Sports Med (2015) 45:1107–1119

DOI 10.1007/s40279-015-0336-5

REVIEW ARTICLE

Gluteal Tendinopathy: A Review of Mechanisms, Assessment

and Management
Alison Grimaldi1 • Rebecca Mellor2 • Paul Hodges3 • Kim Bennell4 •

Henry Wajswelner5 • Bill Vicenzino2

Published online: 13 May 2015

Ó Springer International Publishing Switzerland 2015

Abstract Tendinopathy of the gluteus medius and gluteus utility. On the basis of the few diagnostic utility studies and
minimus tendons is now recognized as a primary local the current understanding of the pathomechanics of gluteal
source of lateral hip pain. The condition mostly occurs in tendinopathy, we propose that a battery of clinical tests
mid-life both in athletes and in subjects who do not utilizing a combination of provocative compressive and
regularly exercise. Females are afflicted more than males. tensile loads is currently best practice in its assessment.
This condition interferes with sleep (side lying) and com- Management of this condition commonly involves corti-
mon weight-bearing tasks, which makes it a debilitating costeroid injection, exercise or shock wave therapy, with
musculoskeletal condition with a significant impact. Me- surgery reserved for recalcitrant cases. There is a dearth of
chanical loading drives the biological processes within a evidence for any treatments, so the approach we recom-
tendon and determines its structural form and load-bearing mend involves managing the load on the tendons through
capacity. The combination of excessive compression and exercise and education on the underlying pathomechanics.
high tensile loads within tendons are thought to be most
damaging. The available evidence suggests that joint posi-
tion (particularly excessive hip adduction), together with
Key Points
muscle and bone elements, are key factors in gluteal
tendinopathy. These factors provide a basis for a clinical
Gluteal tendinopathy is the most prevalent lower
reasoning process in the assessment and management of a
limb tendinopathy, substantially impacting quality of
patient presenting with localized lateral hip pain from glu-
life.
teal tendinopathy. Currently, there is a lack of consensus as
to which clinical examination tests provide best diagnostic Excessive hip adduction, in conjunction with other
muscle and bone factors, is considered a key driver
in the pathomechanics of gluteal tendinopathy.
& Bill Vicenzino
Load and exercise management based on
b.vicenzino@uq.edu.au
pathomechanics is proposed as a biologically
1
Physiotec, 23 Weller Road, Tarragindi, QLD 4121, Australia plausible and viable approach to rehabilitation.
2
School of Health and Rehabilitation Sciences, The University
of Queensland, St Lucia, QLD 4072, Australia
3
NHMRC Centre of Clinical Research Excellence in Spinal
Pain, Injury and Health, The University of Queensland,
1 Introduction
St Lucia, QLD 4072, Australia
4 Gluteal tendinopathy commonly presents as pain and ten-
Department of Physiotherapy, Centre for Health, Exercise
and Sports Medicine, University of Melbourne, Carlton, derness laterally over the greater trochanter (lateral hip
VIC 3053, Australia pain). Studies using various scales rate it as a cause of
5
Department of Physiotherapy and Lifecare Physiotherapy, moderate to severe pain and disability [1–4], with one
LaTrobe University, Bundoora, VIC 3086, Australia study demonstrating quality of life and levels of disability

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1108
similar to those in end-stage hip osteoarthritis [5]. Gluteal
tendinopathy is most prevalent in women aged over
40 years [6, 7], with reports of up to 23.5 % of women and
8.5 % of men between the ages of 50 and 79 years being
afflicted with the condition [7]. It is the most prevalent of
all lower limb tendinopathies [8]. Although this condition
occurs in sedentary individuals, athletes (particularly run-
ners) can also be affected [9]. It is anticipated that the
prevalence of gluteal tendinopathy in athletes will increase
in parallel with the increasing age of society and increasing
participation of females in long-distance running and
triathlons [10–12]. In the USA, the average age of par-
ticipants in road races is 40 years [10] and more than 43 %
of triathletes are over 40 years of age, with females con-
stituting 38 % of all triathletes [12].
Traditionally, lateral hip pain has been diagnosed as
trochanteric bursitis, but this diagnosis has been challenged
by imaging, histological and surgical studies. Non-inflam-
matory insertional tendinopathy of the gluteus medius
(GMed) and/or gluteus minimus (GMin) is now considered
the primary pathology underpinning lateral hip pain [13–18].
Bursal distention may coexist, but this is unlikely to be pri-
marily inflammatory in nature (referring to the suffix ‘‘-itis’’)
[19] and is thought to be secondary [17]. The condition is
sometimes referred to as greater trochanteric pain syndrome,
in acknowledgment of the issues confronting the diagnosis of
lateral hip pain. This review seeks to provide a synopsis of
the current literature on the underlying pathomechanics,
assessment and management of gluteal tendinopathy.
2 Pathomechanics
Understanding of the mechanisms underlying tendon
pathology may provide guidance for optimal management.
Mechanical loading is a potent driver of the biological
processes that occur within a tendon, and these, in turn,
determine its structural form and load-bearing capacity. At
any time, a tendon undergoes both catabolic and anabolic
processes. Under conditions of normal loading, these pro-
cesses are balanced and provide the basis for a healthy
homeostatic state within the tissue. This balance may be
disturbed by the type, intensity and frequency of loading
(see Magnussen et al. [20] for a detailed review). A load
may be applied to a tendon longitudinal to its collagen
fibres (tension or tensile load) or perpendicular to the line
of the fibres (compression), the latter particularly at its
bony enthesis. Tensile loads may be applied actively via
muscle contraction or passively via stretching. Tendon
loads will be particularly high when the muscle is active
and the tendon is lengthening at the same time, i.e. ec-
centric contractions in the outer range, where anatomical
compression may also occur [21].
