Author's Accepted Manuscript

Anatomy and biomechanics of the posterior cruciate

ligament and posterolateral corner
David Barba MD, Lloyd Barker PAC, ATC, MBA,
Anikar Chhabra MD MS

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PII: S1060-1872(15)00081-7
DOI: http://dx.doi.org/10.1053/j.otsm.2015.06.007
Reference: YOTSM50513

To appear in:
Oper Tech Sports Med

Cite this article as: David Barba MD, Lloyd Barker PAC, ATC, MBA, Anikar Chhabra MD
MS, Anatomy and biomechanics of the posterior cruciate ligament and posterolateral
corner,
Oper Tech Sports Med , http://dx.doi.org/10.1053/j.otsm.2015.06.007

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 Anatomy and Biomechanics of the
Posterior Cruciate Ligament and
Posterolateral Corner

Operative Techniques in Orthopedics:

PCL and Posterolateral Corner
Instability of the Knee

Corresponding Author:
Anikar Chhabra, MD MS
Dept of Orthopedics
5777 East Mayo Blvd
Phoenix, AZ 85854

David Barba, MD
Fellow, Orthopedic Sports Medicine
TOCA/Banner Good Samaritan Sports Medicine Fellowship
 Phoenix, Arizona

Lloyd Barker, PAC, ATC, MBA

Department of Orthopedic Surgery
Mayo Clinic Arizona
Assistant Professor of Orthopedics, Mayo College of Medicine
Phoenix, AZ

Anikar Chhabra, MD MS
Department of Orthopedic Surgery
Mayo Clinic Arizona
Assistant Professor of Orthopedics, Mayo College of Medicine
Head Team Orthopedic Surgeon: Arizona State University
Phoenix, AZ

Abstract

The knowledge and understanding of the anatomy and biomechanical function of the

posterior cruciate ligament (PCL) and posterolateral corner (PLC) of the knee is vitally important

when evaluating injury and considering reconstruction. The PCL and PLC both have important

roles to play in the stability of the knee. Through numerous experimental designs, the

biomechanical roles of the PCL and PLC have been clarified. The PCL’s most well defined role is

as a primary restraint and stabilizer to posterior stress. It appears this role is greatest at higher

degrees of knee flexion. The natural history of a PCL deficiency leads to increased contact

pressures and degeneration of both the medial and patellofemoral compartments. The PLC is a
restraint to posterior translation, posterolateral rotation, external rotation and varus loads. It is

important to recognize a PLC injury prior to cruciate ligament reconstruction, since a failure to

diagnose may lead to subsequent graft rupture. Poor surgical outcomes after PCL

reconstruction have been attributed to many factors, the most common of which include:

additional intra-articular pathology, poor fixation methods, insufficient knowledge of PCL or PLC

anatomy leading to improper tunnel placement, and poor surgical candidates. In this article we

attempt to provide a framework for understanding the anatomy and biomechanics of the PCL

and PLC and their surgical implications.

Keywords (7-10 words)

Posterior Cruciate Ligament (PCL), Posterior Lateral Corner (PLC), Popliteofibular Ligament

(PFL), Popliteus Muscle-Tendon Complex (PMTC), Anatomy, MRI, Biomechanics, Lateral

Collateral Ligament (LCL), Knee Instability, Proprioception, Biceps Femoris, Lateral

Gastrocnemius

Overview

The knowledge and understanding of the complex anatomy and biomechanical function

of the native posterior cruciate ligament (PCL) and the posterolateral corner (PLC) is vitally

important when evaluating a knee injury and considering reconstruction.1 Since injuries to the

posterolateral corner are not as frequent as those to the cruciate ligaments or medial

structures of the knee, there is often a delay to diagnosis. PLC injuries, however, typically occur

in combination with either one or both cruciate ligaments, but isolated injuries to the PLC do
occur. DeLee et al. found that only 12 out of 735 (1.6%) knees undergoing ligamentous

treatment were due to acute isolated PLC injury.2 If left untreated, PLC injuries can lead to

residual symptoms of instability, articular cartilage degeneration and failure of cruciate

ligament reconstructions.3, 4 This chapter serves as a foundation for understanding the complex

anatomy and biomechanics of the PCL and PLC, which can help aid in diagnosis and treatment.

