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INTERNATIONAL JOURNAL OF ATHLETIC THERAPY & TRAINING MAY 2017 1
© 2017 Human Kinetics - IJATT 22(3), pp. 1-11
https://doi.org/10.1123/ijatt.2016-0075
CLINICAL COMMENTARY
or many practitioners in the field of sports
medicine, the specific paradigm for insidi-
ous onset, chronic lateral knee pain in run-
ners, cyclists, and rowers has contained the
idea that the iliotibial band (ITB) “moves
over and back of the lateral femoral epicondyle” with
repeated flexion and extension movements of the
knee. Further, it has long been accepted that this bio-
mechanically induced and anatomically based “fric-
tional” force aggravates a subtendinous bursa that sep-
arates the bony prominence from the undersurface of
the tendinous aspect of the ITB, causing localized and
debilitating pain from an inflamed bursa, an inflamed
ITB, or both with chronic knee motion. Many clinicians
know this pathoetiological model as “iliotibial band
friction syndrome”, a nebulous but widely accepted
clinical overuse syndrome first learned in formal edu-
cation and thought to occur more commonly in running
athletes with “tight IT Bands” because of mechanical
“slipping” in the band itself. As a result, ITB friction syn-
drome has long been treated with stretching of the ITB
and deep tissue massage to the irritated aspects of the
tissue itself, in an attempt to loosen the tight tissue and
thus relieve the pain and discomfort. As foundational
knowledge of anatomy, physiology, and biomechanics
has advanced in recent years, the current evidence sup-
ports the approach that stretching and massage to the
ITB is, in the least, ineffective at decreasing symptoms
but rather most likely to exacerbate the problem.1 Poor
treatment outcomes are perhaps just one indication
that our axiomatic conception of the pathoetiology of
the syndrome is inaccurate, and thus it is time for a
new evidence-informed paradigm for assessing and
treating this overuse injury.
Paul R. Geisler, EdD, ATC, and Todd Lazenby, MA, ATC • Ithaca College
Iliotibial Band Impingement Syndrome:
An Evidence-Informed Clinical Paradigm Change
Clinical practice in sports medicine is often guided by axioms or paradigms of practice, some of which have
persisted over time despite a lack of objective evidence to support their validity. Evidence-based practice
compels practicing clinicians to not only seek out and produce evidence that informs their decision-making,
but also to challenge existing paradigms of thought and practice, especially when favorable treatment out-
comes remain elusive. Insidious, load induced lateral knee pain around the iliotibial band in runners, cyclists,
military personnel, rowers, and other athletes has for decades now been conceptualized as iliotibial band
friction syndrome, a biomechanically based and unsubstantiated paradigm based on Renne’s 1975 theory
that the iliotibial band slips back and forth over the lateral femoral epicondyle during flexion and extension
movements of the knee, primarily irritating the underlying bursa and even the iliotibial band itself. Newer
evidence about the anatomy and biomechanics of the iliotibial band, the physiology of the condition, and
interventional outcomes is now available to challenge that long-held paradigm of thought for iliotibial band
related pathology. Given this plethora of new information available for clinical scientists, iliotibial band
impingement syndrome is proposed here as a new, evidence-informed paradigm for evaluating and treating
this problematic overuse syndrome.
F
2 MAY 2017 INTERNATIONAL JOURNAL OF ATHLETIC THERAPY & TRAINING
A Common Problem for Repetitive
Flexion-Extension Athletes
Epidemiologically, ITB-related pain and discomfort
occurs primarily in active persons, with approximately
12% of all runners being affected.2 Though ITB friction
syndrome (ITBFS) is widely reported as the “most
common cause of lateral knee pain in athletes”, its
frequency is varied in both distribution and popula-
tion, with a reported overall incidence range between
1.6% and 52%.3 Orava found ITBFS as the primary
culprit of pain in 6.4% of every 1,000 athletes across
various sports, while Linenger stated it comprised 22%
of all lower extremity injuries,4,5 yet Fredericson and
Wolf reported it accounted for only 12% of all overuse
running injuries.2 Many additional ITBFS studies have
been published focusing on specific populations, as
Renne first reported 1–5% of all military recruits suffer
from the condition and Noble reported that 52% of
long-distance runners presenting with insidious knee
pain had ITBFS.6,7 Devan and his group noted ITBFS to
be the most common lower extremity overuse injury
in female soccer, basketball, and field hockey athletes,
while Holmes et al. reported a 24% occurrence in
road cyclists, and Rumball et al. documented it as a
very common ailment for competitive rowers.8–10 In
addition, recreational exercisers are not immune to
ITB-related lateral knee pain as it has been reported
to be problematic in 15% and 7% of adult women
and men, respectively, who perform general exercise.11
The Current Paradigm
of Practice and Thought
As we have been so often taught, the key to under-
standing complex and troublesome musculoskeletal
syndromes is to first have a solid understanding of
the relevant pillar knowledge that contributes to the
phenomenon at hand—the anatomy, physiology, and
biomechanics of the body part, joint, or system under
investigation. When knowledge of anatomy, physiol-
ogy, and biomechanics is well established and under-
stood, this clinical science and reasoned approach
to problem solving is typically straight forward and
follows a general set of somewhat predictable rules
that make comprehension productive and interven-
tion effective. However, when proper evidence or
knowledge is lacking, particularly in the domains of
anatomy, physiology, and biomechanics, the challenges
presented to the clinician are magnified because of the
increased complexities associated with understanding
the pathophysiological underpinnings of the matter, and
patient outcomes remain bothersome due, at least in
part, because the working paradigm guiding clinical
practice is incomplete or inaccurate. The anatomy and
function of the ITB or iliotibial tract (ITT) exists in some-
what of a “gray zone” for many clinicians, partially
because of what many of us were formally taught, due
to what was actually known for many years about this
long, tough tissue that has its own name. Our clinical
education and best practice of the time led us to assess
ITB tightness or dysfunction with the Ober’s test, and
then to treat any tightness with stretches and massage
techniques focused on lengthening the tissue. Based
on the current evidence, it has become clear that these
common practices should be reexamined and refined.
