European Journal of Radiology 63 (2007) 36–48

Hip osteoarthritis: What the radiologist wants to know

Theofilos Karachalios a,∗ , Apostolos H. Karantanas b , Konstantinos Malizos a
a Department of Orthopaedic Surgery, School of Health Sciences, University of Thessaly, Papakiriazi 22, Larissa 41222, Greece
b Department of Radiology, Medical School, University of Crete, Heraklion, Greece

Received 8 March 2007; received in revised form 9 March 2007; accepted 12 March 2007

Abstract
Osteoarthritis (OA) is the most common disease of the hip joint seen in adults. The diagnosis of OA is based on a combination of radiographic
findings of joint degeneration and characteristic subjective symptoms. The lack of a radiographic consensus definition has resulted in a variation
of the published incidences and prevalence of OA. The chronological sequence of degeneration includes the following plain radiographic findings:
joint space narrowing, development of osteophytes, subchondral sclerosis, and cyst formation. There are cases though, that plain radiographs show
minor changes and the clinical suspicion of early disease can be confirmed with more sophisticated imaging methods, such as multi-detector
computed tomography and MR imaging. The present article will review all the clinical information on the hip OA together with an updated
radiological approach, with emphasis on the early depiction and the differential diagnosis of the disease.
© 2007 Elsevier Ireland Ltd. All rights reserved.

Keywords: MR imaging/diagnosis; Hip disorders; Osteoarthritis; X-ray/diagnosis; Computed tomography

1. Introduction 2. Epidemiology

Osteoarthritis (OA) is a non-inflammatory degenerative joint
disorder associated with various degrees of cartilage degenera-
tion and bony deformity. OA can result in altered joint mechanics
with resultant alignment abnormalities and associated soft tis-
sue contracture leading to limitations in motion. OA is the most
common disease of the hip joint seen in adults [1,2]. Most of
the patients seen in the routine Orthopaedic practice with dis-
comfort, pain, limping or stiffness of the hip joint, are most
commonly suffering from OA.
Clinical and epidemiological data indicate that hip OA is a
distinct entity that behaves differently from OA in other syn-
ovial joints [3]. Our understanding of hip OA comes from
international population studies, joint replacement registries,
and epidemiologic investigations. Understanding the etiology
of hip OA depends on our ability to recognise and discriminate
this entity from other causes of hip disease as well as to dis-
tinguish secondary from idiopathic OA. In the secondary type,
the predisposing cause is well defined and the identification of
the underlying pathology may have an impact on treatment. In
the primary or idiopathic type, the underlying cause cannot be
determined.
∗ Corresponding author. Tel.: +30 2410 682720; fax: +30 2410 670407.
E-mail address: kar@med.uth.gr (T. Karachalios).
The reported incidence of hip OA in the general population
varies considerably, depending on the different methods used for
the selection of the sample, the diagnostic criteria applied, and
the race and age of the subjects participating in different stud-
ies [3–5]. Population studies have shown that there are marked
ethnic and racial differences. The rate of moderate to severe
idiopathic or secondary OA of the hip in Caucasians is 3–6%,
compared with 1% or less in East Indians, Blacks, Hong Kong
Chinese and Native Americans. It seems that the prevalence has
not changed during the last four to five decades, suggesting that
genetic and/or environmental etiological factors remain constant
[6–8]. Studies on patients who underwent total hip replacement
for idiopathic OA, in multiracial countries, showed a virtual
absence of the condition in Asians and low rates in Black and
Spanish populations [9].
3. Etiology of the idiopathic OA
It has been suggested [10,11] that increased anteversion of
the femoral neck may contribute to the development of hip
OA, a statement which has been challenged by others [3,12,13].
Other etiological factors have also been discussed, not without
criticism, in the literature such as farming, occupational heavy
load, overweight and elite sport activity [3,14–19]. The strong

0720-048X/$ – see front matter © 2007 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ejrad.2007.03.022
 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48 37

relationship between race and OA of the hip and the rela-

tively high incidence of the disease in siblings of Swedish and
English patients who underwent total hip replacement because
of idiopathic OA, suggests that genetic factors play an impor-
tant role in the development of the disease [20–24]. As a result,
several attempts have been made in order to identify chomo-
some regions potentially harbouring susceptibility loci for hip
OA [24–28].