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A. Grimaldi et al.
Table 1 Biological responses and outcomes associated with types of
tendon loading
Type of tendon load Biological response Outcome
Compression (transverse) Catabolic Reduced tensile
strength
Tension (longitudinal) Catabolic and Load
anabolic dependent
Less than normal load Catabolic Reduced tensile
(stress deprivation) strength
Normal, regular load Catabolic = anabolic Homeostasis
Slightly greater than Net anabolic Increased
normal load tensile
strength
Much greater than Net catabolic Failure to adapt
normal load
Graduated increases in tensile load with adequate re-
covery and adaptation time induce a net anabolic effect,
with a subsequent increase in the load-bearing capacity of
the tendon [20]. A rapid increase in the intensity and/or
frequency of tensile loading may lead to failure to adapt
and a net catabolic effect. Net catabolism also results from
lack of tensile loading (stress deprivation) and compression
(Table 1). At a cellular level, stress deprivation and com-
pression induce expression of catabolic enzymes, which
break down type 1 collagen [22], and increase tenocyte
expression of large proteoglycans, which cleave apart
collagen fibres [23]. Matrix degradation and changes in
tenocyte behaviour reduce load-bearing capacity and pre-
dispose to injury at relatively low tensile loads [24].
Soslowsky et al. [25] demonstrated in an animal model that
combined compression and high tensile loads are more
damaging than either stimulus alone. Several bony and
muscle factors, and the interaction between them, require
consideration for understanding of how compressive
loading or stress shielding contributes to the underlying
pathomechanics of this disorder.
2.1 Influence of Joint Position
The tendons of GMed and GMin, and the associated bur-
sae, can be compressed by the iliotibial band (ITB) at their
insertion into the greater trochanter. The compressive load
is influenced by the hip joint position. Birnbaum et al. [26]
demonstrated compressive loads in this region of 4 N at 0°
hip adduction, which rise to 36 N at 10° adduction and
106 N at 40° adduction [26]. Accumulation of compressive
tendon loading is likely to result from excessive hip ad-
duction adopted during static postures and dynamic tasks.
Examples include standing with one hip in adduction
(hanging on one hip), sitting with knees together or crossed
in adduction, and an excessive lateral pelvic tilt or shift
during dynamic single-leg loading tasks. Running with a
Gluteal Tendinopathy
midline or cross-midline foot–ground contact pattern, on
the camber of a road or in the same direction around a
track, are examples of dynamic activities that also adduct
the hip and could increase the risk of development of lat-
eral hip pain [27, 28].
Hip adduction might also result in relative stress
shielding of the deeper gluteal tendon fibres from tensile
loads. This has been studied not at the hip but at the
shoulder; the deep fibres of the supraspinatus tendon ad-
jacent to the joint are not only compressed but also
relatively shielded from tensile stress in lower ranges of
shoulder abduction [29]. As the shoulder abducts, the
deeper fibres of the supraspinatus tendon experience in-
creases in tensile loading and reduced compression loading
[29]. This might also occur at the hip, where the deeper
gluteal tendon fibres are not only compressed but also
relatively stress shielded in positions of hip adduction,
potentially resulting in negative structural change over
time.
Higher ranges of hip flexion may also alter ITB tension
because of the substantial fascial confluence of the ITB
with the gluteal fascia and into the lumbodorsal fascia [30,
31], thus potentially contributing to compression of the
GMed and GMin tendons. Patients with gluteal
tendinopathy may experience pain in prolonged sitting,
with subsequent difficulty in rising to standing, particularly
if they have been sitting with more than 90° of hip flexion
in a low lounge or car seat. Sitting with the knees crossed
or adducted in a low seat further increases ITB tension. The
combination of higher ranges of hip flexion and adduction
is likely to induce substantial compressive loading on the
GMed tendon.
Fig. 1 Trochanteric abductors
versus iliotibial band tensioners
1109
2.2 Muscle Factors and Interaction with Joint
Position
The abductor mechanism of the hip involves two muscle
synergies: (1) the trochanteric abductor muscles (GMed
and GMin); and (2) the ITB-tensing muscles or ITBten-
sioners [the upper abducting portion of the gluteus max-
imus (UGM), tensor fascia lata (TFL) and vastus lateralis
(VL)] [26, 32–34] (Fig. 1). Kummer [35] calculated the
potential for trochanteric abductor muscles to provide
70 % of the abductor force required for pelvic control in a
single-leg stance, with the remaining 30 % provided by the
ITB-tensing muscles. The TFL has been shown to hyper-
trophy [36] and GMed and GMin atrophy [18] in those with
gluteal tendon pathology. The latter study assessed patients
following total hip arthroplasty (THA) with and without
trochanteric pain. In this series, abductor tendon defects
and fatty atrophy of the GMed muscle and the posterior
part of the GMin muscle were uncommon in asymptomatic
patients but common in patients with trochanteric pain—
both groups having had hip osteoarthritis and subsequent
THA—suggesting that it was the tendon pathology rather
than the joint issues that held a closer association with this
pattern of muscle atrophy. In another study of patients with
lateral hip pain and without THA, where the most common
pathology seen on magnetic resonance imaging (MRI) was
gluteal tendon pathology with or without bursitis, 40 % had
visibly evident fatty atrophy of GMed and/or GMin. Fatty
atrophy of the gluteus maximus was very uncommon,
evident in only one subject. This pattern of imbalance in
the relative proportions of the trochanteric abductors and
ITB tensioners could feasibly alter the relative contribution
123
1110
of these muscle groups in controlling frontal-plane motion
or postures. Although it is unclear whether these changes
precede or result from tendinopathy, it is tempting to
speculate that the predominant activity of ITB tensioner
muscles could impose greater trochanteric compression in
hip adduction.