First, a Little History
Sixteenth century anatomist Vasalius first described
the tensor fascia lata as a tibial muscle, and given its
clear and palpable tibial insertion, this made sense
at the time.12 Gray’s Anatomy, the much revered text,
described the ITB in a rather pedestrian manner—a
structure “over the lateral femoral aspect (where) the
fascia lata is compacted into a strong iliotibial tract.”13,
p. 339 Kaplan concluded in 1958 that although all quad-
ruped animals have gluteus maximus muscles and
tensor fascia lata, only humans actually have an ITB
because of its developmentally and functionally critical
roles in stabilizing the lateral knee joint and assisting
with erect posture.14 More has been learned in the past
10–15 years in the area of fascial anatomy, histology,
neurophysiology, and force transmission dynamics
alone than in the previous millennia combined, as
recent advances in technology have dramatically
improved our ability to not only visualize living fascia
tissue, but also begin to better understand the function
and components of this constituent, three-dimensional
tension network. In addition, the establishment of the
International Fascia Research Congress has brought
clinicians, scientists, anatomists, and physicians from
a multitude of different disciplines together to share,
discuss, and disseminate their respective research and
clinical and anecdotal experiences in the exploration,
evaluation, and treatment of fascia tissue function
and dysfunction.15 This has led to a realization of the
importance of a greater scientific understanding of this
often ignored, dissected, and discarded tissue in the
overall purpose of the human form and function. As a
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result, our understanding of the anatomy, function, and
purpose of the ITT has increased substantially to the
point that what many of us were taught about the eti-
ology of ITB dysfunction can now be turned on its ear.
Today, many clinicians have generally come to
understand the basic details of the ITB, but perhaps
far too simplistically (see Table 1): that the ITB orig-
inates from the fascia of the tensor fascia lata (TFL)
and gluteus medius muscles and is anchored on the
iliac crest, anterior superior iliac spine, and the cap-
sule of the femoroacetabular joint and distally travels
down the lateral femur with broad insertions to the
linea aspera, is contiguous with fascial tissue that
envelopes the thigh, and has one pronounced and well
versed insertion at Gerdy’s tubercle on the lateral tibial
prominence.16 Indeed, this model is still taught today
in many professional programs and, further, properly
palpating Gerdy’s tubercle (because of its association
with the ITB) remains a key component of many oral
practical examinations at the professional level. In
relating anatomy to biomechanics (and thus, too, to
pathomechanics), it has largely been accepted that
because the ITB originates from two hip joint muscles
and inserts on Gerdy’s tubercle, it was simplistically
considered as a tendon (in that it provided distal
anchoring for the tensor fascia lata muscle), and that
it logically “worked” to transmit the muscular forces
and energy of the TFL and gluteus medius (in other
words, to assist with abduction of the hip, especially
in a flexed hip position).
