As muscles are
exercised against resistance, their size and power will increase.
3. Aerobic exercise.
This is endurance-building exercise that improves cardiopulmonary (heart/lung)
fitness. For most individuals with osteoarthritis, the best aerobic exercises are:

Swimming (especially in a heated pool)

Walking on level ground

Such gentle exercises are less stressful on the joints. Water exercise is especially
recommended for people who have osteoarthritis of the large joints (hips, knees). The
buoyancy of the water makes it possible to exercise while the body weight is supported.
Since pain may worsen with increased activity, people with advanced osteoarthritis may
need to take several rest periods during the day. On the other hand, too much inactivity can
worsen osteoarthritis by causing increasing stiffness. An optimal treatment plan should achieve a
balance between daily exercise and adequate rest. 15

55

Summary of published guidelines for the use of exercise in the management of hip and knee
osteoarthritis. HOA, hip osteoarthritis; KOA, knee osteoarthritis; OA, osteoarthritis; EULAR,
European league against rheumatism; OARSI, osteoarthritis research society international; SRS,
scoliosis research society; ACR, American college of rheumatology; NHS, national health
service. Reproduced with permission from Iversen, MD. Presentation at EULAR meeting,
Copenhagen, DK.
3. Heat And Cold Therapy
Heat and cold treatments are well-known to reduce the pain, stiffness, and occasional
swelling associated with osteoarthritis. But this is generally temporary. There is no 'set'
formula for therapy. Heat works better for some individuals, whereas others favor cold.
Heat often is used to relieve pain or relax muscles before the start of exercise.

56

Heating pads or hot packs can be positioned over stiff joints. Some people prefer "moist
heat" in the form of warm towels, a warm shower or bath, or a heated whirlpool or hot
tub.

Other heat treatments include ultrasound and immersion of painful hands into warm wax.
All are able to bring soothing heat to sore joints.

Heat should be applied at a comfortable temperature and seems to be most beneficial

when used over the muscles adjacent to the joint.

Cold can lessen pain in a sore joint by numbing the local tissues.

It may be applied in the form of a reusable pack or ice.

Ice and cold packs never should be placed directly on the skin, as they are likely to
cause skin damage. Instead, ice and cold packs should be wrapped in a towel before they
are applied.

4.

Acupuncture
Nine SRs of the use of acupuncture for the treatment of OA published between 2006
and 2009 have conrmed that this non-pharmacological modality of treatment does have
some efcacy for relief of pain. The latest MA included results from 11 RCTs . Acupuncture
was compared with sham acupuncture, usual care or waiting list controls.

5.

Electromagnetic therapy
Treatment of OA knee or hip with electromagnetic therapy was not recommended in the
OARSI guidelines despite evidence from a 2002 Cochrane review suggesting that it might be
associated with relatively large improvements in pain in patients with knee OA. The
cumulative data showed that improvement in function was small, and there was no signicant
efcacy for reduction in pain.

6.

Surgical Management

57

Osteoarthritis of the hip is the most common reason for a hip replacement.
Osteoarthritis is caused by the wear and tear of aging. It causes the cartilage covering the
joint surfaces to wear out, resulting in pain and stiffness.
Although recent advances in joint surgery have improved the lives of millions of
people throughout the world, surgery is not the first line of treatment for osteoarthritis.
Before surgery is ever contemplated, simpler treatments must be tried. Moreover,
most surgeons prefer not to perform operative procedures in younger people unless their
quality of life is severely affected by arthritis.
Pain and mobility may worsen with hip osteoarthritis, even when all of the
recommended nonsurgical treatments have been tried. If this happens, the doctor may
recommend surgical treatment.
When surgery is necessary, it is performed by an orthopedic surgeon a specialist in
surgery of the bones and joints. 15
There are four main types of surgery available:
1. Fusion (permanent joining of the bones in a joint, preventing motion)
2. Osteotomy (realigning the joint)
3. "Scoping" the joint (washing out the joint)
4. Total joint replacement (replacement of a damaged joint with an artificial man-made

joint)
1. Fusion
Fusion of the joint, otherwise known as arthrodesis is a procedure in which the
surfaces of the joint are removed and the bone ends are united. This provides pain relief
and stability, but the joint cannot bend.