We propose that a combination of a hip-adducted po-
sition and ITB tensioner muscle activity contribute to the
compression of the tendons of GMed and GMin. A com-
mon clinical observation is that in single-leg standing ac-
tivities, patients adopt a greater hip-adducted position. The
ITB is passively pre-tensioned when the hip is in adduc-
tion, which provides a mechanical advantage for the ITB
tensioners and may provide the basis for an enhanced
contribution to control in the frontal plane. Compressive
loads on the gluteal tendons in passive hip adduction would
then be amplified by added active tensioning by the ITB
tensioner muscles. Detailed biomechanical analysis is re-
quired to test this proposed interaction between muscle
activation and joint position on the tendons of GMed and
GMin in individuals with lateral hip pain.
2.3 Bone Factors and Interaction with Joint Position
Bone morphology influences compressive forces imparted
at the hip by the ITB. Using both cadaveric investigations
and biomechanical modelling, Birnbaum et al. [26, 37]
assessed the effect of alteration of the angle of the femoral
neck from a typical physiological angle of 128° and
showed increased compressive forces as the neck angle
reduced. With a typical femoral neck angle of 128°, the
ITB exerted a compressive force of 656 N at the greater
trochanter, but at 115° (coxa vara), the compressive force
was 997 N [37] (Fig. 2). This concurs with findings that
patients with more severe gluteal tendon pathology have
Fig. 2 Femoral neck angles and
compressive loads at the greater
trochanter. Lower neck angles
(coxa vara) result in higher
compressive forces than normal
neck angles (the numeric values
come from Birnbaum and
Pandorf [92]). N newtons
123
A. Grimaldi et al.
lower femoral neck–shaft angles than pain-free controls or
those with hip osteoarthritis [38].
Viradia et al. [39] recently demonstrated that the dif-
ference between the width of the iliac wings and that of the
greater trochanters (offset) was greater in individuals with
lateral hip pain (mean difference 28 mm) than in a pain-
free control population (mean difference 17 mm). It is
tempting to speculate that the neck–shaft angle would
contribute to this offset, as those with smaller neck–shaft
angles are more likely to have a greater relative width
between trochanters. Thus, in patients with lateral hip pain
who present with a tendency to adopt more adducted hip
joint postures in static and dynamic tasks, a greater
prominence or offset of the greater trochanters would likely
increase compression against the gluteal tendons from the
ITB.
3 Assessment
The differential diagnosis of lateral hip pain may be
challenging because of the possibility of referral from
sources other than the local soft tissues of the greater tro-
chanter—most commonly, the lumbar spine and hip joint
[40, 41]. This section focuses on the key presentation
features, clinical diagnostic tests and radiological investi-
gations that indicate the presence of a local pain source,
primarily gluteal tendinopathy. Clinical tests of underlying
mechanisms are also discussed.
3.1 Key Presentation Features
The most salient feature of the presentation of gluteal
tendinopathy is pain and tenderness primarily at the greater
trochanter [13, 42–44]. There may be some radiation
Gluteal Tendinopathy
around the trochanter and often down the lateral thigh [42,
44]. The onset of pain is frequently insidious, tends to
worsen over time and is sometimes associated with chan-
ges in training load or physical activity [42, 43], though it
can occur acutely after a strong contraction of the abductor
musculature, such as that occurring during a slip or fall or a
forceful sporting action, such as a sidestep.
The impact of this condition can be debilitating, as it
typically disturbs sleep and limits performance of com-
mon functional tasks. Pain is often worst at night—those
affected having difficulty sleeping on their side [14]. This
can have a substantial negative influence on sleep quality.
Other problem functions include single-leg loading tasks,
such as walking, standing on one leg to dress, and
climbing stairs and hills [38, 42]. Patients with gluteal
tendinopathy also frequently report lateral hip pain and
stiffness on extending the hip on rising to stand or
walking after sitting [42]. Pain on extending the hip
during these tasks is also common in hip osteoarthritis,
but a key feature that differentiates these pathologies is
that those with hip osteoarthritis have difficulty with
manipulating shoes and socks, whereas those with
tendinopathy do not [41].
3.2 Clinical Diagnostic Tests
A recent meta-analysis of the diagnostic accuracy of clin-
ical hip tests found only three studies of gluteal
tendinopathy of adequate quality [13, 44, 45] and reported
that the tests generally possessed weak diagnostic proper-
ties [46]. Details of the most common or useful tests em-
ployed and their clinicometric properties are reported in
Table 2. Data from Fearon et al. [38] have also been in-
cluded, as their study compared participants with two dif-
ferent symptomatic hip pathologies—greater trochanteric
pain syndrome and hip osteoarthritis. This information may
be useful in the differential diagnosis of lateral hip pain.
