SYMPOSIUM: PAPERS PRESENTED AT THE ANNUAL CLOSED MEETING OF THE
INTERNATIONAL HIP SOCIETY
The Etiology of Osteoarthritis of the Hip
An Integrated Mechanical Concept
Reinhold Ganz MD, Michael Leunig MD,
Katharina Leunig-Ganz MD, William H. Harris MD, DSc
? The Association of Bone and Joint Surgeons 2008
long been considered secondary (eg, to congenital or
developmental deformities) or primary (presuming some
underlying abnormality of articular cartilage). Recent
information supports a hypothesis that so-called primary
osteoarthritis is also secondary to subtle developmental
abnormalities and the mechanism in these cases is femo-
roacetabular impingement rather than excessive contact
stress. The most frequent location for femoroacetabular
impingement is the anterosuperior rim area and the most
critical motion is internal rotation of the hip in 90? flexion.
Two types of femoroacetabular impingement have been
identified. Cam-type femoroacetabular impingement, more
The etiology of osteoarthritis of the hip has
prevalent in young male patients, is caused by an offset
pathomorphology between head and neck and produces an
outside-in delamination of the acetabulum. Pincer-type
femoroacetabular impingement, more prevalent in middle-
aged women, is produced by a more linear impact between
a local (retroversion of the acetabulum) or general
overcoverage (coxa profunda/protrusio) of the acetabulum.
The damage pattern is more restricted to the rim and the
process of joint degeneration is slower. Most hips, how-
ever, show a mixed femoroacetabular impingement pattern
with cam predominance. Surgical attempts to restore nor-
mal anatomy to avoid femoroacetabular impingement
should be performed in the early stage before major
cartilage damage is present.
Level of Evidence: Level V, therapeutic study. See the
Guidelines for Authors for a complete description of levels
Four decades ago, Murray  suggested a relationship
between a rather subtle deformity of the proximal femur,
which he called the ‘‘tilt deformity,’’ to the subsequent
development of osteoarthritis (OA) of the hip . Because
only anteroposterior (AP) radiographs were available, the
deformity was not fully characterized, but the AP film
suggested a mild degree of the deformity commonly
occurring after a minimal slipped capital femoral epiphysis
(SCFE). It appeared to foretell the later development of OA
in the hip (Figs. 1, 2).
Stimulated by Murray’s observations, Solomon and
colleagues in South Africa [54–58] and Harris and col-
leagues in the United States [20–22, 61, 62] extended
Murray’s original suggestion. From these three sets of
Each author certifies that he or she has no commercial associations
(eg, consultancies, stock ownership, equity interest, patent/licensing
arrangements, etc.) that might pose a conflict of interest in connection
with the submitted article.
R. Ganz, M. Leunig
University of Berne, Berne, Switzerland
Department of Orthopaedics, Balgrist University Hospital,
M. Leunig (&)
Hip Service, Department of Orthopaedics, Schulthess Clinic,
Lengghalde 2, CH-8008 Zurich, Switzerland
Maternity Department, Triemli City Hospital, Zurich,
W. H. Harris
Harvard Medical School, Massachusetts General Hospital Harris
Orthopedic Biomechanics and Biomaterials Lab, Boston, MA,
Clin Orthop Relat Res (2008) 466:264–272
observations grew a controversial hypothesis on the etiol-
ogy of hip OA [20–22, 54–58, 61, 62]: the theory proposes
many cases of osteoarthritis of the hip that previously were
considered ‘‘primary’’ or ‘‘idiopathic’’ are, indeed, caused
by minor developmental deformities that were previously
unrecognized or ignored and these deformities cause
arthritis to develop from what is today called femoroace-
tabular impingement (FAI).
This overview integrates for the first time this previously
proposed hypothesis on the etiology of hip OA into the
concept of FAI recently proposed by Ganz et al. .