4. Etiology of the secondary OA

Hip OA can be secondary to osteonecrosis, trauma, sepsis,

Paget’s disease or as a result of inflammatory arthropathy. Cer-
tain conditions such as congentital hip disease (CHD), Perthe’s
disease and slipped capital femoral epiphysis (SCFE), involve
anatomical structures which lead to the development of OA in
adulthood. Murray [14] stated that minimal anatomical varia-
tions exist in the majority of cases, which had been reported
as idiopathic by previous authors, sometimes so slight that the
radiographic appearance may be regarded as being within nor-
mal limits. He had also observed that minor degrees of SCFE
with no symptoms in adolescence may be the cause of idiopathic
OA. He insisted that the radiographic finding called “tilt defor-
mity” is an indication of pre-existing SCFE. Stulberg in 1975
[29] confirmed Murray’s observations and concluded that an
underlying developmental abnormality is associated with most
cases of so-called idiopathic OA. Resnick [30] pointed out that
tilt deformity results from a remodeling process in hip OA. Har-
ris in 1986 [31] suggested that the idiopathic hip OA, if it does
exist, is very rare and he opposed Resnick’s suggestion that the
“tilt” deformity is the result rather than the cause of OA.
Fig. 1. Plain radiograph of the left hip joint with internal rotation of the feet. The
normal weight-bearing surface of the acetabulum is horizontal and the normal
joint space width measures more than 2.5 mm (arrows).
Normal femoral neck and head anatomy facilitates move-
ment and allows the leg to swing clear of the pelvis. Possible
loss of neck offset, will result in less clearance between the
neck and the bony acetabulum causing impingement of the neck
against the labrum and the acetabular lip within normal range
of motion. Repetitive micro damage causes osteophyte forma-
tion and degeneration of the joint. The “cam” type impingement
syndrome from an anterior femoral offset deficiency (“tilt or
pistol grip” deformity), widely recognized today with mag-
netic resonance imaging (MRI), is accepted as a cause of
hip pain and early OA [32–34]. Either because of “cam”
femoroacetabular impingement (FAI) or from sports injuries,

Fig. 2. A 60-year-old woman with left hip pain. The clinical diagnosis was OA and the radiological investigation revealed an underlying acetabular dysplasia. (a)
The right hip shows a CE angle of 13◦ . The joint space has a normal width (arrow). (b) The left hip shows a reduced joint space width (arrow), a CE angle of 12◦ and
a Sharp’s angle (created by the teardrop horizontal line and the line connecting this to the outer acetabular lip) of 44◦ . The weight-bearing surfaces of the acetabulum
are not horizontal on both sides.
38 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48

acetabular labrum tears and intra-articular chondral lesions and remodelling phenomena are taking place with osteophyte
cause hip pain and are responsible for the development of early development.
OA [35]. Macroscopically, the cartilage shows fibrillation and fissures
It has been also suggested that OA of the hip is due to a extending to subchondral bone. Sclerotic changes then occur
subtle CHD. If this is true, OA should be seen frequently in in the subchondral bone from overload. Juxtaarticular cysts and
Japanese persons, with their extremely high rate of dysplasia; marginal osteophytes eventually form, and joint space narrowing
however idiopathic OA is rare in that population [36]. When and sclerosis occur. Joint capsule shows secondary thickening
controlled studies of acetabular measurements are done and the and fibrosis. Synovium appears mildly inflamed and sometimes
rates of CHD and OA for each racial subgroup are considered, becomes thick, red and villi are developed.
CHD accounts for only a small percentage (5–10%) of hip OA Aging of the cartilage and OA are different processes,
in Caucasians [3]. although aging predisposes to OA in certain joints. Aged car-
tilage usually shows, non-progressive changes of decreased
5. Classification of idiopathic hip OA cellularity, reduced proteoglycan concentration, loss of elasticity
and reduced mechanical properties.
Different classification systems have been described using
as criteria the direction of migration of the femoral head 7. Clinical features
and the evolution of the destructive changes within the joint
[15,37–40]. Most of them agree that there are two main types The symptoms in OA are usually unilateral and asymmet-
of head migration: superior and medial. The superior migra- ric at early stage. In late stages multiple joints may be involved.
tion (or eccentric) may be superolateral or superomedial. The
medial migration (concentric) is also referred to as axial or
global.
The differential diagnosis of the superior migration pattern
of the hip includes the calcium pyrophosphate dihydrate crystal
deposition disease and the osteonecrosis, which might both be
complicated by secondary degenerative changes. The concentric
loss of articular cartilage poses diagnostic difficulties since it
should be differentiated from infectious arthritis and rheumatoid
arthritis. The osteophyte formation and subchondral sclerosis
together with the absence of osteopenia or subchondral erosions,
favour the diagnosis of idiopathic OA.
We use the Altman’s classification [37,41]; eccentric and con-
centric OA which, in our opinion, is simple, convenient and
eliminates the need to quantify the migration of the femoral
head.

