OSSEOUS AND MENISCI
In the majority of the population, the normal mechanical axis of the lower extremity lies slightly medial to the center of the knee. To achieve balance in the stance phase of gait, compressive forces are transmitted through the medial compartment of the knee whereas the lateral structures are under significant tension. During the normal gait cycle, the lateral ligamentous structures of the knee are subjected to greater forces than the medial ligamentous structures and are appropriately more substantial and stronger.11
Likewise, the bony anatomy of the lateral compartment of the knee is quite different from the medial compartment. The medial femoral-tibial compartment has an inherently stable ‘‘cup’’ formation. The convex medial femoral condyle rests in the concavity of the medial tibial plateau. On the contrary, the lateral compartment of the knee is inherently unstable as the convex lateral femoral condyle articulates with a convex lateral tibial plateau. Without additional support these 2 convex surfaces would have minimal surface contact, high contact stresses, and very little stability. The inherently unstable bony geometry of the lateral compartment allows greater motion than the medial compartment, but relies on the posterolateral soft tissue structures to provide the required stability. The roles of the medial and lateral menisci parallel the roles of the medial and lateral osseous compartments. Both menisci add stability to their respective compartments, but the lateral meniscus must do so when accommodating the relatively greater range of motion of the lateral compartment. The lateral meniscus contributes to lateral knee stability by adding concavity to the lateral tibial plateau. To preserve its increased motion across the tibial plateau, it has less restraining static meniscotibial attachments than the medial meniscus, and is dynamically stabilized by a branch of the popliteus tendon.
Because the lateral meniscus is less restrained, it is also less stable than the medial meniscus. This permits it more motion across the tibial plateau with flexion and extension of the knee. The increased excursion of the lateral meniscus limits its ability to compensate for the unstable bony geometry of the lateral tibiofemoral compartment. Therefore, the remaining soft tissues of the PLC must provide significant stability to the lateral side of the knee.25
ANTERIOR-POSTERIOR TRANSLATION
The primary restraint to anterior translation of the tibia relative to the femur is the ACL. It accounts for about 86% of the total resistance to anterior tibial translation.11 Although the posterior horn of the medial meniscus provides some support to this role, especially in the ACL-deficient knee, it is easily injured when the ACL
is compromised. This indicates the minimal amount of support the ACL receives in this role and the necessity of reconstructing it when it is deficient. Several studies have demonstrated that the posterolateral structures do not prevent primary anterior tibial translation.26,27 However, like the posterior horn of the medial meniscus, the PLC helps prevent anterior tibial translation in the ACL-deficient knee. The role of the PLC seems to be more prominent near extension, whereas the role of the posterior horn of the medial meniscus is
more noticeable in flexion. This can be demonstrated on physical examination. Typically, an ACL-deficient knee, with an intact posterior horn of the medial meniscus and a torn PLC, will have a markedly positive Lachman test (greater than +2) and a subtle (grade 1) anterior drawer. Conversely, an ACL-deficient knee, with a torn posterior horn of the medial meniscus and an intact PLC, will have a positive anterior drawer and positive Lachman test. However, in the later example, the Lachman test may not be as prominent. Clinically, if an ACL is reconstructed in a knee with a PLC injury, the reconstructed graft will be at higher risk of failure unless the PLC injury is addressed. This underscores the need to thoroughly exam the PLC in all ACL-deficient knees, before reconstruction.