History of the Theory
The new theory first required an extensive set of exclusion
criteria: inflammatory diseases of the hip (such as rheuma-
toid arthritis, ankylosing spondylitis, Reiter’s syndrome, or
lupus) as well as calcium pyrophosphate disease, diffuse
idiopathic skeletal hyperostosis, gout, and hemochromato-
sis. Also excluded were osteonecrosis and fractures around
or femoral neck. Similarly, cases of damage to the cartilage
from infection or resulting from penetration of a fixation
device into the joint space were excluded. This set of
exclusions was necessary to narrow the definition of hip OA
to those causes that arise within the joint itself without
extraneous inflammatory, traumatic, and metabolic causes,
after rheumatoid arthritis has damaged the joint at an earlier
time and has burned out as an active rheumatoid process.
Second, within this redefined group, several additional
key observations were made. Clearly, many cases of hip
OA result from severe developmental or acquired defor-
mities of the hip that occurred in infancy or childhood.
Children with developmental dysplasia resulting in a
hypoplastic acetabular articulation coupled to a deformed
femoral head often develop progressive and severe arthritis
of the hip in late adolescence or young adult life. Similarly,
some patients with severe SCFE or Legg-Calve ´-Perthes
disease may develop late OA. It is generally agreed hip OA
in these examples is causally related to the gross deformity.
In contrast, the focus of the new concept addressed those
remaining cases of hip OA in which the deformity was
considered mild, slight or even, in the eyes of casual
observers, nonexistent. In the past, such cases have been
commonly considered ‘‘primary’’ (ie, without known
Fig. 1A–D AP
(A) a normal hip and three forms
of abnormalities associated with
mild slipped capital
epiphyses called (B) ‘‘flattening,’’
(C) the ‘‘bump,’’ and (D) the
‘‘hook.’’ Reproduced with per-
Etiology of osteoarthritis of the
Volume 466, Number 2, February 2008Mechanical Damage to the Hip265
It was in this group of patients with mild deformities
that the hypothesis developed. Murray’s  work sug-
gested hip OA could develop secondary to rather subtle,
sometimes previously unrecognized
occurred before full skeletal maturation. One example
was the development of hip OA secondary to a mild,
unrecognized, and untreated SCFE. Harris and Solomon
and their coworkers presented additional longitudinal
data on documented cases of mild developmental hip
disease unrecognized as abnormal by many radiologists
and orthopaedic surgeons, which led years later to hip
OA [20–22, 54–58, 61, 62]. The leading conditions
contributing to these subtle deformities were develop-
mental hip dysplasia, SCFE, Legg-Calve ´-Perthes disease,
multiple epiphyseal dysplasia, and spondyloepiphyseal
This concept was subsequently supported in retrospec-
tive analyses of patients presenting in adult life with hip
OA, without any of the excluded conditions, for whom
prior radiographs were available for analysis after adult-
hood had been reached, but before any radiographic
signs of arthritis were visible. From these studies, a striking
observation was made: 79% of these cases had antecedent
subtle but definite signs of an underlying developmental
abnormality [21, 61, 62].
Among women, unrecognized and untreated develop-
mental dysplasia predominated . Among men, the
dominant abnormality was femoral, not acetabular, and had
the characteristic of the ‘‘tilt’’ deformity on AP radiographs
. When assessed using three radiographic views (AP,
frog lateral, and crosstable lateral), this femoral deformity
was more fully described and named the ‘‘pistol grip’’
deformity [21, 62]. Detailed longitudinal followup studies
of long duration confirmed this characteristic configuration
of the femoral head and neck could be produced by several
etiologies, namely SCFE, Legg-Calve ´-Perthes disease,
multiple epiphyseal dysplasia, and spondyloepiphyseal
dysplasia. This same femoral deformity also existed in
many patients, both male and female, who had develop-
mental acetabular dysplasia. Thus, this common femoral
deformity can exist both with and without an acetabular
dysplasia. Moreover, as is well known, longitudinal studies
show some cases of Legg-Calve ´-Perthes disease that began
as a purely femoral abnormality producing a pistol grip
deformity can secondarily lead to acetabular deformity [21,
Thus, this concept is reinforced by evidence from both
longitudinal studies following known cases of develop-
mental dysplasia of the hip, SCFE, and Legg-Calve ´-Perthes
disease into adulthood and retrospective studies of adult
cases of OA, which showed a high correlation between
these hip deformities resulting from infantile, childhood,
and adolescent conditions and the subsequent adult hip OA.
