Research Review By Dr. Joshua Plener©


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Date Posted:

October 2022

Study Title:

The Iliotibial Band: A Complex Structure with Versatile Functions


Hutchinson L, Lichtwark G, Willy R & Kelly LA

Author's Affiliations:

School of Human Movement and Nutrition, The University of Queensland, Australia; School of Physical Therapy and Rehabilitation Science, University of Montana, United States

Publication Information:

Sports Medicine 2022; 52(5): 995-1008

Background Information:

The iliotibial band (ITB) is made up of tough, fibrous fascial tissues and spans from the iliac crest to the lateral proximal tibia (remember, it is well-accepted now that soft tissues are continuous, integrated structures that don’t ‘start here and stop there’, so to speak). The various functional roles of the ITB appear to be dependent on the posture and activity performed (1-3). This is likely a result of the in-series muscular contributions of the gluteus maximus and tensor fascia latae (TFL), as well as the anatomical path of the ITB crossing the hip and knee joints (4). During walking, the ITB affects the hip and knee, activating as a hip and knee stabilizer, as well as storing elastic energy (5).

ITB pain is common in runners, with a 5-14% prevalence of all running related injuries (6). Recent reviews have suggested a shift away from commonly held beliefs regarding the diagnosis and treatment strategies of ITB syndrome, such as moving away from a friction syndrome model to a compression syndrome or impingement model (7-10).

The current clinical understanding of ITB syndrome is lacking and the purpose of this review is to summarize the current body of literature surrounding the anatomy and biomechanics of the ITB, to better understand the etiology, clinical examination and treatment of ITB syndrome.


Anatomical Variance:
The ITB is unique to humans and is anatomically distinct from the tensor fascia latae (TFL) of other primates. The theory is that humans could walk bipedally following the development of the glute max, the change in position of the pelvis from horizontal to vertical, and the formation of the ITB (5).

The glute max and TFL muscles directly insert into (or, are continuous with) the ITB, contributing to its functional mechanics. The TFL pulls anterosuperiorly on the ITB to flex the hip while the glute max pulls posteriorly to extend the hip (5, 11-13). The insertion of glute max has two distinct portions, the superior portion inserting into the ITB, which ranges from 40-70% of the glute max’s total mass, and the inferior portion inserting into the femur (26). As a result, the ITB broadens the insertion of glute max and facilitates the transmission of forces from the glute max and TFL across both the knee and hip.

The ITB inserts distally at Gerdys tubercle, as well as four other commonly published insertion points, including a shared insertion with the femoral tibial ligament, the supracondylar femur shared with the lateral collateral ligament, along the linea aspera, and to the patella.

Mechanical Function:
The function of the TFL achieves little agreement in the literature but the consensus appears to be that it contributes to hip internal rotation, hip flexion and stabilization of the knee through the ITB, while the TFL’s role in hip abduction is more contested (5). As the TFL shares an insertion (or, integration) with glute max onto the ITB, the mechanical role of the TFL likely depends on the posture of the hip and knee when force is produced.

The glute max is considered a primary extensor of the hip joint. Glute max assists in external hip rotation, hip abduction and tensioning of the ITB, and due to the size of glute max, it is likely to transmit greater force through the ITB than the TFL. Furthermore, as glute max also inserts superiorly on the ITB, it may have a role in hip abduction.

The literature supports the theory that the knee is indirectly stabilized as a by-product of muscles tensioning the ITB. Cadaveric studies suggest the ITB tension can induce lateral patella displacement and external tibial rotation (14), but it is difficult to assess whether passive forces generated in the ITB would be sufficient to counteract the other muscular and external forces acting on the knee during movement, as the information used to inform this theory is based on cadaveric studies. The use of cadaveric studies is a major limitation, as these studies ignore the potentially large forces transmitted from the glute max and TFL during real world activities like walking and running.