6. Pathogenesis of idiopathic OA

On cellular level, at the earliest changes of OA when the car-

tilage is morphologically still intact, an increase in water content
and easier extractability of the proteoglycans is observed. A fail-
ure of the internal collagen network, which normally restrains
the matrix gel, follows. At an intermediate stage, a loss of proteo-
glycans, which weakens the structure making it more susceptible
to injury, is observed and cartilage defects appear. Later as the
cartilage becomes less stiff, secondary damage to chondrocytes
may release, in response to injury, cell degradative enzymes
which can overcome the cartilage repairing system and degrade
matrix and cartilage microstructure [42]. Cartilage deformation
may also add to the stress on the collagen network, which starts
a chain of changes leading to tissue breakdown. Articular carti- Fig. 3. Osteophyte formation in hip osteoarthritis. (a) A 65-year-old male patient
lage distributes loads and, when it loses its structural integrity, with bilateral hip pain and decreased range of motion on the left. The plain
loads are concentrated on the exposed subchondral bone. In the radiograph shows bilaterally subchondral sclerosis and osteophyte formation
subchondral bone, areas with thickened trabeculae, sclerosis, (short white arrows). In addition, on the left there are joint space narrowing
(long arrow), and a large herniation pit (black arrow). (b) A 73-year-old woman
increased vascularity and increased interosseous pressure, or with left hip pain and decreased range of motion. The plain radiograph shows
areas with focal trabecular degeneration, necrosis and cysts for- marginal osteophytes (white arrow) but the joint space appears normal (small
mation are observed. In areas where cartilage is still intact, repair arrow).
 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48 39

Patients usually present after middle age, although in some forms

of secondary OA (e.g. CHD) symptoms start earlier. Pain is the
usual presenting symptom. Initially pain is worsened by activity
and relieved by rest, but eventually rest and night pain develop.
Typically, the symptoms of hip OA follow an intermittent course,
with periods of remission sometimes lasting for months. Pain
arising in the hip joint is felt in the groin, down the front of the
thigh and, sometimes, in the knee; occasionally knee pain is the
only symptom. Pain at the back of the hip is seldom from the
joint, it usually derives from the lumbar spine. Limp is a common
symptom and it may be due to a change in limb length, weak-
ness of the hip abductors or joint instability. Decreased range of
motion and crepitus are also common. Stiffness, deformity, leg
length discrepancy and Trendeleburg’s sign are late symptoms,
associated with pelvic obliquity. Restriction of walking distance,
difficulty in climbing stairs, and progressive inability to per-
form everyday tasks or enjoy recreation may eventually drive the Fig. 4. A 62-year-old patient with medial OA demonstrated with joint space
patient to seek help. The eccentric type of idiopathic OA is more narrowing (black arrow). There is also osteophyte formation (white arrow) pre-
sumably secondary to a long-standing femoroacetabular impingment from an
painful and has poor prognosis due to rapid deterioration. The abnormal head–neck offset (open arrow).
concentric type has a better prognosis and is better tolerated by
patients [41].
9. Radiological appearance of idiopathic and secondary
Since OA can develop in the knees and the lumbar spine of
OA of the hip
the same patient and patients can also experience referred pain
from these sites, a thorough clinical examination and appropriate
9.1. Plain radiographs
imaging must be undertaken before decisions for treatment are
made.
The radiographic evaluation has the following aims: (1) to
confirm the clinical diagnosis of OA; (2) to establish the severity
8. Laboratory investigations of OA; (3) to monitor disease activity and response to treatment
and (4) to depict any complications of the disease or of its treat-
Lab evaluation will reveal a normal ESR, CRP and ment. The conventional radiologic work-up of the hip, includes
CBC, and synovial fluid analysis may show a normal or the anteroposterior and the “frog-leg” view. The latter needs a
slightly elevated WBC count (10,000–20,000) with normal 45◦ of abductions, which is not always achievable when patients
differential. This pattern is found in most non-inflammatory suffer from pain or limitation of motion. Hip radiographs should
arthropathies. be obtained with the joint internally rotated, with an angle of