Anatomy

We first will describe the gross and microscopic anatomy of the PCL, and then describe each

component of the PLC. The main components of the PLC include the iliotibial tract, biceps

femoris, lateral collateral ligament, popliteus muscle-tendon complex (PMTC), popliteofibular

ligament (PFL), fabellofibular ligament and the arcuate ligament. Other smaller contributors

include the popliteotibial fascicle, popliteomeniscal fascicles, middle third of the lateral

capsular ligament, posterior horn of lateral meniscus, coronary ligament, and the posterolateral

part of the joint capsule. In an effort to categorize these structures, Seebacher et al. 5 divided

the lateral structures of the knee into 3 layers, from superficial to deep. Layer I contains the

iliotibial tract and the superficial biceps femoris. Layer II contains the quadriceps retinaculum

anteriorly and the patellofemoral ligament posteriorly. Layer III being the deepest and most

important is further divided into superficial and deep lamina by the lateral geniculate artery

running between the two layers. The superficial lamina includes the LCL and fabellofibular

ligament and the deep lamina contains the coronary ligament, the popliteus tendon,

popliteofibular ligament, the capsule and the arcuate ligament.5

Posterior Cruciate Ligament (PCL)

The PCL is named due to its insertion on the posterior aspect of the proximal tibia, and is

the largest of the intrarticular ligaments. The PCL originates from a broad, concave, semicircular

area along the medial femoral condyle within the intracondylar notch. The PCL inserts into a

depression known as the posterior intercondyloid fossa or PCL fossa, just inferior to joint line,

between the two tibial plateaus, and posterior to the tibial spine (Figure 1).6 The PCL consists

of longitudinally oriented collagen fibers which is narrowest in its middle portion and fans out

superiorly and to a lesser extent inferiorly.7 The fibers of the PCL attach to the femoral

footprint in a lateral to medial orientation and to the tibial footprint in an anterior to posterior

orientation. Average length of the PCL is 38 mm and the average width within the middle

portion is 11 mm.1,7,8 The PCL has a wide variation in shape and size of its femoral

attachments, due to variation in intercondylar notch sizes, whereas the tibial attachments size

and shape are more consistent.9 The substance of the ligament is made up of two distinct but

inseparable bundles that allow for resistance of posterior translation in both extension and

flexion. The bundles are named by their position within the femoral footprint/attachment;

anterolateral bundle & posteromedial bundle (Figure 2). To help identify these bundles during

dissection or arthroscopy, other anatomical landmarks have been identified.

On the femoral side, the medial intercondylar ridge defines the proximal limit of the

insertion of the PCL, whereas the medial bifurcate ridge separates the insertion sites of the two

bundles. 10 (Figure 3B) There is a change in slope as each bundle approaches the femoral

insertion site, putting the bundles in different planes when the knee is flexed. The PCL
footprint on the femur is made up of approximately 55% anterolateral bundle and 45%

posteromedial bundle. The mean distance between the centers of the anterolateral and

posteromedial bundles on the femur is 12.1 mm. The distal margins of the anterolateral and

posteromedial bundles is a mean 1.5 mm and 5.8 mm proximal to the notch articular cartilage,

respectively.11 While the femoral footprint size is nearly equal between the two bundles, the

anterolateral bundle’s cross sectional area is significantly larger than the posteromedial bundle.