Ex vivo and In vivo Material Properties and Elastic Function:
The ITB facilitates the attachment of glute max and TFL to bone and therefore it is likely to have tendon like properties to provide joint stability and contribute to the storage of elastic energy. Human legs have spring like tendons allowing for the storage and release of energy during walking (15-18). For example, the Achilles tendon contributes approximately 35-40% of positive work during the stance phase of running (17), and given the ITB’s size and similar properties, it is plausible that the absorption and dissipation of energy occurs in a similar manner. One model predicted that the ITB stores approximately 14% of the work the Achilles contributes (4), and the posterior ITB, inserted via the glute max, transmits larger forces than the anterior, which is inserted via the TFL. This is an area of research that requires further investigation to understand how tension and/or stress is applied to the ITB to further understand its function.

Clinical Significance:
ITB syndrome is an overuse injury with pain at the lateral knee commonly exacerbated by tensioning the ITB (19). ITB syndrome is the most prevalent overuse injury of the lateral knee, accounting for 12% of all running related injuries, as well as a significant contribution to cycling and military related injuries (19, 20-22). However, the lack of understanding of force transmission within the ITB and stresses and strain placed on it, underpins the lack of evidence and rationale for many treatments.

There are two proposed mechanisms to describe the behavior and function of the ITB. First, ITB syndrome was considered a friction injury (23) as it was believed that the cyclic loading of the ITB moving from the anterior aspect of the lateral femoral epicondyle in full knee extension to the posterior aspect of the lateral femoral epicondyle as the knee is flexed beyond 30 degrees causes irritation during activities such as running. Recently, the mechanism behind this theory has been questioned and many suggest it is not accurate, as the ITB is tethered to the distal femur, except for the upper portion of the lateral femoral condyle (1, 5), thus preventing the ITB from traversing over the lateral femoral condyle. A new theory behind ITB syndrome emerged following MRI scans, which showed that when the knee is flexed past 30 degrees, the band compresses medially against the lateral femoral epicondyle. This compression is suggested to cause irritation to the highly innervated fat between the band and the bone, suggesting that the ITB syndrome is a compression syndrome rather than a friction syndrome (1, 8)

Primarily, the diagnosis of ITB syndrome is one of exclusion. Generally, runners with ITB syndrome report lateral knee pain approximately 2-3 cm proximal to the lateral tibiofemoral joint line in the region of the lateral femoral condyle. The onset of pain is often described as insidious and preceded by a recent increase in running loads, usually due to an increase in running distance or an increase in the volume of downhill running (24, 25). Patients may also report pain reproduction in the stance limb during their descent on stairs as hip extension is coupled with knee flexion and the TFL contracts eccentrically to assist lower limb control (26). Furthermore, running, particular downhill or fast running may exacerbate ITB syndrome (26). Other diagnoses that should be ruled out include patellofemoral pain syndrome, lateral meniscal lesions, lateral synovial plica syndrome, and distal femoral bone stress fracture. In addition, gluteal tendinopathy and lumbar radiculopathy could also cause lateral thigh and knee pain and should be ruled out. Imaging does not assist the clinician in making a diagnosis of ITB syndrome.

Clinical Examination & Considerations:
The Noble compression test is the sole diagnostic test used in clinic for a suspected ITB syndrome. This test is performed by applying manual pressure to the patient’s lateral knee, 1-2 cm proximal to the lateral femoral condyle as the knee is passively extended though a range of motion from 60 degrees to full extension. A positive test is reproduction of the lateral knee pain at approximately 30 degrees of knee flexion (21). Despite its widespread use in clinic, this test has unknown psychometric properties and therefore caution should be used when interpreting its results. Another test that clinicians use to assess the ITB is Ober’s test. The classic Ober’s test is performed with the patient lying on their side and the examiner flexing the affected knee to 90 degrees while adducting and extending the hip posterior to the unaffected leg, allowing gravity to further adduct the leg. A positive test is an inability for the patient to further adduct their leg under gravity past horizontal (27, 28). A modified version Ober’s test consists of keeping the knee fully extended and the pelvis manually stabilized, theoretically reducing the possibility of influence from a tight rectus femoris (28). The Ober’s test is based on the assumption that an injured ITB is tighter than a healthy ITB. However, neither version of the test appears to assess ITB tightness as in cadaveric studies, a positive Ober test was attributed more to restriction of the hip capsule and gluteus medius and minimus musculature (28). Therefore, the usefulness of the Ober’s test to diagnose ITB syndrome is weak.