Fig. 5. Two different patients with advanced hip osteoarthritis demonstrating on plain radiographs severe joint space narrowing with subchondral sclerosis (arrows).
Superolateral migration is seen in (a) and superior migration in (b). Large subchondral cysts are seen in (b) (black arrows). An underlying calcium pyrophosphate
dihydrate crystal deposition disease was found in (b).
40 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48

Fig. 6. Rapidly destructive osteoarthitis of the hip in a 71-year-old man. Radiographs a and b have been obtained within 11 months interval. Joint space narrowing
is rapidly progressing (arrows) with medial migration of the femoral head.

10–20◦ or of 25◦ between the inside of the feet [43] to best completely normal radiographs [49]. In other studies, JSN was
demonstrate the neck (Fig. 1). Joint space width (JSW) is more a better predictor of hip pain compared to osteophytes [50,51].
accurately measured when the hip is radiographed with the joint Asymmetric JSN is a highly reliable sign of OA.
weight bearing and centering of the beam on the hip joint [44]. A
hip is characterized radiologically as normal when the weight- 9.2. Follow-up with plain radiographs
bearing surface of the acetabulum is horizontal, the angle of
Sharp is 40◦ or less and the center-edge (CE) angle is 25◦ or Radiological progression of hip OA seems to be related to the
higher (Figs. 1 and 2) [45,46]. Normal radiological anatomy is femoral head migration pattern. The superolateral migration is
present in more than 80% of patients with idiopathic OA [3]. correlated with rapid and the superomedial or medial with slow
Plain radiographs have been used as the primary diagnos- progression [52]. Evaluation of the disease progression, either
tic method for hip OA for many decades. Radiographs in a hip for the individual patient of for epidemiological studies, needs a
with established idiopathic OA are so characteristic that other quantitative estimation of the radiological findings, particularly
forms of imaging are seldom necessary. The radiological find- the JSW.
ings of OA include osteophyte formation, joint space narrowing
(JSN), subchondral sclerosis and subchondral cyst formation
(Figs. 2–5). Osteoyphytes of the central type represent new
bone formation into the joint and produce an irregular contour
of the articular surface. Marginal osteophytes represent lips of
new bone which typically grow at the joint margins increas-
ing thus the femoral head coverage and reducing the joint stress
(Figs. 3–5) [47]. They are thought to precede JSN (Fig. 3b) which
results from cartilage degeneration, demonstrated radiologically
as a decreased distance between opposing articular bony sur-
faces. Osteophyte formation shows a sensitivity of 89% and a
specificity of 90% for the diagnosis of hip OA [48]. Subchon-
dral sclerosis corresponds to new bone deposition and trabecular
microfractures and is located at sites of maximum stress in the
subchondral bone [47]. Subchondral cysts or geodes, are located
subchondrally, correspond to necrotic areas following microcon-
tusions and contain synovial fluid or proliferated myxomatous
tissue [47]. In the late stage, displacement of the joint is common
and bone destruction may be severe.
Most of the men and half of the women have a hypertrophic
pattern with marked sclerosis and large osteophytes. In about
20% of cases, mostly women, reactive changes are more sub-
Fig. 7. A 5-year postoperative plain radiograph in a patient with avascular necro-
dued, and the hip joint appears atrophic or osteopenic. The sis and persistent hip pain. There is advanced osteoarthritis with joint space
presence of osteophytes and JSN may show discordance with narrowing. Note also the varcularized fibular graft (arrow) and the extensive
the clinical picture and 29% of subjects with hip pain my show osteonecrotic area (open arrows).
 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48 41