Tests include those involving active abductor muscle
contraction—hip abduction and internal rotation, Ober’s
test, single-leg stance assessment, flexion/abduction/exter-
nal rotation (FABER) and palpation. These diagnostic tests
generally impart either a tensile or compressive load—or a
combination of both—across the gluteal tendons. Isometric
hip abduction reported by Woodley et al. [44] and Bird
et al. [13] was performed in both cases in the inner range of
abduction, thereby generating an active tensile load along
the tendon but in the absence of a compressive load in the
abducted hip position. While Woodley et al. [44] found that
weakness on this test was useful in predicting gluteal ten-
don pathology on MRI, assessment of pain reproduction
was less useful in predicting a tendon tear [13]. Using the
principles discussed in Sect. 2.2, adding compression to the
gluteal tendons could potentially enhance pain provocation.
1111
Assessing active abduction in a position of hip adduction
may be more useful.
Active contraction of the GMed and GMin muscles,
which produces tensile loading of their tendons, has also
been assessed via the secondary internal rotation function
of these muscles, all portions internally rotating in higher
ranges of hip flexion [47]. Three studies assessed different
test variations (Table 2) [13, 44, 45], with the most useful
diagnostic properties being reported by Lequesne et al.
[45], who tested resisted hip internal rotation at 90° hip
flexion and maximal external rotation. While no scientific
data are available to confirm the compressive effects of the
ITB on the gluteal tendons in positions of hip flexion and
external rotation, as discussed in Sect. 2.1, the strong
connections of the ITB with the gluteal and thoracodorsal
fascia may impose relatively more compressive load in the
position selected by Lequesne et al. Furthermore, as in-
ternal rotators at 90°of hip flexion, the musculo-tendinous
units of GMed and GMin will be on relative stretch at end-
of-range external rotation, potentially influencing the
provocative value of the test [45, 46]. Cook and Purdam
[21] have also suggested that outer-range positions may
expose a tendon to higher levels of compressive load.
Accordingly, the diagnostic utility of this test may be
further enhanced by the addition of end-of-range passive
hip adduction, maximizing tendon compression.
Ober’s test places the hip in end range passive hip ad-
duction, so while compressive load is imparted, the test is
missing an active tension component, which may explain
its reportedly limited diagnostic utility [41, 44]. On the
basis of the foregoing pathomechanical considerations,
diagnostic tests are more likely to be maximally provoca-
tive of symptoms if they apply both active tensile and
compressive loads simultaneously to the GMed and GMin
tendons.
The sustained single-leg stance test should, in most
cases, provide such a scenario, designed as a pain provo-
cation test [45] rather than a test of muscle function [13,
44] or balance [41]. Unlike the Hardcastle and Nade ver-
sion [48] of the Trendelenburg test used by Woodley et al.
[44], the patient is not instructed to try to hitch the pelvis
into relative hip abduction, a position of relatively less
compressive tendon load. A compensatory trunk lateral
shift is not allowed, resulting necessarily in a position of
hip adduction even in the normal population [49], more so
if the abductors are weak and fatigable. This position of hip
adduction and subsequent exposure of the gluteal tendons
to increased compressive load may be the important ele-
ment that results in pain reproduction over the greater
trochanter—a positive test result. Performed in this man-
ner, the test returned excellent sensitivity and specificity as
a diagnostic test for gluteal tendinopathy [45]. The tradi-
tional Trendelenburg test was reasonably useful in
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Table 2 Methods and clinicometric properties of clinical tests used for diagnosis of gluteal tendinopathy or greater trochanteric pain syndrome
Clinical test Method Positive test result Clinicometric properties
Sensitivity Specificity Likelihood ratio
(%) (%)
Positive Negative

Isometric hip abduction

Woodley et al. [44]a Sidelying, inner-range isometric Reduced abductor strength 80 71 2.8 0.28
abduction
Bird et al. [13]b Supine, 45° hip abduction Pain reproduction at lateral hip 72.7 46.2
Active hip internal rotation
Woodley et al. [44] Sitting, 90° flexion, through range Pain reproduction at lateral hip 31 86 2.15 0.81
active internal rotation
Bird et al. [13] Supine, 45° flexion, isometric Pain reproduction at lateral hip 72.7 46.2
internal rotation at end-of-range
external rotation
Lequesne et al. [45]c Supine, 90° flexion, resisted Pain reproduction at lateral hip 88 97.3
through range from end-of-range
external rotation
Ober’s test
Woodley et al. [44] Sidelying, 0° hip flexion, Restricted range and/or pain Values not reported, not considered useful
90° knee flexion, adduct hip to reproduction at lateral hip
end of range
Fearon et al. [41] Sidelying, 0° hip flexion, Restricted range and pain 41 95 0.94 0.45
90° knee flexion, adduct hip to reproduction at lateral hip
end of range
Single-leg stance
Woodley et al. [44] In single-leg stance, elevate non- Failure to elevate pelvis and/or 23 94 3.64 0.82
weight-bearing side of pelvis and maintain for 30 s
maintain for 30 s; light upper
limb support provided on stance
side by examiner as required
Fearon et al. [41] Balance in single-leg stance for up Duration of single-leg stance Not reported—useful for differentiating