Despite many patients with ITB syndrome presenting with hip abductor weakness, it is not a known risk factor for ITB syndrome, and likely is a result of ITB syndrome rather than a cause (6). The theory is that distal compression of the highly innervated tissues deep to the ITB may inhibit the proximal hip musculature, specifically the TFL and gluteus maximus in order to attempt to reduce ITB tension. However, no prospective study has assessed strength deficits in runners with ITB syndrome and therefore future research may alter our understanding.

Treatment of the ITB:
Generally, there is low quality evidence for the treatment of ITB syndrome, mainly consisting of narrative reviews and/or case series. Progressive overload and graded exposure appear to be a common treatment provided and recommended for this condition. Other treatments that are commonly provided include foam rolling, ITB stretching and hip strengthening (24, 26), even though these treatments are not supported by our current understanding of the structure and function of the ITB.

Foam rolling is typically prescribed for patents with a tight ITB and/or ITB syndrome. Positive results from foam rolling are short lived or insignificant, providing patients with only temporary relief. As ITB syndrome is considered a compression syndrome, additional compression in the form of foam rolling lacks justification and may actually exacerbate symptoms!

Stretching is also problematic and the clinical test to demonstrate ITB tightness, the Ober test, is not sufficient for the reasons stated above (28). One study has shown that there are no differences in ITB stiffness between healthy participants and participants with ITB syndrome (29). Therefore, it is a distinct possibility that increased stiffness does not cause ITB syndrome, making stretching unlikely to proffer significant clinical impact.

Hip strengthening is also provided frequently, based on a cause and effect rationale between hip weakness and ITB syndrome (6). However, the biomechanical rationale to prescribe hip strengthening is lacking for a few reasons. First, hip strength does not appear to be related to hip adduction during running despite this being a widely held belief among clinicians (30, 31); and second, hip strengthening doesn’t result in reduced hip adduction during running (32). Despite the lack of biomechanical rationale for hip strengthening, patients improve with this intervention. A possible reason for this is the alteration of central pain processing and a reduction of local hyperalgesia (33). This certainly remains a treatment option, it just may impart benefit in a different way than previously thought.

Interventions targeting running biomechanics could also alter ITB strain such as running with a wider step width (34), and/or running with a higher cadence (35).

High quality studies via randomized clinical trials (RCTs) for the treatment of individuals with ITB syndrome are still lacking.

Clinical Application & Conclusions:

This narrative review provides clinicians with an in-depth understanding of ITB syndrome. Unfortunately, our understanding remains incomplete currently in many aspects, such as the diagnosis, treatment and pathophysiology of ITB syndrome. Many of our commonly accepted and utilized practice standards need to be challenged and further studied. For example, studies that have assessed the function of the ITB have mainly been performed on cadaveric studies, the mechanism of how the ITB causes pain is controversial, the diagnosis of ITB syndrome in clinic is based on a limited number of appropriate tests, and common treatment interventions provided such as foam rolling lack justification in the literature (and in this case, in logic!). Future research on this topic will hopefully provide much needed answers.

Study Methods:

This study is a narrative review with no study methods mentioned in the article.

Study Strengths / Weaknesses:

  • This is a comprehensive review that is clinically relevant to many practicing clinicians, particularly those who serve active patients.
  • This paper also highlighted the many areas of debate and where future research should be targeted to improve our understanding of the ITB.
  • This is a narrative review and therefore is prone to any inherent biases of the authors.
  • Relevant literature may not have been included, as no formal search strategy was published in the paper.

Additional References:

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