Resistance to posterior tibial translation is far more complex. The stout and centrally located PCL is the primary static stabilizer of the knee and plays a strong role in resisting posterior tibial translation. It provides
95% of the total restraint to posterior tibial displacement forces at all flexion angles.11,22 With the knee in near full extension, isolated sectioning of the posterolateral structures results in increased posterior translation of the lateral tibial plateau. As the knee is flexed to 90 degrees, there is minimal posterior translation. In PCL-deficient knees with transected posterolateral structures, posterior tibial translation of the medial and lateral tibial plateaus is appreciated at 30 and 90 degrees of flexion. Thus, the posterolateral structures are important in resisting posterior tibial translation at small flexion angles (eg, 30 degrees). The PCL and PLC structures work in concert, and injury to both of these structures results in a significant increase in posterior translation of the knee at all flexion angles.23,24
The popliteus is a dynamic stabilizer that assists the PCL by resisting posterior tibial translation. In the intact knee, loading the popliteus has been shown to reduce the in situ forces in the PCL by 9% and 36%, at 90 and 30 degrees of flexion, respectively.28 In the PCL-deficient knee, loading the popliteus has been shown to reduce posterior tibial translation by up to 36%. This amounts to a reduction of posterior translation by approximately 2 to 3 mm. The results of this study confirm that the popliteus muscle complements the PCL in resisting posterior tibial loads and can contribute to knee stability when the ligament in absent.27,28 In a combined PCL and PLC injury model, Harner et al29 demonstrated that a deficiency of the PLC increased posterior tibial translation, in the PCL reconstructed knee, by 4.6 to 6.0 mm. They found a corresponding increase in the in situ forces in the PCL graft of 22% to 150%, if the posterolateral structures were not
repaired or reconstructed. These results demonstrate that an isolated PCL graft reconstruction is rendered ineffective and may be overloaded if the posterolateral structures are deficient. Although the PCL provides the greatest contribution to resisting posterior tibial translation, both biomechanical and clinical studies have shown that it cannot function appropriately in a knee with a deficient PLC. Conversely, clinical studies have demonstrated that many individuals can function with an isolated rupture of the PCL, although their biomechanics may not be identical to that of a healthy knee. These studies demonstrate the importance of a fully functional PLC in resisting posterior tibial translation, and the necessity of repairing or reconstructing the PLC when it is compromised.
VARUS-VALGUS ROTATION
The FCL is the primary restraint to varus stress at all flexion angles of the knee. LaPrade et al30 found that varus forces on the FCL had loading responses from 0 to 90 degrees of flexion, with the greatest being at 30 degrees (12 N/J). Although other soft tissues provide additional support in this function, the FCL receives the least support at 30 degrees of flexion. This makes the FCL most susceptible to injury at 30 degrees of flexion. It has been shown that approximately 300N of force is required to cause failure of this ligament.17 The PCL is considered a secondary restraint to varus rotation; however, sectioning of this structure with an intact FCL does not affect varus rotation. Conversely, when the PLC is deficient and the PCL is intact, the PCL will provide some resistance to varus stress, but it is not as effective in this role as an intact PLC. In a combined PCL and PLC injury model, Harner et al29 demonstrated that a deficiency of the posterolateral structures after PCL reconstruction increased varus rotation up to 7 degrees. Grood et al23 and Veltri et al31 reported that an increase in varus rotation (as much as 19 degrees) can be appreciated with the combined sectioning of the PCL and posterolateral structures. This varus rotation occurred throughout all angles of knee flexion, with the maximal increase observed at 60 degrees. The posterolateral structures act as the primary restraint to varus rotation especially at lesser degrees of knee flexion (maximal restraint at 30 degrees). The PCL acts as secondary restraint that is most noticeable when the PLC is compromised. The PCL is more effective at resisting varus stresses at greater degrees of knee flexion (60 degrees). To a lesser degree, dynamic resistance to varus rotation is provided by the iliotibial band, biceps femoris muscle tendon complex, and lateral gastrocnemius.9