To be sure, the ITB or ITT is a lot of things at once—
by name it connects the hip (“ilia”) to the lower leg
(tibial); by location it runs from the iliac crest, anterior
ilium, and anterior superior iliac spine to the linea
aspera and Gerdy’s tubercle on the tibia; by nature
and depending upon what portion one is referring to,
it is part fascial thickening, part ligament, and part
tendon; by architecture it receives most of the gluteus
maximus muscle fibers and all of the tensor fascia
lata muscle fibers; and by microscope it is a dense,
regular connective tissue composed almost exclusively
of regular collagen with a little bit of elastin content,
and is largely avascular. As with other tissues in the
body, fascia tissue demonstrates an enormous ability to
adapt to mechanical stress and, in particular, repetitive
demands. The ITB is a structural tissue that is not pres-
ent when we are born, but develops over time into a
dense, collagenous-rich fascia along the outside aspect
of the thigh in response to the stress demands placed
on the tissue during bipedal locomotion and functions
to provide stabilization of the hip when walking, run-
ning, and hopping.17 To point, the stiffness noted in the
ITB upon palpation in individuals that walk and/or run
regularly is absent in individuals who are sedentary or
wheelchair bound. To better illustrate the adaptability
of the fascial tissue, el-Labban and his group found the
opposite to be true in horseback riders as the fascia
along the medial aspect of the thigh has been found to
adapt to the stress load patterns associated with saddle
contact over time and therefore develop a thicker,
Table 1 Anatomical Components of Two Paradigms for ITB Pathology
ITB Paradigm Origin Insertion Action(s) or Implication
Old (What we
used to “know”)
Fascial union from TFL
and gluteus maximus
on the iliac crest and
ASIS
– Broad to linea aspera
– Gerdy’s tubercle on tibia
Transmit force of TFL muscle during hip
activity (abduction from a flexed position);
acts as “pelvic deltoid”, stabilizing to stance
stability and “swinging of the knee along
with the hip”; restrict excessive hip adduc-
tion (if tight)
New (What we
now “know”)
Fascial union from TFL
and gluteus maximus
on the iliac crest and
ASIS
– Broad to linea aspera
– Lateral femoral condyle
– Lateral femoral epicondyle
– Patella via lateral retinaculum
– Gerdy’s tubercle (3 layers):
superficial, deep, capsular
osseous
– Fibular head
Passive stability of the hip joint (via gluteus
maximus tensioning in the ITB) during
loading/deceleration in stance and mono-
podal gait; passively resists hip adduction
and internal rotation during loading/decel-
eration in stance; passively limit anterior
translation and internal rotation of the tibia
during loading/deceleration in stance
Abbreviations: ITB = iliotibial band; TFL = tensor fascia lata; ASIS = anterior superior iliac spine.
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more dense fascia traversing the medial aspect of the
thigh.18 Functionally, the ITB is also quite multifaceted
as it crosses two large ambulatory and weight bearing
joints, at times dependent upon position and motion,
working proximally to move the hip in manners con-
cordant with the function of the gluteus maximus
and tensor fascia lata. The ITB also works distally as a
tendon to anchor the aforementioned hip muscles and
even as a ligament to help stabilize the patellofemoral
and knee joints.19
The Origins of a Clinical Paradigm or Axiom
In 1975 and based off early understandings of anatomy
and biomechanics, Renne first described the idea of
ITBFS after noting a preponderance of insidious onset,
lateral knee pain conditions in a population of US
marines undergoing high-level physical training.6 At
that time, it was thought that the anatomical insertion
of the ITB was solely on the lateral tibial prominence
known as Gerdy’s tubercle, therefore Renne hypoth-
esized that the ITB would roll over the lateral femoral
epicondyle with repetitive flexion and extension
movements of the tibiofemoral joint. In full extension,
Renne reasoned the ITB would be “anterior of the
lateral epicondyle”, and once past 30 or so degrees
of flexion, the tendinous aspect of the band would be
positioned posterior to the bony femoral prominence.
With repetition, this movement or “slippage” would
presumably create friction on the undersurface of the
ITB and corresponding subtendinous bursa, creating
inflammation, pain, and degeneration along the supe-
rior lateral aspect of the affected knee joint.16
Just a few short years later, Noble published a pair
of papers that took up Renne’s clinical axiom and
extended the idea that ITB displacement or slippage
was responsible for producing the sharp and pro-
nounced pain at the site of the lateral femoral epicon-
dyle, even coining the now oft used “Noble’s Test” for
diagnostic purposes.7,20 According to Noble, increased
pain with manual compression at the lateral femoral
condyle (LFC) with the knee at 30° of flexion is diag-
nostic for ITBFS in runners “in all cases” and symptoms
are worse with downhill running, stating the source of
the pain was a wounded ITB and/or “bursal type tissue”
or “fascial tissue”, while the effective treatment simply
consisted of rest, addressing training errors, steroid
injections, and, in recalcitrant situations, corrective
surgery. To date there are dozens of papers that have
since taken up and extended Renne and Noble’s “fric-
tion syndrome” paradigm for lateral knee pain and, as
such, it has gradually become the axiomatic standard
for clinical practice despite the absence of compelling
evidence to support the original pathomechanical
underpinnings, anatomical foundations, or the various
interventional strategies employed.2,3,21–24
Our early and limited understandings of the anat-
omy and function of the ITB can now be appreciated as
the root sources of the false clinical axiom that many
have helped to promulgate, a paradigm of thought and
practice we commonly and habitually know as “ilio-
tibial band friction syndrome”. However, more recent
anatomical and biomechanical studies reveal that the
attachments and functions of the ITB are actually far
more complicated and multifactorial than originally
thought. Most importantly, and with profound implica-
tions for an evidence-informed clinical practice, these
new enlightenments shed a brighter light on the clinical
axiom surrounding ITBFS that has been carried forth
from our education and practice. Thankfully, this new
clinical science offers critical evidence and direction for
a new paradigm of thought concerning insidious onset
lateral knee pain in highly active and running-based
individuals.
