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ILLIOTIBIAL BAND Friction Syndrome

Ben Snell, Sian Cook, Paul Wiedersehn

Pathogenesis & Mechanisms

Created by Ben Snell, Sian Cook & Paul Wiedersehn.

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Pathogenesis of ITBFS

The pathogenesis of ITBFS involves inflammation and irritation of the lateral synovial recess, irritation of the posterior fibers of the ITB, and inflammation of the periosteum of the lateral femoral epicondyle (Ellis, Hing, & Reid, 2007). When the knee is flexed greater than 30˚, the ITB lies posterior to the lateral femoral epicondyle; however when the knee is extended the ITB moves anterior to this bony landmark (Beers et al., 2008). This is best described by the concept of an ‘impingement zone’ which occurs at 30˚ of knee flexion during foot-strike and early stance phase. At knee flexion of approximately 30˚ or greater, the ITB passes over and posterior to the lateral femoral epicondyle. During the impingement period, eccentric contraction of the tensor fascia lata and gluteus maximus decelerate the leg, exerting a greater tension through the ITB (Kirk et al., 2000). A cumulative effect of excess friction causes an inflammatory reaction within the iliotibial tract, underlying bursa, and/or periosteum of the lateral femoral epicondyle, inducing lateral knee pain and inflammation (Beers et al., 2008). In contrast to this model, it has been proposed that an illusion of anterior-posterior movement of the ITB results from repetitive cycles of tightening in which the lateral fascia exerts a repetitive compression effect on connective tissues lying deep to the ITB (Lavine, 2010).

Mechanisms of Injury (click here)

Image: Netter FH. Iliotibial band friction syndrome.

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