INTERNAL-EXTERNAL ROTATION
The popliteus complex is usually considered the primary restraint to external rotation of the knee. However, recent studies have shown that this function is shared by the FCL. In selective cutting studies, several authors have demonstrated that sectioning of the FCL, popliteus tendon, and deep ligaments of the lateral knee created increases in external rotation at all angles of knee flexion.22,28 Further studies have identified the specific roles of the FCL and the popliteus complex in resisting external rotation. In a recent cadaveric study, LaPrade et al30 found that the FCL resisted greater external rotation forces in the early range of knee flexion (0 to 30 degrees) when compared to the popliteus complex. The external rotation moment responses for the FCL were fairly constant from 0 to 60 degrees of knee flexion, averaging approximately 10 N/J. The mean load response peaked at 30 degrees of flexion (20 N/J) before falling to 8.1 N/J at 90 degrees of flexion. The popliteus tendon and popliteofibular ligament became more highly loaded by an external rotation torque with higher amounts of knee flexion. The popliteus tendon and the popliteofibular ligament had similar loading patterns to an external rotation torque, from 0 to 90 degrees of knee flexion. Their mean load response generally increased with increasing knee flexion, peaking to approximately 13 N/J at 60 degrees of knee flexion (FCL 10 N/J) before slightly declining to 10 N/J at 90 degrees.30 Therefore, the FCL is the primary restraint to external rotation from 0 to 30 degrees, whereas the popliteus complex (popliteus tendon and popliteofibular ligament) assumes a more important primary role in resisting external rotation at knee flexion angles greater than 60 degrees. The PCL is a secondary stabilizer in resisting external rotation of the tibia. Isolated sectioning of the PCL does not increase external tibial rotation when the PLC is intact. The role of the PCL as a secondary stabilizer becomes significant when the PLC is compromised. In a PCL-intact knee, isolated sectioning of the posterolateral structures increased external rotation of the lateral tibial plateau, with maximal external rotation (average 13 degrees) demonstrated at 30 degrees of knee flexion. At 90 degrees of flexion, a smaller amount (average 5.3 degrees) of external rotation was observed. Combined sectioning of the PLC and the PCL results in an increase in external rotation of the lateral tibial plateau at all angles of knee flexion, with a maximal increase noted at 90 degrees. As much as 20 degrees of increased external rotation can be appreciated at this degree of knee flexion.22,23 This is the basic science behind the external
tibial rotation test (or Dial test) commonly used to distinguish between isolated PLC injuries and combined PCL/PLC injuries.
Thus, the fibular collateral ligament is the primary restraint to external rotation at small degrees of knee flexion (30 degrees) and the popliteus complex is the primary restraint against external rotation at greater degrees of knee flexion (60 degrees). The PCL serves as a secondary restraint when the PLC is injured and is most effective at knee flexion angles of 90 degrees. These basic science studies have important clinical applications. Because isolated sectioning of the PCL does not increase external tibial rotation, any increased tibial external rotation should make a clinician suspicious of a PLC injury. In a combined PCL and PLC injury model, Harner et al29 biomechanically demonstrated that a deficiency of the posterolateral structures after PCL reconstruction increased external rotation up to 14 degrees. If the PLC is not reconstructed when the PCL is reconstructed, this resulting increased external rotation places the patient at increased risk of reinjury. Therefore, it is important to reconstruct the posterolateral complex in addition to the PCL to restore normal external tibial rotation restraints. The posterolateral structures play a small role in preventing primary internal rotation of the knee.31 Because there is a large amount of variability in internal rotation changes within ACL-intact and ACL-deficient knees, this particular knee instability has not demonstrated much clinical significance.