58

Lack of mobility is a serious disadvantage of this procedure. Nevertheless, this is

the preferred surgery for some younger individuals who have a single involved joint.
Mobility in the other joints often will compensate for the loss of movement in the fused
joint. The joints most commonly fused are smaller joints, such as those in the toes or
fingers.
Younger people with severe arthritis of the hip or knee in whom fusion was once
offered, are now considered for total joint replacement (see below), though depending
on the individual, a fusion may sometimes be preferable. 15
2. Osteotomy
Osteotomy is an operation in which the surgeon cuts the bone below the affected
joint, realigns it, and resets it in a better position. This procedure changes and improves
the contact between the remaining healthy areas of cartilage in the joint. Afterwards, the
painful areas do not rub against each other.
Osteotomy provides pain relief and leaves the joint mobile; however, it can only be
performed in a joint that is not already stiff. Osteotomy usually is reserved for joints with
uneven damage. It is not performed frequently, although the procedure sometimes is a
good choice for younger arthritis sufferers, since it can prevent further joint damage and
postpone the need for joint replacement surgery. (For example, osteotomy of the tibia
[shinbone] is performed to correct curvature and weight-bearing in the lower leg of adults
with OA of the knee.)
Candidates for osteotomy include younger patients with early arthritis, particularly
those with an abnormally shallow hip socket (dysplasia). The procedure involves cutting
and realigning the bones of the hip socket and/or thighbone to decrease pressure within
the joint. In some people, this may delay the need for replacement surgery for 10 to 20
years. 15
3. Scoping
59

"Scoping" the joint is an expression used to describe arthroscopy - the examination

of the inside of a joint using a device equipped with a tiny video camera. By means
of arthroscopy, the physician can look for damaged tissue directly within the joint.
A small incision is made through the skin alongside the affected joint. Then,
microsurgical tools are used to remove areas of cartilage or cartilage fragments that are
causing irritation and thoroughly wash out the joint. Arthroscopy is an outpatient
procedure and does not require an overnight stay in the hospital.
Joint "scoping" may provide temporary relief from symptoms - especially those
caused by cartilage tears or particles; however, it does not stop the progression of
osteoarthritis. It may help for a month in some, six months or much longer in others, and
sometimes not at all. 15

(Left) Your surgeon inserts the arthroscope through a small incision about the size of a
buttonhole. (Right) Other instruments are inserted to treat the problem.

During arthroscopy, surgeon can see the structures of your hip in great detail. (Right)
Small instruments are used to repair a labral tear.
60

4. Total joint replacement

Total joint replacement involves the complete removal of the painful joint, which is
exchanged for a man-made appliance. The artificial joint can be fashioned from a
combination of materials, including stainless steel, Vitallium (a cobalt-chromium
alloy), titanium, and high-density polyethylene plastic. Silicone rubber occasionally is
used for joint replacements (hand, base of the thumb), if the surgeon elects not to fuse the
joint.
The hip and knee have shown the greatest successes of all joint replacement
surgery. Over 90 percent of people are free of pain and have good mobility following hip
replacement surgery for osteoarthritis. Other joints that are less commonly replaced are
the shoulder and elbow.
Unfortunately, joint replacements tend to last only 10 to 20 years. But another
replacement generally can be performed, if needed. This repeat surgery is called a
revision.
Types of Hip Replacement
a. Traditional Hip Replacement
Traditional hip replacement surgery involves making a 10- to 12-inch incision
on the side of the hip. The muscles are split or detached from the hip, allowing the hip
to be dislocated.
Once the joint has been opened up and the joint surfaces exposed, the surgeon
removes the ball at the top of the thighbone, or femur. The hip socket is prepared by
removing any remaining cartilage and some of the surrounding bone. A cup-shaped
implant is then pressed into the bone of the hip socket. It may be secured with screws.
A smooth plastic bearing surface is then inserted into the implant so the joint can
move freely.

61

Next, the femur is prepared. A metal stem is placed into the femur to a depth of
about 6 inches. The stem implant is either fixed with bone cement or is implanted
without cement. Cementless implants have a rough, porous surface. It allows bone to
adhere to the implant to hold it in place. A metallic ball is then placed on the top of
the stem. The ball-and-socket joint is recreated. 13
b.

