Interest in the posterolateral corner (PLC) of the knee joint has increased because recent biomechanical and anatomic studies have revealed its importance in knee stability (1). PLC injury of the knee is commonly associated with concomitant ligament disruptions (1). Although PLC injuries of the knee are uncommon, they can lead to chronic disability from persistent instability and resultant articular cartilage degeneration (2). The diagnosis of subtle lesions of the PLC can be elusive unless there is heightened clinical suspicion for possible injury of this region (3). Failure to diagnose and treat PLC injuries may increase the failure rates for both anterior and posterior cruciate ligament (PCL) reconstructions (1). However, early diagnosis may allow for immediate surgical repair of the PLC that has resulted in superior outcomes as compared to delayed reconstruction (1,2).

The complex anatomy of the PLC of the knee is due largely to the evolutionary changes in the anatomic relationships of the fibular head, the popliteus tendon, and the biceps femoris muscle (3). Recent anatomic and biomechanical studies have more clearly defined the various anatomic structures composing the PLC of the knee. These structures include the iliotibial tract, lateral collateral ligament (LCL), popliteus tendon complex, popliteofibular ligament (PFL), and the posterolateral capsule (1,13). The LCL is the primary static restraint to varus opening of the knee (4, 5, 6). The femoral insertion is located proximal and posterior to the lateral epicondyle in a small depression between the lateral epicondyle and the supracondylar process. Distally, the LCL attaches to the fibular head a mean of 8.2 mm posterior to the most anterior aspect of the fibular head (7, 8, 9) (Fig. 38.1).

The popliteus tendon complex consists of the popliteus muscle-tendon unit and the ligamentous connections from the tendon to the proximal fibula, tibia, and meniscus (10). The popliteal muscle originates from the posteromedial aspect of the proximal tibia and gives rise to its tendon, which courses intra-articularly through the popliteal hiatus of the coronary ligament to insert on the popliteal saddle on the lateral femoral condyle (11). The femoral insertion site of the popliteus is consistently anterior and distal to the femoral attachment site of the LCL, according to LaPrade et al. (11). However, Brinkman et al. (12) found more variability in the popliteus tendon femoral insertion site as either anterior or posterior to the LCL. The three popliteomeniscal fascicles extend from the tendon to the lateral meniscus and assist in providing dynamic stability to the meniscus (13).

On the basis of their dissection studies, Sudasna and Harnsiriwattanagit (14) identified a fibular origin of the popliteus (also known as the popliteofibular ligament or PFL) in 98% of the knees, a fabellofibular ligament in 68%, and a thin, membranous arcuate ligament in 24%. The PFL arises from the myotendinous junction of the popliteus and courses distally and laterally to insert on the fibular styloid process.

In addition, the iliotibial band (IT) is composed of multiple layers and blends with a confluence of the short head of the biceps to form an anterolateral sling about the knee. The long and short heads of the biceps femoris muscle provide dynamic stability, with the fabellofibular ligament being a thickening of the distal capsular edge of the short head of the biceps (1). The common peroneal nerve is located on the posterior border of the long head of the biceps (8). The mid third of the lateral capsular ligament is a thickening of the lateral capsule (1). Ultimately, the lateral meniscus increases the tibiofemoral conformity and thus the stability of the lateral compartment.

The primary function of the PLC is to resist varus rotation, external tibial rotation, and posterior tibial translation (4,6). Biomechanical studies involving selective sectioning and joint loading have helped to define the interrelationships between the PLC and the primary functions of the LCL, popliteus tendon, and the PFL (15). The LCL is the primary static restraint to varus opening of the knee (4, 5, 6). The response to direct force measurements of the LCL at 30 degrees of flexion is significantly higher than at 90 degrees of flexion (15). The individual maximum tensile strength of the LCL has been determined to be 295 N (16). The PCL has been found to play a role as a secondary restraint because, when sectioned in isolation, the PCL has no effect on varus rotation but, when the posterolateral structures are deficient, additional PCL sectioning results in a significant increase in varus rotation (4, 5, 6).

Selective ligament sectioning by Nielsen et al. (17, 18, 19, 20) demonstrated the importance of the PLC as the primary stabilizer of external tibial rotation at all knee flexion angles. The LCL and the posterolateral part of the capsule resisted varus and external rotation of the tibia. The popliteus tendon resisted excessive external rotation of the tibia during knee flexion from 20 to 130 degrees, and it resisted excessive varus rotation of the tibia during flexion from 0 to 90 degrees (18). Isolated sectioning of the PCL did not affect varus or external rotation stability, whereas combined sectioning of the LCL and the posterolateral part of the capsule resulted in increased instability (17,19).

Gollehon et al. (4). and Grood et al. (6). found that combined injury to the PCL and posterolateral structures produced significantly greater increases in external tibial rotation, especially at 90 degrees of knee flexion. These studies provide the biomechanical rationale for performing the dial test at 30 and 90 degrees of flexion to determine the presence of an isolated PLC or combined PLC/PCL injury (21).

In a cadaveric study by LaPrade et al. (15), it was found that the mean load responses to external rotation in the LCL were significantly higher than those of the popliteus tendon and PFL at 0 and 30 degrees of flexion. The popliteus tendon and PFL, on the other hand, demonstrated higher loads at higher knee flexions, peaking at 60 degrees. It was concluded that the LCL, popliteus tendon, and PFL performed complementary roles as stabilizers to external rotation with the LCL assuming a primary role at lower knee flexion angles and the popliteus complex assuming a primary role with higher knee flexion.

Due to studies demonstrating that isolated sectioning of the PCL produces increased posterior tibial translation at all angles of knee flexion, with a maximum at 90 degrees, and isolated sectioning of the PLC structures produces increased posterior tibial translation at all angles of knee flexion, with a maximum at early knee flexion, it can be concluded that the PLC, not the PCL, is the primary restraint to posterior tibial translation near full knee extension (6,22). Furthermore, combined sectioning studies of both the PCL and the PLC have demonstrated significant increases in posterior translation at 90 degrees of flexion compared with the intact knee(s) with isolated PCL or posterolateral deficiency (4,6,23).

The interdependent relationship of the PLC structures and the cruciate ligaments is demonstrated through biomechanical analysis of posterolateral deficiency in the setting of ACL or PCL reconstruction (1). LaPrade et al. (24) sectioned the posterolateral structures and noted increased loads in the ACL graft with application of varus and coupled varus-internal rotation moments. Due to these findings, the authors recommend reconstruction or repair of a grade III PLC injury at the time of ACL reconstruction.

Failure to recognize and treat a PLC injury will result in increased stresses and possible failure in PCL reconstruction; therefore, a combined reconstruction is recommended (10). This is demonstrated by Harner et al. (10) as they sectioned the posterolateral structures and, compared to knees with intact posterolateral structures, found an increased posterior tibial translation in the reconstructed knees of 6 mm at 30 degrees and

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