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Osteoarthritis(OA) of the Hip

Osteoarthritis is a chronic disorder of synovial joints in which there is progressive softening and
disintegration of articular cartilage accompanied by new growth of cartilage and bone at the joint margins
(osteophytes), cyst formation and sclerosis in the subchondral bone, mild synovitis and capsular fibrosis.
It differs from simple wear and tear in that it is asymmetrically distributed, often localized to only one
part of a joint and often associated with abnormal loading rather than frictional wear. In its most common form,
it is unaccompanied by any systemic illness and, although there are sometimes local signs of inflammation, it is
not primarily an inflammatory disorder. It is also not a purely degenerative disorder, and the term degenerative
arthritis which is often used as a synonym for OA is a misnomer.
Osteoarthritis is a dynamic phenomenon; it shows features of both destruction and repair. Cartilage
softening and disintegration are accompanied from the very outset by hyperactive new bone formation,
osteophytosis and remodelling. The final picture is determined by the relative vigour of these opposing
processes. In addition,there are various secondary factors which influence the progress of the disorder: the
appearance of calcium-containing crystals in the joint; ischaemic changes (especially in elderly people) which
result in areas of osteonecrosis in the subchondral bone; the appearance of joint instability; and the effects of
prolonged anti-inflammatory medication.

a.

b.

Osteoarthritis: non-progressive and progressive

(a) Non-progressive OA changes are common in older people; here we see them along the inferomedial edge of the femoral head,
while the articular cartilage over the rest of the head looks perfect. (b) Progressive OA changes are seen characteristically in the
maximal load-bearing area; in the hip this is the superior part of the joint. Articular cartilage has been destroyed, leaving a bald patch
on the dome of the femoral head.

The hip is one of the joints most commonly affected by osteoarthritis. In the majority of cases there is no
obvious reason for the development of the degenerative changes. In some cases there may be a relevant history
of hip disease, such as DDH, Perthes disease or other childhood problems. There may be a history of previous
trauma to the hip or pelvis, or other arthritic processes leading to hip joint destruction (e.g. rheumatoid arthritis).

Aetiology
The most obvious thing about OA is that it increases in frequency with age. This does not mean that OA
is simply an expression of senescence. Cartilage does age, showing diminished cellularity, reduced
proteoglycan concentration, loss of elasticity and a decrease in breaking strength with advancing years. These
factors may well predispose to OA, but it is significant that the progressive changes which are associated with

clinical and radiological deterioration are restricted to certain joints, and to specific areas of those joints, while
other areas show little or no progression with age.
Primary changes in cartilage matrix might (theoretically) weaken its structure and thus predispose to
cartilage breakdown; crystal deposition disease and ochronosis are well-known examples.
Inheritance has for many years been thought to play a role in the development of OA. A number of
studies have demonstrated a significant increase in the prevalence of generalized OA in first-degree relatives of
patients with OA as compared with controls (Kellgren, 1963. However, one should bear in mind that OA of
large joints is often attributable to anatomical variations, e.g. acetabular dysplasia and other forms of epiphyseal
dysplasia, and it is these that are inherited rather than any tendency to develop OA as a primary abnormality.
Articular cartilage may be damaged by trauma or previous inflammatory disorders. Enzymes released by
synovial cells and leucocytes can cause leaching of proteoglycans from the matrix, and synovial-derived
interleukin-1 (IL-1) may suppress proteoglycan synthesis. This could explain the appearance of secondary OA
in patients with rheumatoid diseases; whether similar processes operate in primary (idiopathic) OA is
unknown.
In most cases the precipitating cause of OA is increased mechanical stress in some part of the articular
surface. This may be due to increased load (e.g. in deformities that affect the lever system around a joint) or to a
reduction of the articular contact area (e.g. with joint incongruity or instability).
Changes in the subchondral bone may also increase stress concentration in the overlying cartilage,
either by altering the shape of the articular surface or by an increase in bone density (e.g. following fracture
healing) which reduces the shock-absorbing effect of the supporting cancellous bone.
OA is conventionally classified as being primary (idiopathic) or secondary, when it follows some
clearly defined predisposing disorder or disease , but it is becoming increasingly apparent that the development
of all types of OA is associated with multiple aetiological factors.