ARTICULAR CONTACT PRESSURES
The structures of the PLC are important in maintaining joint stability, which can have significant effects on articular contact pressures. Abnormal joint loading patterns and contact pressures can predispose a joint to degeneration. Sectioning the PCL and posterolateral structures has been shown to increase medial, lateral, and patellofemoral compartment contact pressures. 32 In a cadaveric biomechanical model of the knee, Skyhar et al,32 demonstrated that sequentially sectioning the PCL and then the posterolateral structures resulted in a significant increase in patellofemoral contact pressure at all angles of flexion. This finding is a result of 2 interrelated factors. First, with the loss of these structures, posterior tibial translation increases, thus, diminishing the moment arm of the patellar tendon. The angle between the quadriceps and patellar tendon decreases and creates an increase in the reaction force of the patellofemoral joint. This phenomenon is known as the ‘‘reverse Maquet’’ effect. Second, the quadriceps must exert a greater force because it is acting through a diminished lever arm. This increases articular contact pressures even more. The loss of ligamentous support creates instability so that the pressure is less likely to be distributed over the articular surface in a normal pattern. A combined PCL and PLC injury induces external rotation of the tibia on the femur, which creates aberrant medial and lateral contact pressures that are already elevated owing to the increase in quadriceps force. Several authors have postulated that this combined injury shifts the center of rotation further into the medial compartment, increasing shear and/or changing contact areas within these compartments during knee motion, ultimately, resulting in a varus-thrust gait pattern.32,33 The abnormal contact pressures seen in this combined injury may lead to premature degeneration of the joint and underscore the importance of the PLC in maintaining a healthy knee.
GRAFT RECONSTRUCTIONS
From a clinical standpoint, the PLC can have a significant effect on the survival of the native ACL and PCL. Studies have shown that sectioning of the FCL and surrounding posterolateral structures resulted in increased
stresses on the ACL with internal rotation and on the PCL with external rotation.24 Similar to the native ACL or PCL, the reconstructed ACL or PCL is at increased risk of failure in a knee with a deficient PLC. Studies have shown that sectioning the FCL and surrounding posterolateral structures results in increased
stresses on reconstructed ACL and PCL grafts.34,35 LaPrade et al34,35 have shown that coupled loading of varus and internal moments, at 0 and 30 degrees of flexion, significantly increased ACL graft forces. Furthermore, significantly increased forces were demonstrated within PCL grafts with varus and/or coupled external rotation at 30, 60, and 90 degrees of flexion. These studies affirm the recommendation to reconstruct the PLC in both isolated and combined injuries.
95% of the total restraint to posterior tibial displacement forces at all flexion angles.11,22 With the knee in near full extension, isolated sectioning of the posterolateral structures results in increased posterior translation of the lateral tibial plateau. As the knee is flexed to 90 degrees, there is minimal posterior translation. In PCL-deficient knees with transected posterolateral structures, posterior tibial translation of the medial and lateral tibial plateaus is appreciated at 30 and 90 degrees of flexion. Thus, the posterolateral structures are important in resisting posterior tibial translation at small flexion angles (eg, 30 degrees). The PCL and PLC structures work in concert, and injury to both of these structures results in a significant increase in posterior translation of the knee at all flexion angles.23,24
The popliteus is a dynamic stabilizer that assists the PCL by resisting posterior tibial translation. In the intact knee, loading the popliteus has been shown to reduce the in situ forces in the PCL by 9% and 36%, at 90 and 30 degrees of flexion, respectively.28 In the PCL-deficient knee, loading the popliteus has been shown to reduce posterior tibial translation by up to 36%. This amounts to a reduction of posterior translation by approximately 2 to 3 mm. The results of this study confirm that the popliteus muscle complements the PCL in resisting posterior tibial loads and can contribute to knee stability when the ligament in absent.27,28 In a combined PCL and PLC injury model, Harner et al29 demonstrated that a deficiency of the PLC increased posterior tibial translation, in the PCL reconstructed knee, by 4.6 to 6.0 mm. They found a corresponding increase in the in situ forces in the PCL graft of 22% to 150%, if the posterolateral structures were not
repaired or reconstructed. These results demonstrate that an isolated PCL graft reconstruction is rendered ineffective and may be overloaded if the posterolateral structures are deficient. Although the PCL provides the greatest contribution to resisting posterior tibial translation, both biomechanical and clinical studies have shown that it cannot function appropriately in a knee with a deficient PLC. Conversely, clinical studies have demonstrated that many individuals can function with an isolated rupture of the PCL, although their biomechanics may not be identical to that of a healthy knee. These studies demonstrate the importance of a fully functional PLC in resisting posterior tibial translation, and the necessity of repairing or reconstructing the PLC when it is compromised.
