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

1

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

2

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

3

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.

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 mild-

to 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,

Paget’s disease,gout, and chondrocalcinosis. Localized risk factors include joint injury,

developmental deformities (e.g., slipped capital femoral epiphysis), Legg–Calvé–Perthes 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.

4

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 on pain relief and maximizing function and independence.

Pharmacotherapeutic options include acetaminophen, anti-inflammatory 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

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.

5

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.

6

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

7

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

neck’s posterior surface has a concave appearance. The head and neck are at an angle of 130º (±

7º) 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.

8

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

9

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

10

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

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

11

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

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.

12

Hip ligaments.

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.

13

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.

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 Root

level

Sensory Motor

Genitofemoral L1-2 Proximal anteromedial

thigh

None in hip and thigh

Obturator L2-4 Inferomedial thigh Gracilis (anterior division)

14

Adductor longus (anterior division)

Adductor brevis (anterior/posterior

division)

Adductor magnus (posterior division)

Lateral femoral cutaneous L2-3 Lateral thigh None

Femoral L2-4 Anteromedial thigh Psoas major

Sartorius

Articularis genus

Rectus femoris

15

Vastus lateralis

Vastus intermedius

Vastus medialis

Tibial L4-S3 None in thigh Biceps femoris (long head)

Semitendinosus

Semimembranosus

Common fibular (peroneal) L4-S2 None in thigh Biceps femoris (short head)

Posterior femoral

cutaneous nerve

S1-3 Posterior thigh None

16

Hip nerves, lateral view.

Hip nerves, anterior view.

17

Muscular Anatomy

The muscles of the hip joint are outlined in Table and the images below.

Muscles of Hip Joint

Muscle Action Nerve

Sartorius Hip flexion, external rotation Femoral nerve

Iliopsoas Hip flexion Femoral nerve

Pectineus Hip flexion Femoral nerve

Rectus femoris Hip flexion, leg extension Femoral nerve

Adductor magnus (anterior

part)

Hip flexion, adduction Obturator

Adductor magnus (posterior

part)

Thigh extension Tibial

Gracilis Hip flexion, adduction, internal

rotation

Obturator

Tensor fascia lata Hip flexion, abduction Superior gluteal nerve

Adductor brevis Hip adduction Obturator nerve (posterior

division)

Adductor longus Hip adduction Obturator nerve (anterior

division)

Pectineus Hip adduction, flexion Femoral

Obturator externus Thigh external rotation Obturator nerve posterior

division

Gluteus maximus Lateral rotation, extension Inferior gluteal nerve

Piriformis Lateral rotation Nerve to piriformis

Obturator internus Lateral rotation Nerve to obturator internus

Gemellus superior Lateral rotation Nerve to obturator internus

Gemellus inferior Lateral rotation Nerve to quadratus femoris18

Quadratus femoris Lateral rotation Nerve to quadratus femoris

Gluteus medius Hip abduction Superior gluteal nerve

Gluteus minimus Hip abduction Superior gluteal nerve

Semimembranosus Thigh extension, leg flexion Tibial

Semitendinosus Thigh extension, leg flexion Tibial

Biceps femoris, long head Thigh extension, leg flexion Tibial

Biceps femoris, short head Thigh extension, leg flexion Common fibular

Hip muscles, lateral view.

19

Hip muscles, anterior view.

Vasculature

he arteries of the hip are outlined in Table 3 and the image below.

Arteries of Hip Joint

Artery Branches

Obturator Anterior and posterior branches

Femoral 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

20

Superficial external pudendal

Deep external pudendal

Deep femoral artery

Descending genicular artery

Articular branch

Saphenous branch

Deep femoral

artery

Medial circumflex femoral: major supply to femoral neck

21

Lateral circumflex femoral: also supplies femoral neck

Ascending branch

Transverse branch

Descending branch

Perforators/muscular branches

Artery Course

Obturator

Artery of

ligament teres

Runs through ligament of femoral head

Deep femoral Branches from femoral artery in femoral triangle

22

artery

Medial

circumflex

femoral

Ascending

branch

Descending

branch

Lateral

circumflex

femoral

Ascending

branch

Cervical

branches

Between pectineus and iliopsoas to posterior femoral neck

Runs on quadratus femoris deep to sartorius and rectus femoris to greater trochanter

anteriorly

Extracapsular branches of anastomosis

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

Extends laterally

Under rectus femoris

23

Retinacular

arteries

Transverse

branch

Descending

branch

II. PHYSIOLOGY 24

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

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

25

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

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,

26

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

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

27

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

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 long-

term 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.