A retrospective study of Caucasian cases in the United
States suggested 79% of the cases of adult OA were
associated with these deformities, and when the remaining
21% of cases were further examined over a longer time
span, an additional 10% had or subsequently developed
signs of rheumatoid arthritis, hemochromatosis, or calcium
pyrophosphate disease . Thus, after eliminating the
excluded conditions listed above that lead to degenerative
changes in the hip, approximately 90% of the cases of
adult hip OA were associated with some developmental
Solomon et al. [54–58] made similar observations in
Caucasians living in South Africa. Moreover, they made
other relevant observations. They found a markedly lower
incidence of hip OA in Africans in South Africa compared
to Caucasians. This difference also correlated with a
markedly lower incidence of those related developmental
conditions listed above, conditions that were common
among Caucasian children and adolescents in South Africa
but uncommon among Africans. These parallel differences
in Africans further suggested a causal role of develop-
mental deformities of the hip in leading to adult hip OA
. This relationship between developmental deformities
Fig. 2 Comparison of the mild deformity of the proximal femur
secondary to a mild, unrecognized slipped capital femoral epiphysis
and the contour of the grip of a pistol. Because of the similarity, these
types of proximal femoral deformities are called ‘‘pistol grip
deformities.’’ Reproduced with permission and copyright ? 1975
by Elsevier from Stulberg SD. Unrecognized childhood hip disease: a
major cause of idiopathic osteoarthritis of the hip. In: Cordell LD,
Harris WH, Ramsey PL, MacEwen GD, eds. The Hip: Proceedings of
the Third Open Scientific Meeting of the Hip Society. St Louis, MO:
CV Mosby; 1975:212–228.
266Ganz et al.Clinical Orthopaedics and Related Research
and subsequent OA was further reinforced by the identifi-
cation by Solomon and coworkers of two ‘‘geographically
isolated African communities in whom hip OA was
unexpectedly common; in both, there is also a high inci-
dence of hip dysplasia’’ .
A relationship between developmental deformities and
hip OA is not new. For decades, many cases of hip OA
have been called ‘‘secondary,’’ for example, secondary to
severe dysplasia. The distinction here lies in the novel
concept that more subtle deformities, often unrecognized in
the past as meaningful deformities, can produce hip OA
(Fig. 3). This hypothesis proposes most, if not all, hip OA
is secondary, often secondary to subtle but definite and
commonly overlooked, ignored, or not recognized dyspla-
sia or pistol grip deformities.
Problems with the Theory
While the data supporting this hypothesis appeared strong,
several critical pieces were still missing. First was clinical
confirmation. Large-scale radiographic studies of asymp-
tomatic young adults to document the percentage of
individuals with these developmental abnormalities could
potentially provide confirmatory evidence. Prospective
longitudinal long-term followup studies could demonstrate
both the positive and negative predictive power of the
hypothesis. Studies of this nature would contribute to such
important questions as ‘‘do those patients with these
abnormalities always get OA?’’ and ‘‘are these deformities
the only ones to produce OA?’’
The second piece of data missing was the mechanism by
which some of these subtle abnormalities, for example,
subtle femoral head, head-neck, or neck deformities, led to
OA. In contrast to this question in relation to minor defor-
mities, in cases of severe deformities, the joint contact area
was typically reduced by distortion of the acetabulum or
femoral head or both and thus the contact pressure history in
the articular cartilage was increased. However, we do not
believe a major reduction in contact area would be a sat-
isfactory explanation in those cases of subtle deformities,
for example, in cases having a normal acetabular contour
and only a mildly abnormal head-neck contour.