to 30 s with no upper limb timedand compared between controls from those with GTPS but not
support groups useful in differentiating GTPS from hip
osteoarthritis
Bird et al. [13] Visual assessment of pelvic tilt in Positive if pelvic tilt regarded 72.7 76.9
single-leg stance and gait as abnormal by the examiner
Lequesne et al. [45] Single-leg stance maintained for Pain reproduction at lateral hip 100 97.3
30 s, avoiding lateral trunk
displacement and allowing
gentle fingertip support for
balance
Hip FABER
Fearon et al. [41]d Lateral malleolus of test leg is Pain reproduction at lateral hip 82.9 90 0.94 0.72
placed above patella of opposite
leg, pelvis is stabilized via
opposite anterior superior iliac
spine and flexed hip is passively
lowered into abduction and
external rotation
FABER flexion/abduction/external rotation, GTPS greater trochanteric pain syndrome, MRI magnetic resonance imaging
a
Results reflect the usefulness of clinical diagnostic tests in predicting symptomatic gluteal tendon pathology, evident on MRI
b
Results reflect the usefulness of clinical diagnostic tests in predicting the presence of gluteus medius tendinopathy plus a tear on MRI
c
Results reflect the usefulness of clinical diagnostic tests in predicting the presence of local T2 uptake at the greater trochanter on MRI,
interpreted as gluteus medius tendinopathy and/or bursitis, with or without a tendon tear
d
Results reflect the ability of clinical tests to differentiate clinically diagnosed greater trochanteric pain syndrome from advanced hip
osteoarthritis

123
Gluteal Tendinopathy
detection of partial and complete abductor tendon tears
[13]; however, evidence for its applicability as a diagnostic
test at earlier stages of pathology is weak. While further
research with more robust methodology is required, the
sustained single-leg stance test as performed by Lequesne
et al. [45], rather than the Trendelenburg test, is recom-
mended for diagnostic purposes in clinical practice.
The Patrick-FABER test has also been cited historically
as a diagnostic test for trochanteric bursitis and
tendinopathy [50–52]. Although Woodley et al. [44] re-
cently reported that this test was not useful for diagnosis
of pathology at the lateral hip, Fearon et al. [41] selected
this test from amongst others as a key criterion for dif-
ferentiating pathology at the lateral hip from pathology of
the hip joint. The difference may lie in the definition of a
positive test. Woodley et al. [44] considered the test
positive if it reproduced the lateral hip pain or if it was
not possible to move the knee to a position level with the
contralateral thigh. Limitation of range of motion on the
FABER test has not been demonstrated for those with
gluteal tendinopathy but may be limited in those with a
joint-based pathology [53]. Fearon et al. [41] found that
when participants reported pain reproduction at the greater
trochanter on the FABER test, in the absence of difficulty
manipulating shoes and socks (which will be difficult if
limited in FABER), this formed a strong basis for diag-
nosis of greater trochanteric pain syndrome, together with
pain on palpation of the greater trochanter. Taken to-
gether, these data imply that soft tissue pathology of the
greater trochanter is likely to be present when the FABER
test is not limited in terms of range of motion but re-
produces the patient’s lateral hip pain. If motion is lim-
ited, then hip joint–based pathology cannot be excluded.
This holds promise as a tool for differential diagnosis and
is worthy of further study.
Pain on palpation (direct compression) of the soft tissues
overlying the greater trochanter is generally regarded as the
most important sign in the diagnosis of gluteal tendinopa-
thy (±bursal distention). There is widespread agreement
that this is a cardinal sign for the diagnosis of lateral hip
tendinous or bursal pathology [13, 41, 44, 45, 51, 54]. An
absence of tenderness on palpation of the greater trochanter
would raise suspicion that the source of the pain may be
distant to the trochanter, and would warrant a search for an
alternative diagnosis.
The lack of consensus regarding which tests possess
greatest diagnostic utility means that clinical practice in-
volves a battery of tests. Further research is required to
ascertain which combination of tests is likely to provide the
most accurate interpretation of a patient’s presentation. The
underlying pathomechanics related to compression and
tensile loading warrants consideration for selection of the
tests for this clinical battery, and further research that
1113
implements and assesses test modifications may provide a
more useful test battery.
3.3 Tests of Underlying Mechanisms
Although a definitive diagnosis is always desirable as an
assessment priority, identification of potential mechanisms
underlying the presenting problem provides important di-
rection for management. A tendon’s ability to tolerate load
has been suggested as a key factor both in its symptoma-
tology and for determination of appropriate treatment [55].
Cook and Purdam [55] recommend functional loading tests
to assess and monitor a tendon’s response to management
over time. For the gluteal tendons, these authors suggest
standing on one leg as a low-load test and hopping as a
high-load test. Reduced pain on subsequent testing is
thought to reflect improved load tolerance by the tendon.
Improvement after a period of rehabilitation could be
identified as either reduced pain on a specified number of
hops or a greater number of hops before the onset of pain.
Assessment of the quality of functional movement tests
may also highlight potentially negative loading strategies.