Updating the Paradigm
In the mid-2000s, John Fairclough and colleagues
clearly attempted to alter the working paradigm for
ITB-related knee pain with the publication of two
papers on the topic. Experimentally, the UK-based
group put the ITBFS paradigm predicated upon a slip-
ping tissue and a painful subtendinous bursa to the test
with a thought provoking and multi-level study in the
Journal of Anatomy, and followed that up a year later
with an explanatory opinion piece in the Journal of
Science and Medicine in Sport.1,25 Using a combination
of gross anatomical dissection and histology studies
in cadaveric specimens and magnetic resonance
imaging (MRI) scans of healthy and “ITB syndrome”
positive subjects, Fairclough and colleagues put forth
the following claims about ITB anatomy, its function,
and its dysfunction: the ITB does not roll over the fem-
oral epicondyle because it is anchored firmly by the
fascia lata, rather an illusion of movement is created
because of changing tensions in the anterior and pos-
terior fibers of the ITB during flexion and extension,
and, respectively, there is no subtendinous bursa, but
rather a highly innervated fat pad deep to the ITB.25
Further, this study showed two distinct regions of
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the ITB that implicate a multifactorial function of the
tissue, a ‘tendinous’ part proximal to the lateral femoral
epicondyle and a ‘ligamentous’ portion between the
epicondyle and its insertion at Gerdy’s tubercle. The
authors explained the “movement illusion” further
based on a model of sequential “load shifting”. As the
knee flexes, the tendinous or fascial fibers of the ITB
that attach to the patella come under tension as the
patella tracks distally in the trochlear groove of the
femur while the more posterior ligamentous portions
become tensioned as knee flexion increases further. In
short, the various ITB fibers are progressively tensioned
from the anterior to the posterior during increasing
knee flexion and the many fibrous connections of the
ITB limit any significant movement in the area of the
lateral femoral condyle.1
At about the same time, a Brazilian group added
to the complexity with another anatomical dissection
study of the ITT in an attempt to better define its inser-
tional arrangements and its functional relationship with
other structures of the knee.26 Ten detailed dissections
by Vieira and his team26 revealed three specific distal
layers of the ITT (band) that led them to conclude that
not only does the ITB have critical connections to the
femur, the patella, and the lateral tibia, but that it plays
a pivotal role in patella-femoral stability. In addition,
its capsular-osseous layer is an important anterolateral
knee stabilizer that joins the anterior cruciate ligament
in a functional unit, forming a special “horseshoe”
system that helps prevent excessive tibial rotation and
anterior displacement.
Further complicating the issue are at least three
other studies concerning possible anatomical and
noxious sources and contributors of ITB syndrome,
one involving “normal anatomy”, and two concerning
benign tissue abnormalities. In 1996, Nemeth and
Sanders built upon a 1941 report that detailed a “lateral
extension of the synovial pouch” and their own clinical
studies to further investigate chronic ITBFS.27 Although
they weren’t the first (or the last) to report the presence
of this “normal anatomical” feature, they could not
resolutely report that the lateral synovial recess (LSR)
is primarily involved in the pathogenesis of chronic
ITBFS, but their study does point the finger at the LSR
as at least being partially involved in the chronic lateral
knee syndrome we call ITBFS. Based on histological
and imaging (MRI) data, Nemeth and Sanders felt com-
fortable in stating the following; that no bursa exists
under the ITB, there is a highly vascularized adipose
tissue present between the femur and the ITB, and
that histology results of subjects with a history of ITBFS
supports the notion that regular “impingement” of the
LSR and/or adipose tissue in the lateral spaces of the
knee is responsible for the chronic inflammation and
synovitis in the ITBFS patients.27
Grando and colleagues offered direct and more
recent evidence for the role of both extrasynovial tissue
and fat pads in ITB-related pathologies in their 2014
article published in Magnetic Resonance Imaging Clinics
of North America.28 First, they connect the reader to the
utility of fat pads (versus bursa) by succinctly recount-
ing the theoretical work of MacConaill in 195029: “they
not only occupy dead space in the joint but also help
maintain the joint cavity and promote efficient lubri-
cation by helping to distribute synovial fluid…explains
the presence of fat pads in areas of the body exposed
to mechanical stresses, such as the knee”.28, p. 725 More
critically, they provide further imaging evidence of both
normal and pathological adipose and synovial tissue
in the lateral recesses of the knee, between the femur
and the ITB, and specifically refer to an “impingement
zone” in which maximum fat pad and synovial tissue
impingement or compression occurs in the early stance
phase of running, when the knee flexion angle approx-
imates 30°. From 0–30° of flexion during the loading
or deceleration phases of gait (stance), considerable
eccentric energy and control is required to stabilize
and normalize the forces and movements of the weight
bearing lower extremity. This critical zone of stability
requires strength, control, and endurance of muscles
of the hip and thigh in order for reactive forces on the
limb’s inert tissue to be minimized. Incidentally, this
critical zone mirrors quite well the trouble range or
zone that Renne and Noble both described in their
initial ITBFS models.