Pathogenesis
The initial stages of OA have been studied in animal models with induced joint instability and may not
be representative of all types of OA. The earliest changes, while the cartilage is still morphologically intact, are
an increase in water content of the cartilage and easier extractability of the matrix proteoglycans; similar
findings in human cartilage have been ascribed to failure of the internal collagen network that normally restrains
the matrix gel. At a slightly later stage there is loss of proteoglycans and defects appear in the cartilage. As the
cartilage becomes less stiff, secondary damage to chondrocytes may cause release of cell enzymes and further
matrix breakdown. Cartilage deformation may also add to the stress on the collagen network, thus amplifying
the changes in a cycle that leads to tissue breakdown.
Articular cartilage has an important role in distributing and dissipating the forces associated with joint
loading. When it loses its integrity these forces are increasingly concentrated in the subchondral bone. The
result: focal trabecular degeneration and cyst formation,as well as increased vascularity and reactive sclerosis in
the zone of maximal loading. As the articular surfaces become increasingly malapposed and the joint unstable,
cartilage at the edges of the joint reverts to the more youthful activities of growth and endochondral ossification,
giving rise to the bony excrescences, or osteophytes, that so clearly distinguish osteoarthritis (once called
hypertrophic arthritis) from atrophicdisorders such as rheumatoid disease.

Pathology
The cardinal features are: (1) progressive cartilage destruction; (2) subarticular cyst formation, with (3)
sclerosis of the surrounding bone; (4) osteophyte formation; and (5) capsular fibrosis.
Initially the cartilaginous and bony changes are confined to one part of the joint the most heavily
loaded part. There is softening and fraying, or fibrillation, of the normally smooth and glistening cartilage. The
term chondromalacia (Gr = cartilage softening) seems apt for this stage of the disease. With progressive
disintegration of cartilage, the underlying bone becomes exposed and some areas may be polished, or burnished,

to ivory-like smoothness(eburnation). Sometimes small tufts of fibrocartilage may be seen growing out of the
bony surface.
At a distance from the damaged area the articular cartilage looks relatively normal, but at the edges of
the joint there is remodelling and growth of osteophytes covered by thin, bluish cartilage. Beneath the damaged
cartilage the bone is dense and sclerotic. Often within this area of subchondral sclerosis, and immediately
subjacent to the surface, are one or more cysts containing thick, gelatinous material.
The joint capsule usually shows thickening and fibrosis, sometimes of extraordinary degree. The
synovial lining, as a rule, looks only mildly inflamed; sometimes, however, it is thick and red and covered by
villi.

a.

b.

c.

d.
Osteoarthritis pathology
(a) The x-ray shows loss of articular cartilage at the superior pole and cysts in the underlying bone; the specimen (b) shows that the
top of the femoral head was completely denuded of cartilage and there are large osteophytes around the periphery. In the coronal
section (c) the subarticular cysts are clearly revealed. (d) A fine-detail x-ray shows the extent of the subarticular bone destruction.

The histological appearances vary considerably, according to the degree of destruction. Early on, the
cartilage shows small irregularities or splits in the surface, while in the deeper layers there is patchy loss of
metachromasia. Most striking, however, is the increased cellularity, and the appearance of clusters, or clones, of

chondrocytes. In later stages, the clefts become more extensive and in some areas cartilage is lost to the point
where the underlying bone is completely denuded.
The subchondral bone shows marked osteoblastic activity, especially on the deep aspect of any cyst. The
cyst itself contains amorphous material; its origin is from local areas of steonecrosis or from the forceful
pumping of synovial fluid through cracks in the ubchondral bone plate. As in all types of arthritis, small areas
of osteonecrosis are quite common. The osteophytes appear to arise from cartilage hyperplasia and ossification

at the edge of the articular surface. The capsule and synovium are often thickened but cellular activity is slight;
however, sometimes there is marked inflammation or fibrosis of the capsular tissues.