The PCL is stronger than the medial collateral and anterior cruciate ligaments, with the

anterolateral bundle providing the major contribution to PCL strength.12

The tibial insertions of the anterolateral and posteromedial bundle occur within the PCL

fossa which is trapezoidal in shape and becomes wider inferiorly. (Figure 3A) The anterolateral

bundle is attached at the superolateral aspect of the footprint and the posteromedial bundle is

seen in the inferomedial portion of the fossa. Identification of each bundle is made easier with

each bundle attachment having separate slopes. Across 21 knees, this change in slope angle

was found to be an average of 14.5°.13 Also, an extensive portion of the posteromedial bundle

is below the posterior part of the tibial rim, whereas none of the anterolateral bundle

attachment is below the tibial rim. The superolateral and superomedial corners of the footprint

were both represented by depressions and a reproducible ridge represented the inferior

border, all of which could be identified with arthroscopy.14 The average length and width of

the anterolateral tibial insertion site is 7.8 mm and 9.2 mm, respectively. The posteromedial

tibial insertion site average length and width is 9.4 mm and 15.0 mm, respectively.13
Menisci attachments in relation to the PCL

Johannsen et al, analyzed the posterior root attachments of the medial and lateral

menisci, quantifying their position in relation to the PCL (Figure 4).15 The lateral meniscus

posterior root attachment center was 4.3 mm medial to the lateral tibial plateau articular

cartilage edge and directly 12.7 mm to the most anterior edge of the PCL tibial attachment.15

The medial meniscus posterior root attachment center was 9.6 mm posterior and 0.7 mm

lateral from the medial tibial eminence, and 8.2 mm anteromedial from the PCL. This anatomy

is very important during PCL reconstruction as non-anatomic tunnel placement may

compromise the meniscal root attachment.15

Meniscofemoral ligaments

The meniscofemoral ligaments are two distinct structures with variable incidence that run

from the posterior horn of the lateral meniscus to the lateral aspect of the medial femoral

condyle. The ligaments are named based on their location in relation to the PCL. The anterior

meniscofemoral ligament is also known as the ligament of Humphrey, while the posterior

meniscofemoral ligament is also known as the ligament of Wrisberg.16 (Figure 5 A and B) The

anterior meniscofemoral ligament is sometimes confused for the PCL during arthroscopy; albeit

less than 1/3 the diameter of the PCL. The posterior meniscofemoral ligament can be nearly 1/2

the size of the PCL. Tugging on either of the meniscofemoral ligaments should reveal obvious

motion of the lateral meniscus and thus will help you to identify it from the PCL. Studies

looking at cadaver knees found the presence of either the anterior or posterior meniscofemoral
ligaments in approximately 70% of the knees.16 Anderson et al. found that in those knees

where both meniscofemoral ligaments were present, the posterior meniscofemoral ligament,

posteromedial bundle, and anterior meniscofemoral ligament were aligned parallel to each

other, proximally to distally.11 The posterior meniscofemoral origin is proximal to femoral PCL

attachment and it inserts onto posterior aspect of the lateral meniscus beneath the popliteal

hiatus aperture, therefore, it also has a contribution to the posterolateral corner stability.17

There are no attachments from the PCL to the medial meniscus.

Anatomy of PLC components (Figure 6)

Layer I

Iliotibial band (ITB)

The ITB originates from the femoral supracondylar tubercle and inserts onto Gerdy’s

tubercle on the tibia. The superficial layer of the ITB forms Seebacher’s layer I anterior to the

intermuscular septum.5 The deep layer of the iliotibial band attaches to the lateral

intermuscular septum of the distal femur. Even deeper, the capsule-osseous layer of the ITB is

found, which also extends from the region of the lateral intermuscular septum, blends with a

confluence from the short head of the biceps femoris, and attaches just posterior to Gerdy’s

tubercle.5,18

The ITB functions as a lateral compartment stabilizer and as an secondary stabilizer to

anterior translation of the tibia.19 During flexion the ITB externally rotates the tibia and pulls it

posteriorly. It also functions to reduce a posteriorly subluxated tibia during a reverse pivot shift

test examination maneuver. The ITB is typically spared in PLC injuries due to a varus load on a
fully extended leg, since the ITB moves anteriorly with extension. During the pivot shift test, the

ITB improves tibial reduction at high flexion angles while not affecting subluxation at low

flexion angles.19

Biceps Femoris

The biceps femoris has two heads of origin. The long head arises in common with the

semitendinosus muscle from the ischial tuberosity and the inferior aspect of the sacrotuberous

ligament, crosses the sciatic nerve from the medial to lateral side, and then fuses with the short

head that arises from the lateral aspect of the linea aspera, proximal two-thirds of the

supracondylar line, and the lateral intermuscular septum. The distal insertion of the long head

and short head of the biceps femoris at the knee is far more complex. According to Terry and