28

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

29

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 30

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 co-

contractions 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.

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

31

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

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 32

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

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

33

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 34

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 film radiographs is

considered the definitive diagnosis.3

35

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

36

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

findings 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 (flexion,

extension, abduction, adduction, internal rotation, and external rotation) Morning stiffness,

which improves in less than 1 hour Clinical criteria for the classification 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 classified as having hip OA if they (1)

reported experiencing hip pain,and (2) presented with either one of the following clusters of

clinical findings: 3

- Hip internal rotation less than 15°, along with

- Hip flexion less than or equal to 115°

- Age greater than 50 years

Or,

- 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

When patients were classified 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%; specificity, 75%.

37

Hip OA is classified 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

and/or radiological criteria presented above are usually sufficient 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 deficits (b7100 Mobility of a single joint). 3

IMAGING STUDIES

Imaging studies, specifically plain film radiographs, are confirmatory 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 significant 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 deficiencies 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 findings 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 definite osteophytes, definite moderate

narrowing of joint space; grade 4, large osteophytes, severe joint space narrowing, subchondral

sclerosis, and definite deformity of bone contour. A potential caveat when using the Kellgren/

38

Lawrence scale is spurs or osteophytes are emphasized and not all patients with hip OA have

osteophytes. 16

VII. DIFFERENTIAL DIAGNOSIS

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

- Paget’s 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 (Patrick’s) test for labral tears

- Fitzgerald’s test for labral tears

- Flexion-adduction internal rotation tests for labral tears

- Sacroiliac joint provocation tests for sacroiliac joint pain

39

- Femoral nerve stretch test for L2-3 radiculopathy

Clinicians should consider diagnostic classifications other than osteoarthritis of the hip

when the patient’s history, reported activity limitations, or im-pairments of body function and

structure are not consistent with those presented in the diagnosis/classification section of this

guideline, or, when the patient’s symptoms are not diminishing with interventions aimed at

normalization of the patient’s 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 difficulty in walking and climbing stairs in

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)

40

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 first 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.

41

42

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

benefit 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

43

- Opioid analgesics

* 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

antiinflammatory 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

44

interest in such products. Future independent high-quality studies are required to further

clarify the efficacy of both agents. 5 7 17

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 Guidelines-

Guidelines 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 aceta-

minophen 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

45

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

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,

46

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 considera-

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 agent’s overall safety profile and the patient’s 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 non-

cancer 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

47

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

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 well-

recognized 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,

48

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

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 49

evidence

NSAIDs are effective drugs in relieving pain and immobility associated with

osteoarthritis. COX-2 selective agents are equally effective.

A*

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

cardio-renal toxicity. This risk varies between individual treatments within both

groups and is increased with dose and duration of treatment

A*

COX-2 selective agents are associated with a significantly lower gastrointestinal

toxicity (PUBs and dyspepsia) compared to non-selective NSAIDs. Co-

prescribing of aspirin reduces this advantage.

A*

PPI should always be considered with a non-selective NSAID and with a COX-2

agent in higher GI risk patients.

C†

*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. 6

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.

50

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.

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 anti-

inflammatory 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

51

knee in full extension. All injections should be performed in a sterile manner. It’s 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

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 treatment’s 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 52

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

remains somewhat unclear and costs are not insignificant—injections 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

53

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

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

to achieve long-term improvement. For the most part, however, improvements are short-

lived 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 disease-

specific factors in reports of pain intensity and disability in several conditions, including

54

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.

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 benefits 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 self-

management 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).

55

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

specifically 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

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 confirming 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

56

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 efficient 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

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.

57

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

58

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.

59

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 confirmed that this non-pharmacological modality of treatment does have

some efficacy 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 significant

efficacy for reduction in pain.

6. Surgical Management

60

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.

61

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

62

"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.

63

During arthroscopy, surgeon can see the structures of your hip in great detail. (Right)

Small instruments are used to repair a labral tear.

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.

64

A smooth plastic bearing surface is then inserted into the implant so the joint can

move freely.

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.

65

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.

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 X-

rays. 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

66

(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 67

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 moderate-

to-severe hip dysplasia but little osteoarthritis and good range of motion, osteotomies and joint-

preserving 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 68

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 cost-

effective 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 a 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 69

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 non-

operated 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

70

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

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 efficacy 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 patient’s 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 anti-

inflammatory 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

71

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

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.

72

● 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

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.

REFERENCES

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