Prevalence
Osteoarthritis is the commonest of all joint diseases. It is a truly universal disorder, affecting both sexes
and all races; everyone who lives long enough will have it somewhere, in some degree. However, there are
significant differences in its rate of occurrence in different ethnic groups, in the different sexes within any
group, and in the different joints. Reports of prevalence rates vary, depending on the method of evaluation.
Autopsy studies show OA changes in everyone over the age of 65 years. Radiographic and autopsy
surveys show a steady age-related increase in prevalence from the age of 30. By the age of 65, 80% of people
have some radiographic evidence of OA, although only one in four is symptomatic. The joints most frequently
affected are the spine, hips, knees and some of the small joints of the hands and feet.The peak incidence of hip
arthritis is in the sixth decade. Bilateral hip disease is often seen.
OA is the leading cause of physical disability in people over the age of 65. The prevalence of both
radiographically defined OA, and of OA-related disability, is greater in women than in men. Although disability
associated with OA also increases steadily with age, the majority of people with OA-related disability in the
community are between the ages of 55 and 75.
Men and women are equally likely to develop OA, but more joints are affected in women than in men.
Osteoarthritis is much more common in some joints (the fingers, hip, knee and spine) than in others (the elbow,
wrist and ankle). This may simply reflect the fact that some joints are more prone to predisposing abnormalities
than others.
A similar explanation may account for certain geographical and ethnic differences in prevalence. For
example, the female-to-male ratio for OA of the hip is about 1:1 in northern Europe but is nearer 2:1 in southern
Europe where there is a high incidence of acetabular dysplasia in girls. Even more striking is the virtual absence
of hip OA in southern Chinese and African blacks. This may simply be because predisposing disorders such as
developmental displacement of the hip, Perthes disease and slipped femoral epiphysis are uncommon in these
populations. That they have no inherent resistance to OA is shown by the fact that they often develop the
condition in other joints, for example the knee.
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).

Risk factors
Risk factors for OA include constitutional factors such as age, gender, the shape and alignment of
joints, obesity and some genetic determinants, but there are also important environmental triggers, such as
previous injury or the repetitive trauma associated with certain recreational activities, such as weightlifting or
long-distance running, and with some occupations, such as mining and farming.
Mechanical factors play a role in the pathogenesis of all types of primary, as well as secondary, OA.
Joint failure occurs when mechanical stresses overwhelm the capacity of articular tissues to resist and repair the
damage. Structural failure of the articular cartilage, bone and peri-articular tissues can result from abnormal
mechanical stresses damaging previously normal tissues, or from the failure of pathologically impaired joint
tissues in response to physiologically normal mechanical forces.
Obesity, joint malalignment, occupational trauma and muscle weakness are all important, potentially
modifiable, biomechanical risk factors, which determine the site and severity of the disease.
Race and ethnicity have some influence on the probability of developing OA at different sites. While
OA of the knee is prevalent in all ethnic groups (particularly frequent in black women), hip, hand and
generalized OA are seen predominantly in Caucasians.
Genetic factors are known to be important determinants. Twin studies suggest hereditability of up to
65% in primary OA of the hand and knee, but the susceptibility genes themselves still remain largely

undefined.Progress has been made in identifying mutations in collagen genes that are associated with different
types of bone and cartilage dysplasia where OA is part of a more complex phenotype, but none of these single
gene mutations in genes that code for structural matrix proteins appears to be important in determining
susceptibility to the common types of OA. Recently, however, there has been some progress in identifying
polymorphisms in genes that code for signalling proteins involved in the development and maintenance of
articular cartilage, which do appear to be associated with susceptibility to hip OA in certain ethnic groups

Clinical Features (Signs and symptoms)