LaPrade, the components of the long head of the biceps femoris muscle include a reflected

arm, a direct arm, an anterior arm, and a lateral and anterior aponeurosis.20 The short head of

the biceps femoris tendon has a proximal attachment to the long head’s tendon, a capsular

arm, a confluence of the biceps and capsule-osseous layer of the iliotibial tract, a direct arm, an

anterior arm, and a lateral aponeurosis.20 Tubbs et al. found the attachments of the biceps

femoris to include the lateral condyle of the femur, lateral tibial condyle, fibular head, crural

fascia, popliteus tendon, and arcuate popliteal ligament.21

The biceps femoris functions to extend at hip joint, flex at knee joint as well as laterally

rotate the tibia, and has been shown to display increased activity in ACL-deficient knees.19, 22 It

serves as an important dynamic stabilizer of the knee. The multiple attachment sites for the

biceps femoris muscle may increase the stability of the lateral knee. Considering this
attachment to the popliteus tendon, Tubbs et al. deduced that the synergistic action between

the biceps femoris (external rotator of tibia) and the popliteus muscle (internal rotator of tibia)

is important in the stability of the knee.21 The biceps femoris also tensions the LCL while the

knee continues to flex, further stabilizing the knee.21 Tears of the biceps femoris may be

associated with anterolateral-anteromedial rotatory instability of the knee joint.

Layer II

The quadriceps retinaculum and patellofemoral ligament both lie anterior to the midpoint of

the knee and do not contribute significantly to stability of the PLC or lateral side. 5

Layer III, superficial lamina

Lateral (Fibular) Collateral Ligament (LCL)

Femoral attachment is triangular, located in a fovea, posterior (3.1 mm) and proximal

(1.4 mm) to the ridge of the lateral femoral epicondyle.17,18,23 It then inserts onto the

superiorly and laterally facing V-shaped plateau on the lateral aspect of fibular head, just

anterior and distal to the styloid process.17,18,23 (Figure 7) It has a round and well-defined origin

with a distal fan-shaped morphology that blends with the attachment of the biceps femoris

tendon.20 The fibular attachment site is 8.2 mm (range, 6.8 to 9.7) posterior to the anterior

margin of the fibular head and 28.4 mm (range, 25.1 to 30.6) distal to the tip of the fibular

styloid process.18 The LCL is the smallest of the 4 major knee ligaments. The average length of

the LCL is approximately 70 mm (range, 62.6-73.5).24 The cross-sectional area of the LCL

attachment site on the femur is approximately 0.45 cm2 (range 0.43, to 0.52).17, 28 The fibular
attachment cross-sectional area is approximately 0.43 cm2 (range, 0.39 to 0.50).18 The average

distance between the attachment of the LCL and the popliteus tendon on the femur was 18.5

mm (range, 16.8 to 22.9).18

The LCL functions primarily as a static and dynamic stabilizer to varus forces along all

ranges of motion. It is taut in full extension and becomes lax after flexion beyond 30 degrees.24-
26
The LCL is also dynamically controlled by the biceps femoris during flexion and acts

secondarily to limit external rotation.17 It resists external rotation with the knee near extension,

whereas the popliteus complex and popliteofibular ligament have more important roles in

resisting external rotation with increasing knee flexion.23,24,27 In a cadaver study by Gollehon,

isolated sectioning of the LCL caused only a small increase in laxity from 1º to 4º in varus

rotation at all angles of knee flexion.25 This is because the remaining intact PLC structures

afford some stability against varus forces. Injury to the LCL usually occurs as a soft-tissue

avulsion off the proximal attachment on the femur or as a bone avulsion associated with an

arcuate fracture of the fibular head.23,28 (Figure 8)