In the third and most recent study, a Korean group
published a paper that pinpointed “intra-articular
fibroma” in the tendon sheath as a culpable source of
pain in ITBFS patients.30 The authors presented a brief
review of the rare condition (intra-articular fibromas)
and a case involving a 45-year-old male athlete with
recurrent lateral knee pain and a palpable nodule. MRI
revealed a thickened ITB, fatty abnormalities deep to
the ITB, and the presence of an abnormal nodule in
the space between the ITB and the LFC. Arthroscopic
resection revealed an inflamed lateral synovial recess
and a whitish polypoid intra-articular nodule that was
attached to the joint capsule, and histology studies
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demonstrated marked hemorrhage, fibrosis, and
prominent capillary proliferation in the resected fibrous
nodule. Though fibromas of tendon sheaths are rare
overall, they more typically develop in the fingers,
hand, and wrist joint. Extra-articular fibromas in the
knee are exceedingly rare however, (only 7 reported
cases), but tendon sheath fibromas in the knee are
the most common location for intra-articular lesions
in 20–50-year-old males. When they do develop, it is
easier to assess clinically than typical ITBFS because
of the painless mass (31%), sense of fullness, and
mechanical symptoms that typically present as a result
of these fibrotic neoplasm or reactive fibroses (in con-
trast to ITBFS without fibromas). Table 2 summarizes
the “old” and the “new” anatomical and biomechani-
cal evidence that is pertinent to the understanding of
ITB-related pathology and dysfunction over time.
This new anatomical and biomechanical informa-
tion begs for a new paradigm of thought and practice
for IT band related knee pain. To be frank, Craig Den-
egar first made us aware of this paradigm change in
2010 as part of a case study presentation he delivered
on a recalcitrant case of ITBFS in an elite female runner.
Denegar’s evidence-informed experience forced him
to fundamentally reexamine the clinical paradigm or
axiom from which he was initially working to address
this common problem, and the net result of this pre-
sentation was that it forced clinicians in the audience
to reconsider what they “thought they knew” about
ITB-related pathology.31 There is now a firm belief that
the ITB cannot be stretched32 per se because, as Fair-
clough states, “the fascia lata, the lateral intermuscular
septum, and the distal fibrous bands anchoring the ITB
to the femur would all need to be stretched for the ITB
to be lengthened.”1 The 2006 research of Chaudhry
et al. reinforces this notion with a three-dimensional
mathematical model claiming that the forces required
to produce a 1% shear and compression in fascia lata
are far beyond the physiologic range that manual ther-
apy can induce, leading to the conclusion that the fascia
lata remains very stiff under any shearing produced
with stretching.33 They further hypothesized that the
anecdotal relaxation changes reported by therapists
when massaging fascial tissue may be due to a stim-
ulation of fascial mechanoreceptors that then leads to
tonus changes in connected muscle fibers.
Table 2 Summary of Old vs. New Paradigm
Clinical Components for ITB Pathology
Syndrome Component ITB Friction (“Slipping Band”) ITB Impingement (“Compression”)
Pathoetiology Movable ITB, crosses over lateral fem-
oral condyle with knee flexion/exten-
sion, especially at 30° of flexion
ITB does NOT move across the lateral femoral con-
dyle, and thus cannot cause friction-related pathol-
ogy; dynamic valgus collapse due to neuromuscular
factors causes impingement of subtendinous tissue
during repetitive weight bearing flexion/extension
activities
Tissue & anatomy Subtendinous bursa; ITB; ITB inserts
on linea aspera and Gerdy’s tubercle
Extra synovial pouch/recess; highly innervated fat
pad; benign tendon sheath fibroma; ITB?; ITB has
multiple and varied insertions on tibia, patella, lat-
eral retinaculum, and LFE itself
Clinical presentation History concurrent with ITB presenta-
tion, including pain over lateral femoral
condyle, overuse, increased mileage,
other modifiable risk factors common
in runners; positive Ober’s test; posi-
tive Noble’s test
History concurrent with ITB presentation, including
pain over lateral femoral condyle, overuse, increased
mileage, other modifiable risk factors common in
runners; inconclusive Ober’s test; positive Noble’s
test
Treatment Steroidal injections; stretching of ITB;
deep tissue/friction massage; therapeu-
tic modalities; activity modifications;
surgery (recalcitrant cases)
Activity modifications; address modifiable risk fac-
tors; hip strengthening and neuromuscular training
Outcomes Not supported Supported
Abbreviation: ITB = iliotibial band.
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Rather than the ITB being “stretched” over a subly-
ing bursa and slipping fore and aft over the lateral fem-
oral condyle, the new theory put forth for those who
suffer from pain and discomfort is that the ITB band
does move medially and laterally due to the varying ten-
sioning forces. These forces are enough to compress a
highly vascularized and innervated fat pad that “works
as a bursa would” and sits underneath the IT band and
in effect prevents undue forces on vulnerable tissue
(as MacConaill described and detailed prior). Because
the fat pad between the ITT and the epicondyle is a
richly vascularized and innervated connective tissue,
it may contain pressure-sensitive Pacinian corpuscles,
pain-sensitive nociceptors, and proprioceptive nerve
endings that may, through neural feedback, play an
important pathoetiological role in the perpetuation of
ITB syndrome.1 Grando emphasizes the importance
and under appreciation of fat pads in and around the
knee by summarily informing us that fat pads should
be appreciated as more than passive, space occupying
structures. Rather, fat pads of the knee are critical in
that they protect the joint by remodeling their shape
according to flexion angles and assist in preserving the
various compartments by modulating direct contact.