Symptoms of hip OA vary. Typical presenting symptoms are indolent onset of anterior thigh or groin
pain that is deep and activity related. Occasionally, the pain is referred to the buttocks or distal thigh with
possible radiation into the knee. As degeneration of the articular cartilage progresses, the duration and the
frequency of the pain intensify. Pain at rest or pain that wakens the patient at night is associated with severe
arthritis. Typically, the symptoms of OA follow an intermittent course, with periods of remission sometimes
lasting for months. The pain in osteoarthritis is generally worse with activity and is relieved by rest.
In inflammatory arthritis, the patient may experience stiffness with inactivity and some improvement of
this symptom with movement of the hip joint. Some patients experience very little pain but complain of
stiffness, limping, and functional decline.
The onset of pain and functional decline can be quite insidious, occurring over many years. Some
patients consider these progressive symptoms to represent part of normal aging and do not seek help until quite
late in the disease process.
Functionally, the combination of stiffness and pain leads to complaints of a limp, difficulty getting up
out of low chairs, difficulty descending and ascending stairs (requiring 36 and 67 of flexion respectively),
inability to squat (120 of flexion, 20 of abduction, and 20 of hip external rotation required), and trouble with
daily activities, such as putting on socks and shoes (Duvernay sign).
Physical findings may include a combined Trendelenburg and antalgic gait (Duchenne), witch is more
common due to a desire to off-load the hip abductor muscles and hence reduce the joint reaction force, which is
often three times body weight in single-leg stance.
Actual or functional shortening of the limb due to collapse of the hip joint, and soft-tissue contractures
and moderate muscular atrophy around the hip joint.
Early hip joint arthritis is associated with pain on hip extension and internal rotation, as the capsule
tightens, and early loss of internal rotation in flexion and extension. Fixed flexion deformity and limited
abduction and adduction are common with more advanced disease. The Thomas test may reveal a fixed flexion
deformity. The FABER test (Flexion, ABduction, and
External Rotation) is also known as the Patrick test,
but the ankle-to-knee or heel-to-knee test is the most
common term for it. With the patient in the supine
position, the affected hip is externally rotated with the
knee flexed, so that the affected ankle can be placed on
top of the opposite knee in a number-four position.
Applying downward pressure to the affected knee
stresses the hip joint and may cause typical hip pain.
Trendelenburg test. When patient is standing
on the affected side, the pelvis on the opposite side
drops, indicating either actual weakness of the gluteus
medius muscle, functional weakness of the hip
abductors secondary to altered alignment of the hip
joint, or a painful arthritic hip joint that cannot tolerate
the normal force of hip abductor contraction during
single-legged stance. The trunk shifts to the left as
patient attempts to decrease biomechanical stresses

across involved hip and thereby maintain balance.

An often used functional outcome measure is the Harris Hip Score. The Harris Hip Score is derived
from scoring 10 different variables, including pain, ROM, gait/limp, gait distance, function, activities of daily
living, and deformity. Scores range from 0 (worst) to 100. Score before and after interventions intended to
alleviate the impairments of body function and structure, activity limitations, and participation restrictions
associated with hip osteoarthritis.

Imaging
X-rays. X-ray appearances are so characteristic that other forms of imaging are seldom necessary for
ordinary clinical assessment. The cardinal signs are asymmetrical loss of cartilage (narrowing of the joint
space), sclerosis of the subchondral bone under the area of cartilage loss, cysts close to the articular surface,
osteophytes at the margins of the joint and remodelling of the bone ends on either side of the joint. Late features
may include joint displacement and bone destruction.

Fig . The cardinal features of osteoarthritis


are remarkably constant
Radiographs of early disease show changes concentrated in the
superolateral aspect of the joint, the area under most mechanical stress.
Joint space narrowing is followed by osteophyte formation, sclerosis,
and cyst formation. Remodeling of the medial and lateral femoral head
occurs and can lead to its collapse and flattening. The medial
acetabulum space fills in with osteophytes, resulting in gradual
superolateral migration of the femoral head (Figure 6-4). The cortex
may thicken with new bone formation along the medial aspect of the
femoral head (buttressing). In contrast, chronic inflammatory arthritis,
such as rheumatoid arthritis, will typically lead to diffuse loss of joint
space and medial migration along the axis of the femoral head, or
protrusio acetabuli.
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.

Fig. Osteoarthritis of the hip. An


AP radiograph of the hip joint
illustrates superolateral migration
of the femoral head (arrow) with
asymmetric joint space narrowing

Fig. AP radiograph of the hip showing


degeneration of cartilage and osteophytes
at margins of acetabulum

Fig. Protruzio acetabuli

Look carefully for signs of previous disorders (e.g.congenital defects, old fractures, Perthes disease or
rheumatoid arthritis). Such cases are usually designated as secondary osteoarthritis.

Fig. Perthes disease showing fragmentation of


the head.

Fig. The flattened femoralhead and


shortened femoral neck are tell-tale signs
of multiple epiphyseal dysplasia in this
patient with secondary OA of the hip

Radionuclide scanning Scanning with 99mTc-HDP shows increased activity during the bone phase in
the subchondral regions of affected joints. This is due to increased vascularity and new bone formation. Bone
scintigraphy is indicated for the detection of osteonecrosis, stress fractures and bone metastases.