Poor lateral pelvic control in single-leg loading tests (sin-
gle-leg stance, single-leg squat, step-up, hop) induces
greater hip adduction and higher compressive loads of the
gluteal tendons beneath the ITB. Inadequate ability to ec-
centrically control hip adduction on landing during walk-
ing, running or hopping produces the provocative
combination of a higher tensile load (active lengthening at
speed), with a high compressive force (adduction). As
appropriate for the athlete, video analysis of running and
change of direction is recommended to assess pelvic tilt
and femoral adduction. The running cadence and stride
length will also influence frontal-plane hip and pelvic
mechanics. A slower cadence and longer stride length have
been associated with greater peak hip adduction and higher
energy absorption and generation around the hip during the
stance phase of running [56]. Greater ranges of lateral
pelvic tilt have also been associated with a less efficient
cutting manoeuvre, where more time is required to perform
the task, therefore exposing the gluteal tendons to longer
durations of eccentric loading [57]. Assessment and
monitoring of improvements in abductor control may guide
appropriate exercise prescription and readiness for return to
activity. A detailed description of assessment of hip ab-
ductor muscles has previously been presented by Grimaldi
[32].
A static measure of hip girth at the level of the greater
trochanters might have clinical utility as a simple surrogate
measure of the neck–shaft angle (i.e. the larger the girth,
the more likely the neck–shaft angle will be smaller) [38]
or as a measure of gynoid (peripheral) adiposity, which has
been shown to be associated with Achilles tendinopathy
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[58] or a combination of both bone and metabolic factors.
Fearon et al. [38] showed that participants with lateral hip
pain had a larger girth at the greater trochanters
(104–106 cm) than pain-free individuals (mean 99 cm) and
those with hip osteoarthritis (mean 100 cm). Although
bone factors that contribute to gluteal tendinopathy are
unmodifiable, weight loss should be considered as a strat-
egy in the management of tendinopathy. Further research
with larger sample sizes is required to identify optimal
girth dimensions.
3.4 Radiological Investigations
Early imaging may be required following acute trauma
and/or a marked loss of function. It may be necessary to
exclude bony or significant soft tissue injury that could
require surgical intervention. Imaging of the hip and lum-
bar spine may also assist if the differential diagnosis is
unclear. Caution is required, as tendon and lumbar
pathology often coexist and occur frequently in the
asymptomatic population [59, 60]. To be relevant, findings
on imaging should correlate with clinical features.
Ultrasound and MRI are the predominant investigations
for lateral hip pain. Ultrasound is usually offered first,
because of cost and availability. Greyscale ultrasound is
less sensitive than MRI for detection of gluteal tendon
pathology, but this might reflect operator experience and
other patient characteristics (e.g. body fat [61]). The sen-
sitivity of greyscale ultrasound to surgically confirmed
GMed tendon tears has been reported as being as low as
61 %, and the diagnostic utility for GMin tears remains to
be elucidated [15]. Distention of the bursa is readily evi-
dent on ultrasound [15], and ultrasound is superior to MRI
with respect to imaging calcifications within the tendon
[17]. Greyscale ultrasound is less sensitive to minor
changes in tendon structure, as a consequence of limita-
tions in the resolution of greyscale imaging [62]. Several
new techniques, such as ultrasound tissue characterization
(UTC) [62] and elastography [63], potentially offer greater
detail regarding assessment of tendon structure. These new
technologies are not widely available in clinical practice,
and further research is required to establish their clinical
utility.
MRI is considered the gold standard for assessment of
gluteal tendons [13, 17, 44, 64, 65], though it is more ex-
pensive and less available than ultrasound. Short echo time
(STE) and ultrashort echo time (UTE) techniques, with or
without the use of intravenous gadolinium, provide supe-
rior enhancement of signal changes and detection of tendon
pathology [66]. MRI has the advantage of allowing
assessment of both direct signs of gluteal tendinopathy—
such as soft tissue oedema, tendon thickening, intrasub-
stance signal abnormality and focal discontinuity or
123
A. Grimaldi et al.
absence of tendon fibres—and associated indirect signs,
including fatty atrophy of the GMed and GMin muscles
[17]. Other causes of lateral hip pain within the pelvis can
also be excluded.
4 Management
Evidence regarding the best management of gluteal
tendinopathy remains elusive. A recent review [9] could
not draw definitive conclusions, because of limited avail-
ability of studies of adequate quality. Many of the proposed
treatment modalities are yet to be tested in randomized
clinical trials. Management techniques include exercise
and strategies to manage tendon load, shock wave therapy
(SWT), corticosteroid injection and surgical interventions.
4.1 Exercise and Strategies to Manage Tendon Load
Cook and Purdam [67] recently proposed that effective
non-surgical management of tendinopathies requires a
specific approach underpinned by management of tendon
load and exercise. Mechanical stimulation induced by ex-
ercise is thought to induce beneficial biochemical processes
within tendon tissue [68]. No randomized clinical trial has
assessed the benefits of approaches that consider manage-
ment of tendon load, and only one clinical trial, which was
not randomized, has studied an exercise programme for
gluteal tendinopathy [54]. In that study, the 12-week ex-
ercise programme included piriformis stretches, ITB
stretches and sagittal plane strengthening, such as straight
leg raises, wall squats, and prone hip extension. Although
there was an 80 % positive response at 15 months, only
7 % of subjects had improved after 4 weeks and 40 % after
4 months. As the benefits of a 12-week exercise pro-
gramme would be expected to be evident by 4 months, this
implies that the intervention was largely unhelpful. This
poor response might be explained by the absence of pre-
scribed management of overall loading at the hip tendons
via advice and education, inclusion of exercises that would
be likely to compress the tendon early in rehabilitation (e.g.
piriformis and ITB stretches), and omission of any frontal-
plane abductor muscle strengthening. In summary, this
programme appears to have paid inadequate attention to the
pathomechanics of the condition in selection of the exer-
cises, particularly for early rehabilitation. Further research
is required for better understanding of the role of exercise
in gluteal tendinopathy, and for assessment of the effects of
a programme more targeted towards improving abductor
muscle function and frontal-plane femoro-pelvic control.