VARUS-VALGUS ROTATION
The FCL is the primary restraint to varus stress at all flexion angles of the knee. LaPrade et al30 found that varus forces on the FCL had loading responses from 0 to 90 degrees of flexion, with the greatest being at 30 degrees (12 N/J). Although other soft tissues provide additional support in this function, the FCL receives the least support at 30 degrees of flexion. This makes the FCL most susceptible to injury at 30 degrees of flexion. It has been shown that approximately 300N of force is required to cause failure of this ligament.17 The PCL is considered a secondary restraint to varus rotation; however, sectioning of this structure with an intact FCL does not affect varus rotation. Conversely, when the PLC is deficient and the PCL is intact, the PCL will provide some resistance to varus stress, but it is not as effective in this role as an intact PLC. In a combined PCL and PLC injury model, Harner et al29 demonstrated that a deficiency of the posterolateral structures after PCL reconstruction increased varus rotation up to 7 degrees. Grood et al23 and Veltri et al31 reported that an increase in varus rotation (as much as 19 degrees) can be appreciated with the combined sectioning of the PCL and posterolateral structures. This varus rotation occurred throughout all angles of knee flexion, with the maximal increase observed at 60 degrees. The posterolateral structures act as the primary restraint to varus rotation especially at lesser degrees of knee flexion (maximal restraint at 30 degrees). The PCL acts as secondary restraint that is most noticeable when the PLC is compromised. The PCL is more effective at resisting varus stresses at greater degrees of knee flexion (60 degrees). To a lesser degree, dynamic resistance to varus rotation is provided by the iliotibial band, biceps femoris muscle tendon complex, and lateral gastrocnemius.9
INTERNAL-EXTERNAL ROTATION
The popliteus complex is usually considered the primary restraint to external rotation of the knee. However, recent studies have shown that this function is shared by the FCL. In selective cutting studies, several authors have demonstrated that sectioning of the FCL, popliteus tendon, and deep ligaments of the lateral knee created increases in external rotation at all angles of knee flexion.22,28 Further studies have identified the specific roles of the FCL and the popliteus complex in resisting external rotation. In a recent cadaveric study, LaPrade et al30 found that the FCL resisted greater external rotation forces in the early range of knee flexion (0 to 30 degrees) when compared to the popliteus complex. The external rotation moment responses for the FCL were fairly constant from 0 to 60 degrees of knee flexion, averaging approximately 10 N/J. The mean load response peaked at 30 degrees of flexion (20 N/J) before falling to 8.1 N/J at 90 degrees of flexion. The popliteus tendon and popliteofibular ligament became more highly loaded by an external rotation torque with higher amounts of knee flexion. The popliteus tendon and the popliteofibular ligament had similar loading patterns to an external rotation torque, from 0 to 90 degrees of knee flexion. Their mean load response generally increased with increasing knee flexion, peaking to approximately 13 N/J at 60 degrees of knee flexion (FCL 10 N/J) before slightly declining to 10 N/J at 90 degrees.30 Therefore, the FCL is the primary restraint to external rotation from 0 to 30 degrees, whereas the popliteus complex (popliteus tendon and popliteofibular ligament) assumes a more important primary role in resisting external rotation at knee flexion angles greater than 60 degrees. The PCL is a secondary stabilizer in resisting external rotation of the tibia. Isolated sectioning of the PCL does not increase external tibial rotation when the PLC is intact. The role of the PCL as a secondary stabilizer becomes significant when the PLC is compromised. In a PCL-intact knee, isolated sectioning of the posterolateral structures increased external rotation of the lateral tibial plateau, with maximal external rotation (average 13 degrees) demonstrated at 30 degrees of knee flexion. At 90 degrees of flexion, a smaller amount (average 5.3 degrees) of external rotation was observed. Combined sectioning of the PLC and the PCL results in an increase in external rotation of the lateral tibial plateau at all angles of knee flexion, with a maximal increase noted at 90 degrees. As much as 20 degrees of increased external rotation can be appreciated at this degree of knee flexion.22,23 This is the basic science behind the external
tibial rotation test (or Dial test) commonly used to distinguish between isolated PLC injuries and combined PCL/PLC injuries.