CT and MRI Advanced imaging is sometimes needed to elucidate a specific problem, e.g. early
detection of an osteocartilaginous fracture, bone oedema or avascular necrosis. These methods are also used for
severity grading in clinical trials.
Blood tests are not helpful in the diagnosis or management of OA and are largely used to exclude other
diseases associated with systemic inflammation or metabolic abnormalities.
Although cartilage degradation products, such as hyaluronan, keratan sulphate and cartilage oligomeric
protein, and cartilage synthesis markers, such as Type II collagen c-propeptide, have been shown to be
increased in the plasma, synovial fluid or urine of patients with OA, there are currently no biochemical or
molecular markers that have clinical utility for diagnosis, monitoring the progress of structural changes or
assessing the prognosis of OA in clinical practice.
Synovial fluid analysis in OA is really only indicated to exclude bacterial joint infection. The fluid is
usually clear and viscous with a low cell count. Detection of crystals by polarizing light microscopy is not
helpful in distinguishing OA from primary crystal deposition disorders.

Differential Diagnoses
The following differential diagnoses should be considered in an individual with signs or symptoms suggestive
of hip OA:
Bursitis or tendinitis
Chondral damage or loose bodies
Femoral neck or pubic ramus stress fracture
Labral tear
Muscle strain
Neoplasm
Osteonecrosis of the femoral head
Pagets disease
Piriformis syndrome
Psoriatic arthritis
Rheumatoid arthritis
Sacroiliac joint dysfunction
Septic hip arthritis
Referred pain as a result of an L2-3 radiculopathy
Based on Aetiology there are several forms of secondary hip osteoarthritis:
Developmental dysplasia of the hip - Most at risk are those babies born to families with a positive family
history, or with breech presentation. Ultrasound scanning should detect most at - risk cases, but late presentation
may occur as delay in walking, a limp or a leg length discrepancy. Missed DDH often leads to a non - congruent
joint and the early development of osteoarthritis in adult life.
Perthes disease - This is a condition seen most commonly in boys between the ages of 5 and 10. It is
considered to be due to segmental avascular necrosis of the femoral head with associated disintegration, and
subsequent healing and deformity. A limp, hip pain or knee pain may be the presenting feature. The clinical
signs are usually minor, perhaps slight restriction of movements of the hip, especially internal rotation,
associated with some spasm.
Slipped upper femoral epiphysis - This is a condition whereby the developing epiphysis of the hip, often
in an overweight hypogonadal boy, partially slips, leading to hip pain or referred pain to the knee. Diagnosis
may be difficult and therefore delayed, but a frog lateral X - ray will show the deformity. The condition
requires urgent surgical stabilization with pins to prevent further slippage of the epiphysis The contralateral hip
is at high risk of slippage, and patients and parents should be warned to return if any further knee or hip pain
occurs.

Avascular necrosis - Avascular necrosis (AVN) of the femoral head can lead to an effusion in the hip
joint, causing pain and stiffness, but if the process continues the femoral head may collapse, producing
secondary osteoarthritis. MRI allows the diagnosis to be made in the early stages, but if radiological evidence of
AVN is present, surgical treatment to arrest the disease is less successful. Arthroplasty may be required.
Infection - Primary septic arthritis of the hip is very rare in adults, but may be present in
immunocompromised patients. The incidence of septic arthritis of the hip in intravenous drug abusers appears to
be rising, especially if intravenous injection has been attempted in the groin. Surgical drainage is usually
necessary. Ultrasound scanning may be required to demonstrate the presence of an effusion. Tuberculosis (TB)
of the hip is occasionally seen in the UK, especially in immigrants. TB of the hip, however, is much more
common in underdeveloped countrie The joint surfaces are destroyed, and the capsule becomes distended with
pus. This may break through to the surface of the skin, forming a sinus, which may become secondarily
infected. The management of TB relies heavily on antibiotic therapy with drainage of chronic abscesses and
removal of necrotic bone.
Trauma
Fractures of the neck of femur (NOF) are epidemic in the developed world, usually secondary to
osteoporosis. Femoral neck fractures may occur occasionally in young patients through normal bone, but the
energy required for such an injury to occur is usually very high. In osteoporotic NOF fractures, the bone is by
defi nition pathological, and the injury required to produce the fracture is often minimal. Relatively few patients
return to full mobility following these injuries. The patients are often elderly and frail, and co - existent medical
conditions may need to be assessed and treated prior to surgical treatment of the fractures.
Intertrochanteric fractures.These fractures are extracapsular and occur in the wide metaphyseal
region between the two trochanters in the femur. Because the blood supply to the fracture is adequate, such
fractures tend to unite without difficulty. Internal fi xation of intertrochanteric fractures with the dynamic hip
screw (DHS) is the preferred treatment method.
Dislocations.The hip joint is anatomically strong, but dislocation can occur, usually as a result of
considerable violence. These injuries are often caused by car accidents in which a front seat traveller is involved
in a head - on collision and strikes his/her knee under the dashboard. The acetabular fracture may be through the
back, the floor or, less commonly, the front of the acetabulum.