The third missing piece, and perhaps most important to
the patient with the subtle abnormality, was a way to treat
the deformity and halt or delay the process. If these
abnormalities were causally related to the generation of the
OA, what could be done, surgically or otherwise, that could
retard or eliminate the progression of the disease under
circumstances of sufficiently low risk that such early
intervention would be warranted?
Thus, this hypothesis lay in an uncertain state for
40 years, unconfirmed and yet tantalizing in its possible
suggestion that if the mechanism of the osteoarthritic
process from these deformities could be established, a
solution to retard progressive damage might ensue.
Fig. 3A–C (A) FAI is shown in a
34-year-old man with an appar-
ently normal AP radiograph. (B)
The nonspherical femoral head
leading to reduced offset at the
neck and predisposition to cam
FAI is visible on the lateral
radiograph. (C) The MRI scan
confirmed the labral tear and
chondral injury resulting from
FAI. Reproduced with permission
from Ganz R, Parvizi J, Beck M,
Leunig M, No ¨tzli H, Siebenrock
KA. Femoroacetabular impinge-
ment. Clin Orthop Relat Res.
Volume 466, Number 2, February 2008Mechanical Damage to the Hip267
Recent Evidence in Support of the Theory
Two recent developments strengthen the hypothesis and
play a predictive role in confirming the hypothesis. The
two key developments are (1) the recognition of the
mechanism for the development of the hip OA caused by
mild deformities and (2) the possibility that correction of
that mechanism could retard the development of the OA.
First pioneered and stimulated by Ganz and coworkers
[4–6, 12, 14, 16–18, 23, 24, 30–36, 39–41, 47, 52, 53, 60,
66], and now confirmed by a variety of observations from
many centers worldwide [1–3, 7–11, 19, 25, 27, 28, 42, 43,
45, 48–51, 59, 63–65, 68, 69], a mechanism has been
defined that explains how these subtle developmental
abnormalities adversely affect the joint and lead to OA in
many cases. The dominant mechanism is FAI-induced by
motion of the well-constrained hip. In those cases of severe
deformity of the hip secondary to developmental abnor-
malities, the mechanism of OA is excessive contact stress
history on the cartilage secondary to reduced contact area.
This is not so for the more subtle deformities that produce
FAI since the contact areas are not reduced. The recogni-
tion of this important mechanism, however, could not be
made until after the technique of surgical dislocation of the
hip could be executed without the risk of avascular necrosis
and had been developed in a way that produced little or no
morbidity from the procedure [15, 16, 18]. Surgical dislo-
cation of the hip allowed not only for in situ observation of
the FAI process but also for the attribution of the various
damage patterns within the joint to different FAI mor-
phologies . Although FAI can take place everywhere
around the femoroacetabular joint, the most common site is
anterolateral and is produced by internal rotation of the
femur in flexion.
Two distinct types of FAI have been identified (Fig. 4).
The first is characterized by the linear impact of the
acetabular rim against the head-neck junction in a local (eg,
acetabular retroversion) or global (eg, coxa profunda or
protrusio) overcoverage of the acetabulum; it is therefore
named pincer FAI. The second type occurs with the jam-
ming of a nonspherical extension of the femoral head into
the acetabular cavity; it is therefore named cam FAI .
Fig. 4A–D Diagrams
the proposed mechanisms of joint
damage in FAI. (A) In pincer
FAI, linear impact due to the
acetabular overcoverage occurs
anteriorly. The persistent anterior
abutment with chronic leverage of
the head in the acetabulum some-
times results in chondral injury in
the ‘‘contrecoup’’ region of the
posterior-inferior acetabulum. (B)
In cam FAI, the prominent fem-
oral head/neck junction (C) is
jammed into the acetabulum caus-
ing damage to the peripheral
cartilage at flexion and internal
rotation (D). Reproduced with
Parvizi J, Beck M, Siebenrock
KA, Ganz R, Leunig M. Anterior
Part I. Techniques of joint pre-
Relat Res. 2004;418:71.