The richly innervated and vascularized fat pads in our
knees function as “windows between the synovium
and the capsular layers”, and therefore “extrasynovial
impingement and inflammation syndromes about the
knee should be in the differential diagnosis for patients
presenting with knee pain”.28, p. 739
In addition, Vieira’s anatomical work has expanded
our notion of what the ITB “does” and thus has lent
significant credence toward the idea that the ITB (or as
he calls it, ITT) is essential to both static and dynamic
stability of both the patellofemoral and knee joints.
Because the ITB crosses both the hip and the knee
joints, proper tensioning and function in the ITB is
crucial for normal biomechanical function at each
level.26 Ward et al. recently wrote a very salient lit-
erature-review-based editorial suggesting a profound
chemico-physical relationship between fat pads and
tendon pain, adding some interesting insight to the
controversy surrounding the true nature of common
tendinopathies (inflammation or degeneration?) at the
knee and ankle.34 They propose that fat pads share an
anatomic and functional relationship with adjacent
tendons and shared vascularization, innervation, and
further that the fat pad’s production of inflammatory
cytokines contribute to the development of clinical
tendinopathies. In citing several histological and imag-
ing findings, Ward and colleagues34 link the size and
location of fat pads around the patellofemoral joint
and Achilles’ tendon to inflammatory and vascular
changes that effectively contribute to, or produce the
perception or manifestation of “tendon pain”. Hoffa’s
fat pad (knee) and Kager’s fat pad (retro calcaneal)
are known to produce greater inflammatory cytokines
and to possess a complex network of surface vessels,
and structurally they contact the under surface of the
proximal tendons (patellar and Achilles’, respectively).
Together, these properties in effect provide extrinsic
blood supply that at times may become the “root” for
neovascularization of the tendon to occur as a tendi-
nopathy develops. They term this neovascularization
phenomenon as “parainflammation”, operationally
defined as “chronic, low-grade inflammation associated
with repetitive tissue stress”.40 Given this biochemical
evidence, Ward et al. hypothesize that “fat pads adja-
cent to common sites of tendinopathy are a key source
of cytokines and influence the pathophysiology of
tendinopathy via parainflammation pathways”.34, p. 1492
Summarily, we now have compelling evidence that
(a) the ITB is extremely functional and important to
lower quarter mechanics; (b) the ITB has several, mul-
tifunctional insertions that contribute to patellofemoral
and knee joint stability, including along the linea aspera
itself; (c) ITB syndrome is related to compressive or
impingement type forces (and not friction, slippage,
or tightness of the ITB); (d) there is no subtendinous
iliotibial bursa present; and (e) the noxious producing
tissue is either a richly innervated fat pad or an extra
synovial pouch, or some combination thereof. Given
this plethora of new information from basic sciences
(anatomy, physiology, and biomechanics), we have
the underpinnings for a new working paradigm of
ITB pathology for clinicians that treat runners, rowers,
soldiers, cyclists, and other athletes with insidious
onset, lateral knee pain, one specifically inspired by
the intersection of Grando’s extrasynovial and fat pad
tissue imaging data and Denegar’s paradigm change
articulation–ITB impingement syndrome. Before we
move on, however, we need to first consider the “how”
and “why” impingement serves as an apt conceptual
model for ITB pathology.
Biomechanics and Pathomechanics
If the ITB is not “slipping” over and back of the lateral
femoral condyle at the 30° of flexion point with repet-
itive running-based activities, as Renne first proposed,
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then why do some people experience insidious lateral
knee pain in their knee, while like activities and volume
are immune to it? What is the precise pathoetiology for
this troublesome syndrome, and how can it be fixed
or prevented? Why doesn’t the standard treatment
protocol of stretching and massage relieve the pain
and discomfort associated with this type of lateral
knee condition in runners?3,32 If we accept Denegar’s
contention that “understanding pathology informs
treatment”, we must first understand how or why the
synovial pouches and/or fat pads of some runners
are impinged, yet are not so in others undertaking
the same mode and volume of activity.31 Perhaps the
answer lies in a combination of information from
Fairclough’s proposed entrapment theory, Vieira’s
functional and anatomical elaboration, and numerous
biomechanical investigations concerning the intercon-
nection between hip musculature and knee function
during closed chain activities.1,26,31
After debunking Renne’s original “friction” or
tissue slippage theory, Fairclough and colleagues were
obligated to offer an alternative mechanical cause for
the pain that ITBFS sufferers reported. If the ITB did
not roll over the lateral femoral condyle, and if the
subtendinous fat pad was being compressed (rather
than a bursa), what was causing this compression in
some athletes (but not others)? Pathomechanically,
what exactly induces this pain in some people and
not in others? Interestingly, Fairclough did not have
to look very hard for an answer, because there were
already at least two studies published by Fredericson
and colleagues that offered an explanation.2,35 Although
he produced no original data of his own making to sup-
port his alternative theory, but based on Fredericson’s
prior work, Fairclough contended that “ITB syndrome
is related to impaired function of the hip musculature”
and that “resolution of the syndrome can only be
properly achieved when the biomechanics of the hip
muscle function are properly addressed.”1, p. 315 Not
only did Fredericson find that long distance runners
with ITBS had weaker hip abduction strength in their
affected legs, but also that their conditions resolved and
that they returned to preinjury training after achiev-
ing improvements in their hip abductor strength.35
Although not a definitively established cause-effect
relationship as of yet (Grau et al. reported in their 2008
study that hip abductor weakness did “not” factor
into ITB syndrome36), there are indeed several studies
documenting at least a role of the hip musculature in
causing ITB impingement syndrome (ITBIS), including
an award winning 2007 prospective paper in Clinical
Biomechanics by Noehren, et al., in which they found
ITB syndrome to be related to peak hip adduction and
knee internal rotation moments, and that treatment
interventions should focus on controlling these energy
absorbing forces and planar movements during the
stance phase of gait.37
Like many syndromes, ITB indeed seems to comply
with the tenets of “systems theory” in that it likely
involves many interconnected factors both etiologi-
cally and pathomechanically and, indeed, Louw and
Deary’s16 systematic review on the etiology of ITB syn-
drome in runners revealed exactly this type of segmen-
tal interconnectedness or “regional interdependence”.