Natural history
Osteoarthritis usually evolves as a slowly progressive disorder. Osteoarthritis generally develops
progressively over several years, although symptoms may remain stable for prolonged periods within that time
frame. Previous trauma, causing articular, meniscal, or ligamental damage or joint incongruity, can reveal or
accelerate the disorder . The correlation between clinical outcome and radiographic course is poor at the
individual level. Although symptoms can improve, the radiographic picture rarely does, radiographic
deterioration is observed in 30% to 60% of patients. Osteoarthritis usually takes years to develop to the level
where it begins to interfere with the persons life.
The natural history of individual hip OA is imperfectly understood. Many different factors contribute to
this. The clinical manifestations that develop in patients with hip OA include changes in the shape, density,
length, and function of the bones, cartilage, and fibrous tissue surrounding the hip joint itself as well as the
surrounding muscles.
The changes that occur around the arthritic hip include a decrease in the joint space between the femur
and acetabulum (more common superior and lateral than medial), shortening of the fibrous joint capsule,
flattening of the femoral head, the appearance of osteophytic growth around the margins of the femoral head
and acetabulum (in some individuals boney overgrowth does not occur), a superior-lateral or medial migration
of the femoral head, and the development of subchondral sclerosis or cysts in the femoral head and acetabulum.
Changes that occur outside of the hip joint include a decreased amount of hip joint ROM (usually mostly
affecting internal rotation and then flexion) and muscle weakness (particularly the abductor muscles), which
eventually may result in difficulty with ambulation.The progression of these changes are usually slow but may

be quite rapid in some cases. Currently, there is no reliable, generally accepted classification of the stages or
severity of hip OA and the rate of progression varies from patient to patient, even when the demographics of the
patients are similar.
However, there is considerable variation between patients in the degrees of destruction and repair. Most
of the men and half of the women have a hypertrophic reaction, with marked sclerosis and large osteophytes. In
about 20 per cent of cases most of them women reactive changes are more subdued, inviting descriptions
such as atrophic or osteopaenic OA. Occasionally OA takes the form of a rapidly progressive disorder.
Rapidly destructive osteoarthritis
Fig. X-ray obtained when the patient was first
seen, complaining of pain in the left hip. This
shows the typical features of an atrophic form
of osteoarthritis on the painful side.

Fig. Eleven months later there is marked


destruction of the left hip, with crumbling
of both the femoral head and the acetabular
floor, and similar features are beginning to
appear on the right side

PROGNOSIS
In most cases, OA of the hip progresses slowly 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. A
patients baseline Kellgren/Lawrence radiographic grade is an important predictive factor for having THA. a
Kellgren/Lawrence score of II or higher is a strong predictor of progression in patients with hip OA. Gossec

et al. also reported that the most important predictive factors of having a THA include Kellgren/Lawrence
radiographic grades of III or higher, a high global assessment of pain, and a previous trial of nonsteroidal antiinflammatory drugs (NSAIDs). Joint space narrowing and the Kellgren/Lawrence scale are important
prognostic predictors of OA while joint space narrowingmay be the best indicator of structural OA progression
in patients with hip OA.