Hip OA is defined according to minimum joint spaces of
<2.5 mm (“probable” OA) and <1.5 mm (“definite” OA) [50].
However, various studies have challenged the application of
absolute measurements. One study showed that a wide JSW
variation exists normally, ranging from 3 to 8 mm and from 2 to
6 mm at the superolateral and superomedial sites, respectively;
with an associated right/left asymmetry in 5.9% of subjects [53].
In the same study the JSW was related to acetabular anatomy,
being larger in dysplasia and smaller in coxa profunda, regard-
less of the presence of OA. In another study, the minimum JSW
decreased progressively with age in women but it was unaltered
in men [54]. A study on 78 normal radiographs showed that no
difference exists between right and left sides but women show a
narrower mean JSW compared to men [55].
Occasionally OA of the hip takes a pattern of a rapid pro-
gression. Rapidly destructive osteoarthritis of the hip is a unique
disorder characterized by rapid chondrolysis (more than 2 mm
or 50% of the joint space in 1 year) with no evidence of infec-
tion or crystal induced joint disease. The plain radiographs show
erosions, osteophytes, osteosclerosis, subchondral cysts, occa-
sionally subluxation and a JSN occurring within a few months
(Fig. 6) [56]. Its precise pathogenesis remains unclear. The
patients are usually elderly women, older than most patients
with hip OA. The use of NSAIDs, especially indomethacin, has
been implicated as pathogenetic cause but this has been chal-
lenged [57,58]. Others suggested the presence of insufficiency
fractures in the subchondral femoral head as the initial stimulus
[59]. The mechanism though of the rapid progression of chon-
drolysis, remains to be clarified. Major differentials of this entity
are septic arthritis and neuropathic arthropathy. Familiarity with
this disorder will obviate the need for extensive work-up to rule
out infection.

Fig. 8. A 33-year-old elite wrestling athlete with persistent bilateral pain, mainly on the left side. (a) The plain radiographs show bilateral congenital dysplasia, with
abnormal CE angle on the left side. Narrowing of the joint space with subchondral acetabular sclerosis is obvious on the left (arrow) suggesting early osteoarthritis.
The calculation of the acetabular head index (AHI) is also shown. (b) The axial CT image discloses narrowed acetabuli (double arrow) and confirms the congenital
dysplasia. (c) The coronal fat suppressed T2-w TSE image, shows bone marrow edema in the left hip (arrow), a moderate joint effusion and loss of the femoral head
sphericity. (d) The axial oblique T2-gradient echo MR image confirms the anterior joint space narrowing (short open arrow), and in addition shows a subchondral
acetabular cyst (open arrow) and a paralabral cyst (white arrow) with associated labral degeneration. Marginal osteophytes are obvious anteriorly and posteriorly
(thin white arrows).
42 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48

Follow-up studies may demonstrate secondary hip OA due

to an underlying disease such as osteonecrosis (Fig. 7), Paget’s,
Perthe’s, SCFE and trauma.

9.3. Plain radiographs and hip dysplasia

It has been suggested that idiopathic OA may be related

to a structural abnormality of the hip including CHD, SCFE,
Legg–Calve–Perthe’s, multiple epiphyseal dysplasia, acetabular
retroversion and FAI [31,60].
Acetabular dysplasia can be radiologically assessed using
simple measurements. The CE angle, as defined by Wiberg [61],
is the angle formed by a line from the center of the femoral
head to the lateral margin of the acetabular roof, and a line per-
pendicular to that joining the centers of the two femoral heads
(Figs. 2 and 8a). The acetabular head index (AHI) is the ratio
of the covered part of the head to the whole head, expressed
as a percentage (Fig. 8) [62]. The acetabular angle or Sharp’s
angle, is formed by a horizontal line connecting the two tear
drops and a line connecting the tear drop to the lateral acetabu- Fig. 10. A 48-year-old male who was an elite athlete in long jump, presenting
lar margin on each side (Fig. 2b). Acetabular dysplasia in adults with a dull persistent pain in the hip. The plain MRI (not shown) was normal.
is defined as the presence of a CE angle of <25◦ , AHI<75% and
The MR arthrogram with fat suppressed T1-w spin echo image in the sagittal
plane, shows central osteophytes (arrows) and articular cartilage defects (open
Sharp’s angle >40◦ . In CHD, the dysplastic acetabulum may be arrows), in keeping with early osteoarthritis.
associated with degenerative OA (Fig. 8) [63–65]. In one study,
acetabular dysplasia was shown to be a strong independent deter- 9.4. Cross sectional imaging
minant of incident radiographic hip OA [66]. Others showed that
mild to moderate hip dysplasia is higher than expected and it Although plain radiographs are a cost-effective means to eval-
significantly influences the prevalence of hip OA [67]. uate joint space when there is suspected hip OA, they do not
Other deformities may also contribute to early onset of hip directly depict the radiolucent articular cartilage. It has been
OA. It seems that acetabular retroversion is associated with hip reported that assessment of JSW alone is not an accurate indi-
OA, since its prevalence is 20% among patients with idiopathic cator of the structural integrity of the articular cartilage [69].
hip OA and 5% among the general population [60]. In addition, Others suggested that routine use of plain radiography in patients
cartilage lesions, as shown with MR arthrography, are common suspected of having hip OA is not indicated and in clinical prac-
in young and middle-aged patients who are suspected of having tice radiographs are used to rule out other conditions such as
FAI (Fig. 9) [68]. osteonecrosis [70,71].