Fabellofibular Ligament

The fabellofibular ligament has its origin on the lateral aspect of fabella and the

posterior portion of the supracondylar process of the femur. It inserts on the posterior and

lateral edge of the fibular styloid process and blends posteriorly with the fibers of the arcuate

ligament.17,29 The fabellofibular ligament has a length of 33 ± 4mm and a diameter of 4 ±1

mm.17 It tends to have a variable occurrence, depending on the presence of a fabellae. 30 In a

cadaveric study of knees by Sudasna and Harnsiriwattanagit the fabellofibular ligament was

identified in 36 of 50 knees (72%).30 In 34 of these knees the fabella was present, and in the
other 2 absent. In the knees with an absent fabella, the ligaments were wider 4.3-4.7 mm

compared to about 2.8 mm in fabella present knees.30 If no fabella is present, the

fabellofibular ligament arises from the posterior aspect of the supracondylar process of the

femur. The fabellofibular ligament becomes tight in extension and serves as a capsular

reinforcement. It does not play a severe role as a static stabilizer of the knee.

Layer III, deep lamina

Popliteus muscle tendon complex (PMTC)

The PMTC has a broad muscular origin at the posteromedial surface of the

proximal tibial metaphysis. It then courses around the lateral side of the knee through an

opening in the coronary ligament (popliteal hiatus) behind the lateral meniscus and deep to the

LCL. It subsequently inserts into the proximal half and anterior one fifth of the popliteus sulcus

of the femur.17 ,18 The average cross-sectional area of the femoral attachment is 0.59 mm2

(range, 053 to 0.62).18 The popliteal tendon footprint is about 10 mm anteroposterior and

about 6 mm superoinferior.17 The length of tendon is 54.5 mm (range 50.5 to 61.2) from the

musculotendinous junction to the femoral attachment.18 The average diameter is 8.40 ±1.31

mm.17

Three popliteomeniscal fascicles (sometimes referred to as ligaments) extend from the

popliteus tendon to the lateral meniscus. The popliteomeniscal fascicles originate at the

anterior surface of the popliteal tendon at the level of the posterior transition between joint

cartilage and tibia bone. The posterosuperior fascicle attaches to the upper border of the

posterior horn of the lateral meniscus. The anteroinferior fascicle attaches to the bottom edge
of the posterior horn of the lateral meniscus and blends into the popliteofibular ligament.31

The third fascicle is the posteroinferior and it attaches to the inferior margin of the posterior

horn of the lateral meniscus.32 The popliteomeniscal fascicles functions to connect the inferior

surface of the lateral meniscus to the articular cartilage border of the lateral tibial plateau,

thereby providing stability to the lateral meniscus.32,33 The popliteomeniscal fascicle

attachments also help to prevent lateral meniscal entrapment during knee flexion. 33

The popliteus muscle tendon complex provides both dynamic and static stability to the

PLC of the knee. It functions as a weak knee flexor and also reinforces the posterior third of the

capsule. The PMTC unlocks the fully extended knee by internally rotating the tibia around the

femur, and also restrains posterior translation and external rotation and varus rotation of the

knee. It is an important structure preventing external rotation and posterior translation of the

lateral tibial plateau from a slightly flexed position to about 90° of flexion.30 LaPrade et al.

established that at an average of 112° of knee flexion, the popliteus tendon fell into the

popliteal sulcus and remained in the sulcus with further knee flexion; it anteriorly subluxated

out of the sulcus when the knee was extended past this position.18 The popliteus tendon

attachment on the femur was always anterior to the fibular collateral ligament femoral

attachment. The average distance between the fibular collateral ligament and the popliteus

tendon femoral attachments was 18.5 mm.18

Popliteofibular ligament (PFL)

Present in 94-100% of knees, the PFL originates at the popliteal musculotendinous

junction along the anterior aspect of the lateral femoral condyle17,34 and inserts on the deep

portion of the posterosuperior aspect of the styloid process with a fan shaped footprint that is

angled distolaterally to its attachment on the fibula.17,18 In relation to other PLC structures, the

PFL is described as posterior, medial and proximal to the LCL fibular attachment and distal,

posterior and medial to the tip of the fibular styloid process. Sugita and Amis revealed that the