Thus, the fibular collateral ligament is the primary restraint to external rotation at small degrees of knee flexion (30 degrees) and the popliteus complex is the primary restraint against external rotation at greater degrees of knee flexion (60 degrees). The PCL serves as a secondary restraint when the PLC is injured and is most effective at knee flexion angles of 90 degrees. These basic science studies have important clinical applications. Because isolated sectioning of the PCL does not increase external tibial rotation, any increased tibial external rotation should make a clinician suspicious of a PLC injury. In a combined PCL and PLC injury model, Harner et al29 biomechanically demonstrated that a deficiency of the posterolateral structures after PCL reconstruction increased external rotation up to 14 degrees. If the PLC is not reconstructed when the PCL is reconstructed, this resulting increased external rotation places the patient at increased risk of reinjury. Therefore, it is important to reconstruct the posterolateral complex in addition to the PCL to restore normal external tibial rotation restraints. The posterolateral structures play a small role in preventing primary internal rotation of the knee.31 Because there is a large amount of variability in internal rotation changes within ACL-intact and ACL-deficient knees, this particular knee instability has not demonstrated much clinical significance.
ARTICULAR CONTACT PRESSURES
The structures of the PLC are important in maintaining joint stability, which can have significant effects on articular contact pressures. Abnormal joint loading patterns and contact pressures can predispose a joint to degeneration. Sectioning the PCL and posterolateral structures has been shown to increase medial, lateral, and patellofemoral compartment contact pressures. 32 In a cadaveric biomechanical model of the knee, Skyhar et al,32 demonstrated that sequentially sectioning the PCL and then the posterolateral structures resulted in a significant increase in patellofemoral contact pressure at all angles of flexion. This finding is a result of 2 interrelated factors. First, with the loss of these structures, posterior tibial translation increases, thus, diminishing the moment arm of the patellar tendon. The angle between the quadriceps and patellar tendon decreases and creates an increase in the reaction force of the patellofemoral joint. This phenomenon is known as the ‘‘reverse Maquet’’ effect. Second, the quadriceps must exert a greater force because it is acting through a diminished lever arm. This increases articular contact pressures even more. The loss of ligamentous support creates instability so that the pressure is less likely to be distributed over the articular surface in a normal pattern. A combined PCL and PLC injury induces external rotation of the tibia on the femur, which creates aberrant medial and lateral contact pressures that are already elevated owing to the increase in quadriceps force. Several authors have postulated that this combined injury shifts the center of rotation further into the medial compartment, increasing shear and/or changing contact areas within these compartments during knee motion, ultimately, resulting in a varus-thrust gait pattern.32,33 The abnormal contact pressures seen in this combined injury may lead to premature degeneration of the joint and underscore the importance of the PLC in maintaining a healthy knee.
GRAFT RECONSTRUCTIONS
From a clinical standpoint, the PLC can have a significant effect on the survival of the native ACL and PCL. Studies have shown that sectioning of the FCL and surrounding posterolateral structures resulted in increased
stresses on the ACL with internal rotation and on the PCL with external rotation.24 Similar to the native ACL or PCL, the reconstructed ACL or PCL is at increased risk of failure in a knee with a deficient PLC. Studies have shown that sectioning the FCL and surrounding posterolateral structures results in increased
stresses on reconstructed ACL and PCL grafts.34,35 LaPrade et al34,35 have shown that coupled loading of varus and internal moments, at 0 and 30 degrees of flexion, significantly increased ACL graft forces. Furthermore, significantly increased forces were demonstrated within PCL grafts with varus and/or coupled external rotation at 30, 60, and 90 degrees of flexion. These studies affirm the recommendation to reconstruct the PLC in both isolated and combined injuries.
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