MANAGEMENT
The management of OA depends on the joint (or joints) involved, the stage of the disorder, the severity
of the symptoms, the age of the patient and his or her functional needs. Three observations should be borne in
mind: (1) symptoms characteristically wax and wane, and pain may subside spontaneously for long periods; (2)
some forms of OA actually become less painful with the passage of time and the patient may need no more than
reassurance and a prescription for pain killers; (3) at the other extreme, the recognition(from serial x-rays) that
the patient has a rapidly progressive type of OA may warrant an early move to reconstructive surgery before
bone loss compromises the outcome of any operation.
EARLY TREATMENT
There is, as yet, no drug that can modify the effects of OA. Treatment is, therefore, symptomatic. The
principles are: (1) maintain movement and muscle strength; (2) protect the joint from overload; (3) relieve
pain; and (4) modify daily activities.
Physical therapy The mainstay of treatment in the early case is physical therapy, which should be
directed at maintaining joint mobility and improving muscle strength. The programme can include aerobic
exercise, but care should be taken to avoid activities which increase impact loading. Other measures, such as
massage and the application of warmth, may reduce pain but improvement is short-lived and the treatment has
to be repeated.
The use of aquatic exercise (hydrotherapy) in the treatment of patients with OA of the hip has been
assessed. Aquatic exercise appears to have some beneficial short-term effects for patients with hip and/or knee
OA while no long-term effects have been documented. In a recent study Hinman et al. used a randomized
controlled trial and compared a 6-week program of aquatic physical therapy to no intervention. The aquatic
physical therapy group demonstrated significantly less pain and improved physical function, strength, and
quality of life after the intervention. However, effect size calculations revealed only small benefits of aquatic
physical therapy for pain, stiffness, right hip abductors strength, and quality of life, and doubtful clinical
benefits for physical function and left hip abductors strength Patients who have an intolerance to land-based
exercise because of pain or obesity may better tolerate aquatic based exercise.
Load reduction .Protecting the joint from excessive load may slow down the rate of cartilage loss. It is
also effective in relieving pain. Common sense measures such as weight reduction for obese patients, wearing
shock-absorbing shoes, avoiding activities like climbing stairs and using a walking stick are worthwhile.
Analgesic medication Pain relief is important, but not all patients require drug therapy and those who do
may not need it all the time. If other measures do not provide symptomatic improvement, patients may respond
to a simple analgesic such as paracetamol.In patients who do not respond adequately to a trial of paracetamol,
the choice of alternative or additional analgesics needs to take into account both the relative efficacy and safety
of the drug or drug combination being considered as well as concomitant medication and comorbidities.
In some patients who do not respond adequately to paracetamol, NSAIDs at the lowest effective doses
can be added or substituted, but long-term use of NSAIDs should be avoided if possible. In patients with
increased gastrointestinal risk, a COX2 selective agent or a non-selective NSAID with co-prescription of a
proton pump inhibitor or misoprostol for gastroprotection can be considered.
All NSAIDs (including COX2 selective agents) should be used with caution in patients with
cardiovascular risk factors.
Topical NSAIDs or topical capsaicin can be effective as adjuncts or alternatives to oral analgesics in
some patients with symptomatic OA. Treatment with glucosamine and/or chondroitin sulfate may provide
symptomatic benefit. If no response is apparent within 6 months, treatment should be discontinued. The

evidence that these agents may also have structure-modifying effects in slowing the progression of articular
cartilage loss remains inconclusive.
The use of opioids and narcotic analgesics can be considered in exceptional circumstances for the
treatment of severe, refractory pain where other pharmacological agents have been ineffective or are contraindicated. Non-pharmacological therapies should be continued in such patients and surgical treatments should
be considered.
INTERMEDIATE TREATMENT
Joint debridement (removal of loose bodies, cartilage tags, interfering osteophytes or a torn or impinging
acetabular or glenoid labrum) may give some improvement. This may be done either by arthroscopy or by open
operation. If appropriate radiographic images suggest that symptoms are due to localized articular overload
arising from joint malalignment (e.g. varus deformity) or incongruity (e.g. acetabular and femoral head
dysplasia), a corrective osteotomy may prevent or delay progression of the cartilage damage.
LATE TREATMENT
Progressive joint destruction, with increasing pain, instability and deformity (particularly of one of the
weight-bearing joints), usually requires reconstructive surgery. Three types of operation have, at different times,
held the field: realignment osteotomy, arthroplasty and arthrodesis.

Realignment osteotomy. Until the development of joint replacement surgery in the 1970s, realignment
osteotomy was widely employed. Refinements in techniques, fixation devices and instrumentation led to
acceptable results from operations on the hip and knee, ensuring that this approach has not been completely
abandoned. Intertrochanteric femoral osteotomy is sometimes preferred for young patients with localized
destructive OA of the hip. These operations should be done while the joint is still stable and mobile and x-rays
show that a major part of the articular surface (the radiographic joint space) is preserved. Pain relief is often
dramatic and is ascribed to (1) vascular decompression of the subchondral bone, and (2) redistribution of
loading forces towards less damaged parts of the joint. Afterload redistribution, fibrocartilage may grow to
cover exposed bone.
Joint replacement Joint replacement, in one form or another, is nowadays the procedure of choice for
OA in patients with intolerable symptoms, marked loss of function and severe restriction of daily activities. For
OA of the hip and knee in middle-aged and older patients, total joint replacement by modern techniques
promises improvement lasting for 15 years or longer.