For athletes, controlling tendon load will be a central
tenet of management of gluteal tendinopathy. While com-
plete rest is catabolic for tendons, avoiding rapid changes
Gluteal Tendinopathy
in loading/training and reducing activities involving
provocative combinations of compression and high tensile
load are recommended [67]. This may involve restriction of
longer-distance and higher-speed running and other ac-
tivities involving high eccentric abductor loads, such as
hopping and bounding. Modifications of running technique
might also be required. Reductions in peak hip adduction in
running can be successfully altered with visual biofeedback
[69] and increases in cadence [70]. Increasing cadence by
10 % has also been shown to result in increased activity of
GMed during the late swing phase but not during the stance
phase [71]. This enhanced pre-activation may explain the
subsequent improvement in lateral pelvic control, without
requiring more work from the muscle during the stance
phase [71]. Other tasks specific to the athlete that may
place the gluteal tendons under high tensile load in posi-
tions of hip adduction should also be assessed and modified
where possible. Stretching exercises for lower limb inser-
tional tendinopathies are not recommended [67]. It would
also seem prudent to avoid hip flexion/adduction stretches
(e.g.ITB and gluteal stretches), as these place compressive
and tensile loads on the gluteal tendon insertions.
4.2 Shock Wave Therapy
Radial SWT has been proposed as an alternative treatment
approach for gluteal tendinopathy, with effects explained
by a mechanobiological mechanism [3, 54]. Radial SWT
produces shock waves that can penetrate soft tissues to a
depth of up to 40 mm [72]. This technology is reported to
have both analgesic and healing effects on painful tendons,
although most research has involved animal or in vitro
preparations, and was on ‘‘focused’’ rather than ‘‘radial’’
SWT [72]. The aforementioned non-randomized trial of
exercise for gluteal pain also included a group that received
radial SWT (weekly sessions for 3 weeks) [54]. Although
the response was poor at 4 weeks (a 13 % positive re-
sponse), the outcomes at 4 months were superior to those
achieved with exercise (a 68 % positive response versus a
41 % positive response) [54]. Without randomization or a
control group, it is unclear whether the SWT group fared
best, because they were not exposed to the potentially
negative effects of stretching (tendon compression) [55,
67] or the anticipated medium-term recurrences experi-
enced after corticosteroid injection. Another non-random-
ized clinical trial also showed favourable outcomes of
SWT, relative to a control group who underwent other
forms of non-operative therapy [3], but the details of the
control intervention were unclear, and it is not clear whe-
ther this group was provided with the same exercise pro-
gramme as was used in the earlier study [54]. Although
SWT might be effective for management of gluteal
tendinopathy, high-quality trials are required to test its
1115
efficacy, and cost and availability may also limit its clinical
applicability. Another issue that has been discussed is the
potential for greater gynoid adiposity to reduce the effec-
tiveness of SWT. Measurements of subcutaneous fat
thickness (e.g. with ultrasound imaging) are required to test
this. If adiposity reduces the mechanical effect of SWT,
then any effect of this treatment is likely to be a more
central effect via neurobiological mechanisms.
4.3 Corticosteroid Injection
A review of treatment of gluteal tendinopathy noted that in
surgical studies in which the numbers of pre-operative
corticosteroid injections were recorded, all patients had
received at least one corticosteroid injection, but the ma-
jority had received between two and four injections, and
one study reported patients who had received over 20 in-
jections [73]. Corticosteroid injection provides a substan-
tial early reduction in pain for those with GMed
tendinopathy, with a 72–75 % positive response at 4 weeks
[4, 52]. As patients and their medical practitioners aim to
achieve early pain relief, it is not surprising that corticos-
teroid injections are commonly recommended [4, 54, 74].
However, corticosteroid injection does not completely al-
leviate the pain (average pain reduction 55 % [4]), and
medium- and longer-term responses are much lower than
its initial effects. Positive responses drop to 41–55 % at
3–4 months [1, 2, 54], and after 12 months, Brinks et al.
[1] showed no difference in outcomes between subjects
receiving corticosteroid injection and those receiving usual
care (analgesics as required). This pattern of poorer out-
comes in the longer term, with high rates of recurrence, has
been shown for other insertional tendinopathies, such as
tendinopathy of the lateral elbow [75, 76].
The mode of effect of corticosteroid injection for
treatment of tendinopathy, and the safety, particularly of
repeated use, remain unclear. Corticosteroid drugs are po-
tent anti-inflammatory medications. Yet substantial signs
of inflammation have been absent in the available
histopathological studies of gluteal tendinopathy [14, 15,
19]. Instead, most studies have reported degenerative
pathology of the gluteal tendons and bursae. This is con-
sistent with findings in other tendinopathies. Rather than an
effect via its anti-inflammatory properties, corticosteroid
injection has been suggested to provide an analgesic effect
related to its interaction with local neuropeptides and
neurotransmitters [75, 77], which have been proposed as
local drivers of painful tendinopathy [78]. Recurrence of
pain following corticosteroid injection may reflect the
failure of this intervention to address the underlying
pathology and the associated central mechanisms now
thought to be important co-drivers of longer-term tendon
pain [78–80]. Corticosteroid injection might even hinder
123
1116
tendon capacity to respond appropriately to loading via
down-regulation of fibroblastic production of collagen [75,
77].