Their intensive review of 12 quality studies (out of
1,732 identified) revealed that runners suffering from
ITB syndrome display decreased rear foot eversion,
tibial internal rotation, and hip adduction angles at heel
strike while having greater maximum internal rotation
angles at the knee and decreased total abduction and
adduction range of motion at the hip during the stance
phase, concluding that a “clear biomechanical cause for
ITBS could not be devised due to the lack of prospective
research”. The biomechanical work on ITB strain rate
and the pathogenesis of ITBS by Hamill et al. lends
further objective support to the notion that stretching
a “tight” ITB does not help reduce pain (due to com-
pression or impingement), and that increased dynamic
valgus collapse of the knee joint during stance plays
a role in the development of ITB syndrome because
of the speed in which it induces strain on the ITB.38
They found that “strain rate” (an indirect measure of
tension in the collagen-based viscoelastic tissue) and
not the absolute magnitude and increased adduction
and internal rotation of the femur and tibia, respec-
tively, were related to the presence of ITBS, especially
at midsupport where the knee is flexed to its maximum
range (in normal running). They thus concluded that
since ITB syndrome subjects exhibited greater strain in
their ITB throughout the support period, as compared
with their control group, that strain rate is a major
factor in the development of ITB syndrome.
Lastly, a thoughtful study by Miller et al. in 2007
sought to test the relation between hip musculature
performance and ITBS by inducing fatigue in runners
to see if their lower quarter mechanics changed as a
result.39 In their eight subjects (runners) with a history
of ITB syndrome, an exhausting run caused them
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to display increased knee flexion and tibial internal
rotation angles at heel strike, and to produce higher
ITB strain rates throughout the entire stance phase as
compared with healthy control runners. Given that
the functional utility of the stance phase of walking,
running, and landing gait is to essentially absorb body
weight and ground reaction forces through decelerative
muscle action (eccentric contractions), exaggerated or
excessive joint motions in the lower extremity indicate
that the ITBs in susceptible runners’ knees are in the
“impingement zone” longer, and that endurance runs
that fatigue the pelvic muscles further decrease the
ability of these vulnerable tissues to effectively absorb
the energy loads that are produced, creating a cyclical
recipe for insidious onset pathology. In concluding that
ITB syndrome pathomechanics appear to be related
to changes in knee flexion at heel strike and internal
rotation of the leg, the authors suggest that kinematic
discriminators for the clinical assessment of ITB syn-
drome are supported by their findings.
One final overarching consideration is the recent
acceptance of the biomechanical concept of tensegrity.
The architectural theory of tensegrity was first intro-
duced through the indirectly linked efforts of sculptor,
Kenneth Snelson, and system theorist and architect,
Buckminster Fuller. Based on the design concepts of
Snelson’s sculptures, Fuller developed architectural
structures that were supported utilizing compression
and tension elements, coining the term “tensegrity”
in naming the unique designs.40 As it relates to human
form, the compression struts in a “tensegrity” design
are represented by bones which in essence float within
the structure, they are not continuous with each other
and therefore do not transmit compression to adjacent
bones. The tension elements are muscles, tendons,
and, in essence, the fascia tissue itself, as they directly
distribute their tension load to adjacent tension ele-
ments.41 Biotensegrity, coined by Dr. Steven Levin in
1981 and further developed on a cellular level by Dr.
Donald Ingber, builds upon Fuller’s model and provides
an explanation for how dynamic forces and cellular
signaling are transmitted throughout the body, which
is of utmost importance to address ITB issues from a
holistic approach. Biotensegrity provides for not only a
structural approach and understanding as to how force
is transmitted through the three-dimensional construct
of the constituent tissues of the body (the fascial tissue
as defined by Guimberteau & Armstrong42) but, more
importantly, how the body itself changes and adapts
to stress through the “sensing” of tension, a process
known as mechanotransduction. Adaptation is a
product of biotensegrity and mechanotransduction
as cells “sense” and/or message each other through
the connection each cell has with each adjoining and
connected cell.43 The nucleus of the cells are signaled
or stimulated to transcribe DNA leading to adaptations
occurring in the tissue.