Total prosthetic joint replacement in the hip was pioneered in


the early 1970s by Sir John Charnley and others, following largely
unsuccessful attempts at joint resurfacing using cup arthroplasties or
acrylic femoral head replacements. Most designs of hip replacement
have a metal femoral stem and an ultra - high - molecular - weight
polyethylene ( UHMWPE ) acetabular component (Fig. 21.11 ).
Implants can be fi xed to the underlying bone with polymethyl
methacrylate bone cement or may be uncemented . Various surface
fi nishes have been applied to prosthetic surfaces to encourage bone
ingrowth, including beads, mesh and plasma - sprayed titanium.
Hydroxyapatite is a synthetic bone substitute, and has been applied to
many prostheses to encourage bony incorporation.Alternative bearing
surfaces, such as ceramic on ceramic or metal on metal bearings, are
becoming more popular, as there is good evidence that particles of
UHMWPE are responsible for the loosening process that is observed in
hip replacement patients. However, joint replacement operations are
highly dependent on technical skills, implant design, appropriate
instrumentation and postoperative care requirements that cannot
always be met, or may not be cost-effective, in all parts of the world.

Fig. Cemented THA

Fig. Charnley hip prosthesis

Fig. Cementless THA

Arthrodesis Arthrodesis is still a reasonable choice if the stiffness is acceptable and neighbouring joints
are not likely to be prejudiced. This is most likely to apply to small joints that are prone to OA. Arthrodesis
should be considered for adolescents or young adults with unilateral end-stage arthritis and no other significant
limb dysfunction.

Risks
The significant risks of the surgery include:
1 Infection. This may occur in approximately 0.5% of patients, and can have signifi cant consequences.
The prosthetic joint will require removal to eradicate the infection, and once the infection has settled a further
joint may be inserted. Total hip replacement is performed in ultra - clean air theatres, with antibiotic
prophylactic cover, by surgeons and assistants usually wearing body exhaust gowns.
2 Thromboembolism. Fatal pulmonary embolism may occur in between 1 in 200 and 1 in 300 patients.
Deep vein thrombosis is seen clinically in perhaps 1 in 20 patients after hip replacement, and patients are given
thromboembolic prophylaxis to reduce the incidence of deep vein thrombosis. There is little evidence so far that
thromboembolic prophylaxis has an effect on the fatal pulmonary embolism rate.
3 Dislocation. The ball and socket of the hip joint may come apart if the patient twists or bends without
care. Dislocation may require a manipulation of the hip under anaesthesia. The risk of dislocation is low at
between 1% and 2%.

Fig. THA dislocation

The long-term concern of total joint arthroplasty is aseptic loosening. When a joint implant is loose and
has to be revised, less bone stock is available and the rates of all complications are higher, particularly the rate
of recurrent loosening. The risk of needing to replace a hip arthroplasty is very low in a patient older than 65
years, who typically places moderate demands on the joint and who has a limited life expectancy, but it is
virtually universal in a young adult who is in good health and places more strenuous demands on the joint.
Appropriate preoperative planning and better implants have improved the results of both primary and
revision arthroplasty.
The procedure is now highly developed, and over 90% of patients have an excellent outcome from surgery.
Data from the Swedish Hip Registry suggest that patients should expect a greater than 80% chance of their hip
replacement lasting more than 20 years.

References

S.Terry Canale, James H.Beaty : Campbells Operative Orthopaedics 11th edition, 2010
Louis Solomon, David Warwick, Selvadurai Nayagam: Apleys System of Orthopaedics and fractures 9th
edition, 2010
John A. Craig, MD, and Carlos A. G. Machado, MD: Netters Orthopaedics
Dr.Tudor Pop Sorin et al: Elemente de ortopedie curs pentru studenti, 2005
Prof.Univ.Dr.Nagy Ors, Prof.Univ.Dr.Bataga Tiberiu, Dr.Tudor Pop Sorin, Dr.Balint C.Andor
Traumatologie Osteoarticulara curs pentru student, 2001