Minimally Invasive Hip Replacement

Minimally invasive hip replacement surgery allows the surgeon to perform the hip

replacement through one or two smaller incisions.

Candidates for minimal incision procedures are typically thinner, younger, healthier,
and more motivated to have a quick recovery compared with patients who undergo the
traditional surgery.
Before you decide to have a minimally invasive hip replacement, get a thorough
evaluation from your surgeon. Discuss with him or her the risks and benefits. Both
traditional and minimally invasive hip replacement procedures are technically
demanding. They require that the surgeon and operating team have considerable
experience.
Technique
The artificial implants used for the minimally invasive hip replacement procedures
are the same as those used for traditional hip replacement. Specially designed instruments
are needed to prepare the socket and femur and to place the implants properly.
The surgical procedure is similar, but there is less soft-tissue dissection. A single
minimally invasive hip incision may measure only 3 to 6 inches. It depends on the size of
the patient and the difficulty of the procedure.
The incision is usually placed over the outside of the hip. The muscles and tendons
are split or detached, but to a lesser extent than in the traditional hip replacement
operation. They are routinely repaired after the surgeon places the implants. This
encourages healing and helps prevent dislocation of the hip.
62

Two-incision hip replacement involves making a 2- to 3-inch incision over the groin
for placement of the socket. A 1- to 2-inch incision is made over the buttock for
placement of the stem.
To perform the two-incision procedure, the surgeon may need guidance from Xrays. It may take longer to perform this surgery than it does to perform traditional hip
replacement surgery.
Benefits
Reported benefits of less invasive hip replacement include:

Less pain

More cosmetic incisions

Less muscle damage

Rehabilitation is faster

Hospital stays are shorter

For traditional hip replacement, hospital stays average 4 to 5 days. Many patients

need extensive rehabilitation afterward. With less-invasive procedures, the hospital stay
may be as short as 1 or 2 days. Some patients can go home the day of surgery.
Early studies suggest that minimally invasive hip replacement surgery streamlines
the recovery process, but the risks and long-term benefits of less-invasive techniques
have not yet been documented. 13

63

(Left) The individual components of a total hip replacement. (Center) The components
merged into an implant. (Right) The implant as it fits into the hip

X-rays before and after total hip replacement. In this case, non-cemented components
were used.
Surgical Approaches
Total hip replacement is an effective treatment for reducing pain and disability and should
be considered in patients with osteoarthritis that causes chronic discomfort and substantial
functional impairment. The optimal time for joint-replacement surgery is not known. Although
surgery has typically been deferred until late in the course of arthritis, data from a prospective
cohort study have indicated that patients with higher functional status before surgery were more
64

likely to function independently 2 years after the procedure than were those with lower
functional status before surgery. These findings suggest a potential benefit of surgery earlier in
the disease course, before there is substantive functional decline. All total hip arthroplasties
consist of a femoral and acetabular component and a bearing surface (the area where the two
joint surfaces are in contact). The available systems use a separate femoral stem, femoral head,
acetabular liner, and acetabular shell. Fixation is achieved with cement or through bony ingrowth
into or onto the porous implant surface. Although earlier populationbased data suggested a
failure rate of 1% a year over a period of 10 years, advances in prostheses and fixation
techniques may result in a substantially longer life span for the replacement, although more data
are needed. Advances in instrumentation have allowed for smaller surgical incisions, with lower
complication rates, more prompt mobility, and shorter hospital stays, as compared with earlier
surgical approaches. Patients undergoing joint replacement may have better outcomes and fewer
complications if surgeons and hospitals perform an increased volume of arthroplasties annually.
A rehabilitation program that may continue for several months, depending on individual needs, is
indicated postoperatively for patients to regain reasonable useof the involved hip joint. Maximal
reduction in pain and improvement in function after a total joint replacement can take up to 12
months. Resurfacing arthroplasty (i.e., resurfacing of the arthritic femoral head and acetabular
bearing surface) has been used as an alternative to total hip replacement. Improvements in this
technique, such as the use of metal-on-metal bearings, rather than the earlier use of a cemented
polyethylene cup in the acetabulum, may reduce the risk of failure, but data from long-term
studies are lacking.56 Osteotomy (surgery to realign the femur or pelvis) is used to shift weight
from a damaged bone surface to a less damaged or normal one. In patients who have moderateto-severe hip dysplasia but little osteoarthritis and good range of motion, osteotomies and jointpreserving surgical procedures appear to be useful when total hip replacement is not yet justified.
Case series suggest that osteotomies may prevent the development of hip osteoarthritis, but more
outcome data are needed. 3
Patients in whom function and mobility remain compromised despite maximal medical
therapy, and those in whom the joint is structurally unstable, should be considered for surgical
intervention. Patients in whom pain has progressed to unacceptable levels-that is, pain at rest
and/or nighttime pain-should also be considered as surgical candidates. Surgical options include
65