Once the concepts of biotensegrity and mechano-
transduction are better understood, it becomes impera-
tive to not just address the local tissues when evaluating
a patient with complaints of lateral knee pain, but also
to take multiple other structures into consideration.
Biotensegrity dictates that tension and forces from
adjacent and, quite plausibly, structures somewhat
remote from the presenting dysfunction could be
contributing to the dysfunction. In other words, restric-
tions in tissues away from the site of symptoms and/
or dysfunction may actually be the root cause of the
problem. In the case of ITBIS, a dysfunction in the
thoracolumbar fascia (TLF) may be contributing and/or
causing the symptoms being experienced in the lateral
knee; this occurs due to the interconnectedness of all
tissues in the body. Tension and strain are produced in
a muscle or deep fascial tissue and the resulting force is
transmitted through the myriad of fascial connections
into adjacent tissues up and down the line from the
point of origin. Therefore, if there is a restriction in any
of the tissues along the line, the transmission of force
will be altered leading to abnormal loading of said
tissue or adjoining tissues ending in dysfunction and
potential pathology. In the case of ITB tissue, pathol-
ogy can lead to symptoms being experienced in the
lateral aspect of the knee. Franklyn-Miller and his group
performed a study on fresh cadavers investigating
microstrain levels produced in various interconnected
tissue groups when a straight leg raise is performed.44
Their results strengthened the biotensegrity theory of
transmission of strain to adjacent structures as there
was over a 200% greater strain produced in the ITB,
a 146% greater strain produced in the ipsilateral TLF,
and a 102% and 100.6% greater strain produced in
the lateral compartment of the lower leg and Achil-
les, respectively, than that produced in the posterior
thigh. These results were found on nonliving tissue
and if extrapolated to potential in-vivo findings, one
can conclude that transmission of force will occur in
an active setting as well, with one expecting to find
significant, though perhaps lower strain, values, as
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living muscle fibers would be able to absorb some of
the force transmission. Therefore, ITBIS is likely to be
a multifactoral issue and not just a problem in local
tissue, so examining other related areas of the body for
restrictions and or dysfunctions is indeed warranted.
An Evidence Informed
Summary and Conclusion
Indeed, there is a need for high-quality prospective
studies to test any new theory or paradigm of thought
or axiom for clinical practice if we are to become and
be an evidence-informed profession; in this case,
there is certainly room for more objective and clear-
cut evidence for resolving ITB- related pathology. But,
given that there is very little to no evidence to support
Renne’s original “friction” theory for ITB pain and
dysfunction, and very little credible and nonanecdotal
evidence to support the way that many of us have
been treating this difficult clinical problem in runners,
cyclists, and rowers for years, there is certainly room for
a new way of thinking and addressing ITB dysfunction
if we hope to establish better patient outcomes in those
that suffer. New evidence from our pillar sciences of
anatomy, physiology, and biomechanics has emerged
that directly challenges both the name and the nature
of the paradigm many of us regularly use and refer to
as iliotibial band friction syndrome. Considerable evi-
dence now exists to help provide a scientific platform
for a new and more informed paradigm for ITB-related
pathology in running-based athletes. Iliotibial band
impingement syndrome, or ITBIS, is proposed here as
a more apropos paradigm because it is based on new
information not only about the basic anatomy of the
ITB and surrounding tissues, but also from physiolog-
ical evidence that implicates extrasynovial tissue and
fat pads as the pathologically insulted and painful
sources, as well as biomechanical data that implicates
neuromuscular dysfunction at the hip, and possibly
tissue further away, as a primary etiological contributor
to the syndrome (or cocontributor, at least).
Combining this science-based evidence with the
clinical science data conducted on the condition in
the laboratory provides a tenuous but plausible evi-
dence-informed paradigm for insidious onset, lateral
knee pain. Given this information, it is thus recom-
mended that clinicians cease from attempting to
stretch and massage the ITB, limit their use of modality
application to the ITB itself, and, rather, begin to use a
regional interdependence quality assessment approach
to treating ITBIS—look at athletes’ landing and stance
mechanics, assess the biomechanics of femoral and
tibial responses to loading, ascertain if athletes with
ITB-related lateral knee pain have a pronounced or
exaggerated “impingement” period or zone during
early to midstance. If so, look up the chain and down
the chain, assess and address tissue dysfunctions that
can contribute to a change in force transmission as
well as neuromuscular issues at the hip to assess and
address biomechanical flaws in the foot and ankle, see
what kind of outcomes are generated with this rela-
tively common problem, and don’t forget to document
and share the results.
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Paul R. Geisler and Todd Lazenby are with the Athletic Training Edu-
cation Program in the Department of Exercise and Sport Sciences,
Ithaca College, Ithaca, NY.
Luke Donovan, PhD, MEd, University of North Carolina at Charlotte,
is the report editor for this article.
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