Fig. 9. Bilateral hip pain with mild reduction of motion range, in a 39-year-old woman. The plain radiograph shows normal joint space (open arrows) but an abnormal
contour in the femoral head–neck offset (arrows), suggesting the presence of femoroacetabular impingment.
 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48 43

Fig. 11. A 37-year-old man with a history of an acetabular fracture during a motor vehicle accident and persistent hip pain for 13 months. (a) The plain radiograph
is of limited value due to the presence of the metallic implants. The MDCT arthrographic images in axial (b) and coronal (c) planes, show cartilage defects and
thinning (open arrows) and significant joint space narrowing (arrow) in keeping with post-traumatic osteoarthritis.

MRI is able to visualize directly the articular cartilage with
its superb contrast resolution and multiplanar imaging capabil-
ity (Figs. 8c and d and 10). MRI combined with arthrography,
is able to depict small osteophytes of central type (Fig. 10).
Patients with metallic components in the hip area or other con-
traindications for MRI may undergo multi-detector computed
tomography (MDCT) after arthrography (Fig. 11). Both MRI
and MDCT might be useful for diagnosing post-traumatic OA
(Figs. 12 and 13) or for identifying an underlying cause of OA
such as FAI and osteonecrosis (Figs. 14–16). MDCT is also
able to depict small intra-articular loose bodies and estimate the
femoral neck anteversion which might be a causative factor for
OA (11).
One study in patients with CHD showed that MDCT arthrog-
raphy was more accurate and reproducible compared to MRI
for cartilage degeneration [72]. In another study in patients
with hip pain and inconclusive radiographs, MDCT arthrogra-
phy revealed cartilage lesions [73]. Nishii et al. showed that
in patients with painful dysplastic hips and normal JSW on
plain radiographs, MRI shows cartilage lesions particularly in
the acetabular articular surface [74]. FAI is strongly associated
with early presentation of OA [75]. MR arthrography shows
abnormal alpha angles, cartilage lesions anterosuperiorly and
abnormal neck contour in cam type FAI and deep acetabu-
lum with posteroinferior cartilage lesion in pincer FAI [76].
In rapidly destructive OA of the hip, the MRI findings include
femoral head flattening, subchondral cyst formation, cartilage
degeneration and marrow edema of the proximal femur (100%)
and acetabulum (83%) [77].
A recently developed technique with I.V. contrast administra-
tion, named delayed gadolinium-enhanced magnetic resonance
imaging of cartilage, was developed to quantify the lost charges
of articular cartilage degradation in OA [78]. Normal articu-
lar cartilage has a high fixed-negative-charge density. In OA,
glycosaminoglycans, which are the negatively charged matrix
molecules, are lost. Therefore, the concentration of the anionic
molecule Gd-DTPA2− will be high in OA cartilage and can be
quantified with T1 MR imaging relaxometry.
44 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48

Fig. 12. A 15-year-old boy with persistent left hip pain and significant reduction of the range of motion, following a hip dislocation during a motor-vehicle accident.
(a) The plain radiographs show a rapid destructive process involving the left hip joint in a period of 11 months (arrows), with joint space narrowing, deformity of the
femoral head which migrates superiorly, subchondral sclerosis and osteopenia. (b) MDCT corresponding to the latest plain radiograph. The coronal and oblique axial
images show the difference between the right and the left joint spaces. (c) The fat-suppressed T2-w TSE MR coronal image shows the joint effusion, the bone marrow
edema (arrows) and the cranial migration of the femoral head. The delayed Gd-enhanced fat-suppressed T1-w Spin Echo oblique axial MR image (d), shows the
enhancing reactive bone marrow edema in the acetabulum (thin arrow), the joint space narrowing due to chondrolysis (arrows) and the labral degeneration anteriorly
(open arrow).
 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48 45

Fig. 13. A 70-year-old male patient with a history of a fractured acetabulum 12 months prior to imaging and unable to walk. The coronal MDCT image shows a
post-traumatic osteoarthritis of the left hip joint with joint space narrowing, and osteophyte and subchondral cyst formation.