arthroscopy, osteotomy and arthroplasty. Arthroscopic removal of intra-articular loose bodies and
repair of degenerative menisci may be indicated in some patients with knee OA. Tibial
osteotomy is an option for some patients who have a relatively small varus angulation (less than
10 degrees) and stable ligamentous support. Total knee arthroplasty is recommended for patients
with more severe varus, or any valgus, deformity and ligamentous instability. Arthroplasty is also
indicated for patients who have had ineffective pain relief following a tibial osteotomy, and for
those with advanced hip OA. Patients who have not yet developed appreciable muscle weakness,
generalized or cardiovascular deconditioning and who would medically withstand the stress of
surgery are ideal surgical candidates. In contrast, full mobility and function may not be
realistically expected in patients with significant cognitive impairment or symptomatic
cardiopulmonary disease, since these conditions can impede post-operative rehabilitation. 3

Surgical modalities of treatment

Patients with hip or knee OA who are not obtaining adequate pain relief and functional
improvement from a combination of non-pharmacological an pharmacological treatment should
be considered for joint replacement surgery. Replacement arthroplasties are effective, and costeffective interventions for patients with significant symptoms, and/or functional limitations
associated with a reduced health-related quality of life, despite conservative therapy.
Total hip arthroplasty (THA) and knee joint arthroplasty (TKA) are universally
recommended in 14/14 existing treatment guidelines, and generally accepted as reliable and
appropriate surgical procedures to restore function and improve health-related quality of life in
patients with hip and knee OA who are not obtaining adequate pain relief and functional
improvement

with

combination

of

pharmacological

and

non-pharmacological

treatments147,148. As ethical and methodological considerations have precluded evaluation of

total joint replacement with RCTs, evidence to support their efficacy is based substantially on
numerous uncontrolled observational studies and a very small number of cohort studies where
outcomes have been compared with standard medical care (LoE III). These are well summarised
in a 2004 qualitative and systematic review of the scientific literature relating to health-related
quality of life outcomes following THA and TKA149. This analysed the outcomes in 74
arthroplasty studies (32 hip and knee, 26 THA and 16 TKA alone) involving many thousands of
66

patients with OA. The Short Form-36 (SF-36) (40 studies) and the WOMAC index (28 studies)
were the instruments most frequently employed. Most studies reported on post-operative
outcomes up to 6 or 12 months but there were some data on clinical outcomes up to 7 years
following surgery. All studies reported substantial improvements in pain and physical
functioning but the effects on mental health and social functioning were more variable149. Pain
scores improved more quickly and more dramatically than physical functional outcomes with
maximal improvements in the first 3e6 months149. An earlier systematic review of outcomes
following THR with different types of prosthesis in 118 uncontrolled studies involving 77,375
patients with a mean follow up of 9.4 years (range 2e20 years) found that 43% (95% CI 34, 49)
to 84 (95% CI 46, 100) were free from pain, depending on the type of prosthesis used. Revision
rates ranged from 0.18 (S.E.M. 0.04) to 2.04 (S.E.M. 0.19)/100 person years150. MA of
functional outcomes following unicompartmental, bicompartmental151 and tricompartmental
knee arthroplasty showed mean improvements in a global knee score, incorporating pain,
function and range of motion,of 63%, 93%, and 100%, respectively, 4e6 years after surgery.
Cumulative revision rates at 10 years following THA and TKA for OA hip and knee were 7%153
and 10% respectively. A number of studies have shown that quality of life indices following THA
approximate to those in the age and gender matched population155e157 a year after surgery.
Overall THA is more effective than TKA in restoring patients with hip or knee OA to normal
function and age is not an obstacle to effective surgery149. However higher age, more
preoperative pain, musculoskeletal co-morbidities such as low back pain, and OA in the nonoperated hip, predict a poorer outcome following THA158. More severe pain, functional
limitation, low mental health scores and medical co-morbidities have also been shown to predict
a poorer outcome following TKA159. Following development and evaluation of explicit criteria
for the appropriateness of indication for THA160 and TKA161, based on a method that combines
expert opinion with available scientific evidence, it has recently been demonstrated that physical
and social functions as assessed by the SF-36 and WOMAC instruments improved to a
significantly greater extent following THA and TKA in patients where the indications for surgery
were appropriate163. THA and TKA were shown to be more cost-effective treatments for the
management of hip and knee OA than current pharmacological modalities of therapy in the first
part of this report4. The most recently published data suggest that the cost per QUALY gained
from TKA is twice that gained from THA. 1
67