268Ganz et al.Clinical Orthopaedics and Related Research
Both morphologic abnormalities are frequent and often
combined . With retroversion of the acetabulum, the
ischial spine is in most cases visible in the pelvic cavity
, suggesting a true rotational abnormality of the ace-
tabulum. The nonsphericity of the femoral head is mostly
located anterolaterally and therefore not necessarily visible
on AP radiographs . When it is seen on AP radio-
graphs, it is known as pistol grip deformity .
Nonspherical extensions of the head are frequently the
result of an abnormality of the capital femoral epiphysis
 and are covered by hyaline cartilage . However,
the metaphysis in SCFE [37, 38], as well as other defor-
mities of the proximal femur like Legg-Calve ´-Perthes
disease  or the retrotilt of an otherwise perfectly healed
femoral neck fracture , can also produce a cam FAI.
The damage pattern of pincer and cam FAI differ sub-
stantially when one of these two types exists as an isolated
deformity (Fig. 5). In pincer FAI, the first structure to fail
is the labrum, showing intrasubstance fissuring and intra-
substance ganglion formation. With time, bone apposition
occurs on the osseous rim next to the labrum, pushing the
labrum forward. The labrum itself becomes thinner and
thinner until it finally is no longer distinguishable. The
bone apposition is visible on MRI  as well as on
standard radiographs as a double line of the involved rim;
as such, it increases impingement. The acetabular cartilage
adjacent to the involved labrum undergoes degeneration,
but in a rather thin strip. With time, the impact area on the
femoral neck shows a saddlelike callus formation with
central ulcerations of the periosteum. The femoral head
cartilage remains uninvolved over a long period; only late
in the process will there be cartilage abrasion in the pos-
teroinferior joint, on the head, and/or on the acetabulum
called ‘‘contrecoup lesion’’ .
In contrast, with isolated cam FAI, the labrum remains
uninvolved over a rather long period. What appears on
MRI as rupture of the labrum is in fact an avulsion of the
acetabular cartilage from the labrum and then of the sub-
chondral bone. Such a cartilage cleavage can become as
deep as 2 cm and will be destroyed with time. When the
involved area is large enough, the femoral head will
migrate into the defect, which can be seen first in MRI and
somewhat later in conventional radiography as joint space
narrowing. It is only then that the cartilage of the spherical
portion of the head (weightbearing area) becomes involved,
while the cartilage of the nonspherical portion of the head
(nonweightbearing area) shows surface damage early in the
disease process [17, 66]. Very often with cam FAI, cysts
develop in the head or near the head-neck junction but
always distal to the physis; we believe they reflect the
effects of the jamming process .
The pincer-type FAI produces a rather slow process of
degeneration and occurs more often in women between 30
and 40 years of age engaging in activities with high
demands on motion like yoga and aerobics. The cam-type
FAI is typically seen in athletic men on average a decade
younger. Both FAI types produce damage first on the
acetabular side, but cam FAI is clearly more destructive
than pincer FAI, although the symptoms are often less
pronounced. The more severe damage to the labrum,
known to contain nociceptive fibers , is the most likely
explanation for the increased pain reported by women
suffering from pincer FAI compared to men with cam FAI.
The described damages to the hip produced by
impingement are more than just precursors. They are the
early stages of an extensive, generalized arthritic process of
the joint. This concept of FAI applies to both the subtle and
some of the larger deformities of the acetabular and the
femoral side compromising the clearance of the hip for
motion; it even includes a small group of patients with
rather normal hip morphology but supraphysiologic
demands on hip motion. Hips with cam FAI fail toward an
anterosuperior OA while hips with pincer FAI fail toward a
posteroinferior or central OA.
Fig. 5A–B Intraoperative photographs show acetabular cartilage
damage during the treatment of young adult patients suffering from
FAI. (A) In pincer FAI, the linear impact leads to substantial labral
damage, while in early phases the adjacent cartilage remains intact.