4.4 Surgical Interventions
For those with gluteal tendinopathy who have failed
pharmacological intervention and conservative rehabilita-
tion, surgical intervention is considered. The surgical lit-
erature can be divided into surgical repair of tendon tears
and surgical solutions for other refractory lateral hip pain.
The evidence for outcomes of surgical repair of gluteal
tendon tears is limited to case reports, which provide only
weak evidence. Patients who have failed conservative re-
habilitation, have significant abductor muscle weakness
and have a muscle tear identified on MRI are generally
reported to do well in the 1- to 2-year follow-up period
following surgery [15, 81–85]. But, in the absence of a
control group, it is unclear whether this is better than the
natural course. The largest case series reported that 90 % of
72 patients who underwent repair of the GMed tendon were
painfree or had minimal pain 12 months after surgery, and
the percentage of patients who considered their walking
ability to be ‘‘normal’’ increased from 5 to 78 % [84]. The
longest period of follow-up after open tendon repair has
been 5 years, after which 16 of 19 patients maintained
significant improvements gained in the first 12 months, as
measured by the Harris Hip Score and Lower Extremity
Activity Scale. Gluteal tendon repairs can now be per-
formed endoscopically [81, 83, 86], which is less invasive
and is associated with reduced post-operative infection,
scarring and pain, and more accelerated rehabilitation [86].
Endoscopic techniques, however, require greater surgical
skill and are generally unsuitable for larger tears or tendon
detachments where there is retraction of the muscle and
greater visualization is required [83]. Endoscopic repairs
have returned good to excellent results in the limited case
series available [81, 83], but no randomized clinical trials
have compared outcomes of open and endoscopic tech-
niques. Walsh et al. [84] detailed complications in their
case series of 72 patients, with a complication rate of 19 %,
most commonly involving deep vein thrombosis, tendon
re-tear and wound haematoma, plus single episodes each of
pulmonary emboli, pressure sores, wound infection and a
fracture of the greater trochanter.
Surgical interventions have also been performed in pa-
tients without gluteal tears, with the main aim being to
remove the trochanteric bursa and usually release the ITB.
This surgery is performed either as an open or an arthro-
scopic procedure, and the technique of ITB release varies
from proximal Z-plasty to proximal longitudinal release,
T-section and distal Z-plasty [73, 87–91]. There are no data
on the comparative efficacy of these procedures, and all
123
A. Grimaldi et al.
studies (case series) have reported good to excellent short-
to medium-term outcomes. The rationale and mechanism
for the efficacy of these surgical techniques remain unclear.
Conceivably, pain relief could be afforded by removal of
an inflamed bursa, but this would not likely address any
underlying tendinopathy-related symptoms or pathome-
chanics. The rationale for ITB release has generally been
based on the premise that the condition presents with re-
duced length of the ITB and surgical lengthening of the
structure would reduce pressure/friction on the underlying
soft tissue structures. However, no study has demonstrated
that this population has a limited hip adduction range of
motion or ITB tightness. It is equally plausible that the
compression beneath the ITB is secondary to excessive use
of the hip in an adducted position during function in as-
sociation with a lengthened and dysfunctional hip abductor
muscle mechanism—in which case, although surgical re-
lease of the ITB would provide relief of symptoms through
some immediate reduction in compression of the underly-
ing tissues, some of the following concerns would remain.
First, the technique does not resolve the issue of poor
control by the hip abductor muscles. Second, excessive
resection of the ITB may result in herniation of the un-
derlying soft tissue and painful external snapping [81].
Third, it could also have a deleterious effect on abductor
muscle function as a result of reduced potential for the
gluteus maximus and TFL to control the hip via their at-
tachments to the ITB [86]. Fourth, because of compromise
of one of the pelvic postural control structures, the patient
may resort to trunk lateral flexion to control the motion of
the pelvis relative to the hip. This could increase stress on
the hip, pelvis and lumbar spine, which could conceivably
predispose to other problems. Fifth, there is limited detail
of post-operative rehabilitation in the surgical literature,
which makes it difficult to establish whether the presently
reported outcomes are explained only by the surgical in-
tervention and the associated period of convalescence, or
this combined withanypost-operative rehabilitation
programme.
5 Conclusion
Gluteal tendinopathy is common in both sedentary and
athletic adults, particularly females aged over 40 years.
The evidence for the best management is poor, and the
underlying mechanisms of the condition are only beginning
to be understood. Compression and stress shielding of the
deep fibres of the gluteal tendons in hip adduction are
likely to be central to the development of tendon degen-
eration. Interventions reported in the literature do little to
address potential underlying mechanisms. The primary aim
of existing treatments is to relieve pain via some form of
Gluteal Tendinopathy
pharmacological or physical manipulation of the local tis-
sues. High-quality trials are required to test the short- and
long-term efficacy and safety of current and emerging
methods of management. Clarification of underlying
mechanisms may guide development of more robust
management strategies.
Acknowledgments This paper is a review only and does not contain
individual patient data or clinical studies. None of the authors has any
conflict of interest nor any financial relationships with any sponsoring
organization.
Kim Bennell and Paul Hodges are supported by National Health
and Medical Research Council Fellowships (#1058440 and #1002190,
respectively).
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