10. Basic management strategies
Treatment of hip OA depends upon the stage of the disease,
the patient’s age and the functional impairment. The goals of
treatment are pain relief, maintenance and restoration of func-
tion, and prevention of advanced changes.
At early stages the goals are: Maintenance of range of
movement and muscle strength with physiotherapy and exer-
cise, relieve pain with acetaminophen, paracetamol, classic
NSAID’s and modern anti-COX-2 NSAID’s [79,80], modi-
fication of daily activities and protection of the joint from
overload using a cane on the side opposite to their painful
hip. Cartilage structure modifying agents, such as condroitin
sulfate, hyaluronate acid, diacerhein and glucosamine have
been also used in early disease with controversial clinical
results [81]. Arthroscopic intervention in selected cases with
labral or chondral lesions and anterior impingement is also
advocated.

Fig. 14. A 56-year-old woman with pain and restricted motion bilaterally. The plain radiographs (a and b) show joint space narrowing and subchondral sclerosis
(open arrows) along with a deformity of the outer femoral head–neck offset (arrows). (c) The fat-suppressed T2-w TSE coronal MR image, shows extensive reactive
bone marrow edema (arrows) and a subchondral cyst in the right acetabulum (thick arrow) in keeping with osteoarthritis secondary to bilateral femoroacetabular
impingment.
46 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48

Fig. 15. A 30-year-old male elite Kick-box athlete complainting of left hip pain during exercise. (a) The plain radiograph shows an abnormal contour suggesting
femoroacetabular impingment (arrow). (b) The coronal contrast-enhanced fat-suppressed T1-w MR image shows bone marrow edema corresponding to stress injury
or bony contusion (long arrow) and iliofemoral tendinitis (short arrow). (c) The MRI examination after 12 weeks of rest and NSAIDS, there is resolution of the bone
marrow edema but the tendinitis persists due to a tear of the labrum (open arrow) which was subsequently surgically confirmed.

At intermediate stages and in young adult patients, varus

or valgus osteotomy is an option in order to help unload the
degenerative cartilage. Re-directional pelvic osteotomy can be
an effective means of treatment in appropriate cases.
Advanced cases of hip OA can be successfully treated with
total hip replacement. Hip joint replacements, both cemented
and cementless, have shown above 90% survival rates of both
components, with a failure rate for aseptic loosening at the level
of 1.5–2% at 10–15 years follow-up.
New frontiers for treatment and prevention of OA include
identifying genetic and biochemical markers. These areas are
currently under investigation but not yet clinically applicable.
Chondrocyte transplantation has received significant attention,
especially for the knee joint; however this is intended for acute
traumatic chondral defects as opposed to degenerative changes
in articular cartilage.

11. Conclusion

To evaluate the symptoms of hip OA and come to a decision as

Fig. 16. Secondary hip osteoarhtritis in a patient with advanced avascular necro-
sis. The fat-suppressed contrast-enhanced T1-w oblique axial MR image shows
the collapsed femoral head with the subchondral necrosis (thin arrow), the bone
marrow edema in the acetabulum and femoral head and neck (arrows) and the
joint effusion (open arrow).
to the proper surgical treatment, the clinical picture, activities of
daily living as well as plain radiographs should be carefully stud-
ied. It is often though difficult to evaluate the disease based on
clinical and radiographic grounds alone. If plain radiographs are
inconclusive, MRI and/or MDCT, especially if combined with
 T. Karachalios et al. / European Journal of Radiology 63 (2007) 36–48
arthrography, may offer a direct demonstration of the cartilage,
and illustrate erosions as well as bone marrow edema and labral
tears. The multiplanar capability of the cross sectional imag-
ing, may disclose occult to plain radiographs mild dysplasias or
deformities which might predispose to early OA. Early detection
is clinically important in the light of new treatment options.
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