(B) In contrast, cam FAI frequently reveals deep-reaching flaplike
cleavage lesions of cartilage from the subchondral bone early in the
Volume 466, Number 2, February 2008Mechanical Damage to the Hip 269
More than 40 years ago, Murray , Solomon et al. [54–
58], and Harris et al. [20–22, 61, 62] made the remarkable
observation that primary OA of the hip could frequently be
attributed to minor morphologic abnormalities such as
pistol grip deformity. Until recently, the pathophysiology
of this etiologic concept remained under debate.
To date, however, there is increasing evidence the FAI
mechanism is the cornerstone of this mechanical etiologic
concept of hip OA, which evolved some 40 years ago [21,
46, 54], leaving few cases with so-called primary OA. With
proposing this ‘‘novel’’ FAI concept, we also realized
clinical and radiographic methods routinely used for
advanced hip OA are limited, if not insufficient, for FAI
assessment and documentation of treatment outcome.
Nonetheless, further steps are required to evaluate this
hypothesis of OA of the hip. All are in process. In an
unpublished sheep model, a 15? varus osteotomy of the
proximal femur produced an impingement of the hip and
consequently showed lesions of the acetabular rim and of
the adjacent cartilage typically seen in a mixed impinge-
ment. Increasing numbers of patients have been reported
with detailed visual [4, 34] or arthroscopic documentation
[10, 11, 19, 28, 49–51, 68] of the FAI partially followed by
abnormality leading to FAI. The short-term outcomes
appear favorable [6, 10, 14, 19, 25, 28, 45, 48–52, 63],
especially when comparing refixation of the labrum as part
of the treatment steps versus de ´bridement of the labrum
. The results of the joint reconstruction together with
labral refixation favor the expectations of good long-term
results. Substantial retardation of the development of OA
would be both beneficial to the patient and supportive of
the concept that such OA is caused in the described way.
Nevertheless, before FAI treatment can be widely pro-
moted, we require greater scrutiny to determine the right
patient, the right time, and the right surgeon. It will not be
the type of procedure (open or arthroscopic), but rather the
possible intraarticular reconstruction that will determine
treatment success or failure. The achievable intraarticular
reconstruction will depend on the complexity of the FAI
morphology and the degree of secondary degeneration.
Since 2005, a prospective population-based study has
been underway (NFP53 405340-104778). Based on a
cohort of more than 1100 young men, this study was ini-
tiated to address the prevalence of FAI in this population
and to determine whether these morphologic alterations are
associated with an increased rate of early OA (natural
course study). Preliminary results suggest a decrease of
internal rotation of the hip while at 90? of flexion by 10?
increases the prevalence of acetabular rim pathology by a
factor of two.
of the morphologic
There is an increasing body of evidence that most hips
that fail to OA without severe deformities of the joint do so
with the mechanism of FAI based on subtle or moderate
morphologic abnormalities of the joint components. An
increasing number of such hips fail at a rather young age.
Consequently, the strategy of treatment should be to
reconstruct a hip morphology allowing motion not inter-
rupted by FAI before major rim and cartilage damage is
established. Because FAI treatment is most successful in
the absence of secondary degenerative changes, this raises
the question whether FAI treatment should be performed in
‘‘asymptomatic’’ patients. Most authors and surgeons view
symptomatic as having pain. If the patient has a limited hip
range of motion (flexion/internal rotation) and degenerative
changes on MRI or radiography, treatment of FAI might be
warranted even in the absence of pain. Presentation of a
pain-free patient in the doctor’s office is a rather rare
situation and the decision-making process should involve
To have a standardized instrument for evaluation of
such surgical indications but also for more accurate
followup data, new scores for clinical evaluation, and
imaging classification for the FAI hip ahead of the well-
established OA are currently under development. A num-
ber of aspects of the concept of FAI are still not adequately
confirmed; others are in the process of evaluation. Despite
the increasing evidence favoring the concept, we believe
treatment of FAI should currently be restricted to centers
experienced in this pathology and staffed by surgeons
adequately trained in techniques addressing FAI. Clinical
and radiographic assessment and followup have to at
least meet those required for total hip arthroplasty. If the
above-mentioned developments and data collection take
place, FAI treatment might become a mainstay in joint-
preserving treatment of the hip similar to that of hip
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