Osteotomy and joint preserving surgical procedures should be considered in young

adults with symptomatic hip OA, especially in the presence of dysplasia.

Osteotomy is

recommended as a modality of treatment in 10/10 existing guidelines for the management of hip
or knee OA where this was considered . Intertrochanteric varus or valgus osteotomy has been
used as a treatment for hip OA for nearly a century and pelvic or femoral osteotomies are widely
advocated to correct the biomechanics and joint congruency in young patients with hip
dysplasias before the development of symptomatic hip OA edence to support the efcacy of
these procedures is limited to analysis of clinical outcomes in three uncontrolled prospective and
nine retrospective cohort studies (LoE III). 1
IX.

PROGNOSIS
In

most

cases,

OA of

the

hip

progresses

slowly197

with

total

hip

replacement/arthroplasty (THR/THA) being the primary clinical endpoint for individuals

with severe hip OA.69 The prognosis of hip OA depends primarily on the extent of
radiographic evidence of hip OA. The severity and progression of hip OA is commonly
assessed with the Kellgren/Lawrence scale of joint space narrowing on plain film
radiographs.99 A patients baseline Kellgren/Lawrence radiographic grade is an important
predictive factor for having THA. Reijman et al found that a Kellgren/Lawrence score of II
or higher is a strong predictor of progression in patients with hip OA. Gossec et al70 reported
that a Kellgren/Lawrence grade of III had an odds ratio of 3.3 and a grade of IV had an odds
ratio of 5.3 that patients would have a THA. Gossec et al70 also reported that the most
important predictive factors of having a THA include Kellgren/Lawrence radiographic grades
of III or higher, a high global assessment of pain, and a previous trial of nonsteroidal antiinflammatory drugs (NSAIDs). Altman et al5 have suggested that the measurement of
individual radiographic features may be superior to the Kellgren/Lawrence global
measurement in detecting arthritic progression. In OA of the hip, a single anteroposterior
radiograph assessing for joint space narrowing and cyst formation yielded high sensitivity in
detecting change. The MCID for joint space narrowing progression is greater than 0.5
mm/y.4,43 The rate of joint space narrowing in patients with slowly developing hip OA is
68

less than 0.2 mm/y and in patients with rapidly developing hip OA greater than 0.2 mm/y.66
In summary, joint space narrowing and the Kellgren/Lawrence scale are important prognostic
predictors of OA while joint space narrowing may be the best indicator of structural OA
progression in patients with hip OA. 16

CHAPTER III
CONCLUSION
Treatment of OA of the hip is directed towards:

Reducing joint pain and stiffness.

Maintaining and improving joint mobility.

Reducing physical disability and handicap.

Improving health-related quality of life.

Limiting the progression of joint damage.

Educating patients about the nature of the disorder and its management.

More than 50 modalities of non-pharmacological, phar- macological and surgical

therapy for knee and hip OA are described in the medical literature. Over the years a number of
69

National and Regional Guidelines have been developed to assist physicians, allied health
professionals and patients in their choice of therapy for the management of the hip OA, but
internationally agreed and universally applicable guidelines for the management of these global
disorders have been lacking.
Opioid analgesics are strongly recommended only for patients with symptomatic hip OA
who have not had an adequate response to both nonpharmacologic and pharmacologic modalities
and are either unwilling to undergo or are not candidates for total joint arthroplasty.
Although recent advances in joint surgery have improved the lives of millions of people
throughout the world, surgery is not the first line of treatment for osteoarthritis.

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