PFL has a load to failure of 186 N compared with 309 N for the LCL.23 Three morphologic

variations have been described with respective frequency of occurrence: singular bundle (60%),

double ligament (26.7%), and a Y-shaped ligament (13.3%).17 Average length is 14.06 ±3.2 mm

anterior and 12.45 ±2.21 mm posterior.17 The posterior division was consistently larger than

the anterior division.18 Average width of about 7 mm.17 In cross-sectional area, the PFL is only

slightly smaller than the LCL.35 The PFL is a strong, direct attachment of the popliteus tendon to

the fibula, with a mean width of 9.3 mm (range, 3.8 to 16.4 mm) at the fibular origin.34-36 The

PFL functions as a direct static stabilizer with its attachment of the femur to the tibia and shares

the resistance to posterior tibial translation and external and varus rotation. 23 The PFL is better

oriented than the LCL to resist external rotation at all flexion angles.
Arcuate Ligament Complex (ALC) (aka arcuate popliteal ligament or short lateral ligament)

The Arcuate Ligament Complex has its origin at the posterior capsule and the lateral

femoral condyle forming a triangular thickening of the posterior capsule and then inserting

onto the lateral edge of the fibular styloid process, just lateral to PFL attachment. Fibers from

the popliteus muscle blend into the ascending limb of the arcuate ligament. The arcuate

ligament is a narrow and thin fiber in about 60% of knees. In relation to other structures, the

arcuate ligament crosses superficial to the popliteus tendon and and deep to the Oblique

Popliteal Ligament (OPL). It is always posterior and deep to the fabellofibular ligament. In a

cadaveric study of knees by Sudasna and Harnsiriwattanagit, the arcuate ligament was

identified in 12 of 50 knees (24%).30 When the arcuate ligament was present it covered the

origin of the popliteus. The function of the arcuate ligament is to stabilize against

hyperextension and also serves as a capsular reinforcement.30 It does not play a severe role as

a static stabilizer of the knee. The arcuate ligament, like the fabellofibular ligament are of

variable size and are not uniformly present in all knees.5, 34, 37

Capsule

The posterior joint capsule runs in near continuation with the PCL. The posterior joint

capsule originates above the femoral condyles and extends distally to the posterior margin of

the tibial plateau. The posterior capsule is within 1-2 mm of the posterior aspect of the tibial

attachment of the PCL. The anterior wall of the popliteal artery lies approximately 7-10mm

from the posterior border of the PCL at 90° of flexion.1 Matava et al. found the distance

between the PCL and popliteal artery was maximal at 100° of knee flexion, with measurements
of 9.9 mm in the axial plane and 9.3 mm in the sagittal plane, using MRI.38 There is an anterior

septum between the capsule and PCL that is made up of fatty tissue wrapped in a thin synovial

membrane which creases a triangular thickening. In the upper third of this tissue is the entry

point for the bundle of the middle genicular artery, above the oblique popliteal ligament.

The mid-third lateral capsular ligament is a thickening of the lateral joint capsule and

contributes to the PLC.15 This ligament arises from the femur, has attachments to the lateral

meniscus, and then courses to the tibia. The tibial attachment is from just posterior to Gerdy’s

tubercle to the popliteal hiatus. The posterior part of the lateral capsule is reinforced by the

arcuate ligament and the fabellofibular ligament.29

Meniscotibial (Coronary) Ligament

The meniscotibial or coronary ligament serves as a capsular attachment from the lateral

edge of the lateral meniscus to the lateral tibial condyle that functions to secure the posterior

horn of the lateral meniscus.2 It may be injured with excessive rotation of the tibia. Rupture of

the coronary ligament may lead to increased mobility of the lateral meniscus, posterior knee

pain, and a gap in the posterior capsule.39

Other Associated PLC Structures

Lateral Gastrocnemius tendon

The lateral gastrocnemius tendon originates near the supracondylar process of the distal

femur. In relation to the posterolateral corner, the lateral gastrocnemius tendon blends with

the arcuate ligament and the lateral capsular thickening. At the level of the fabella, it becomes

adherent and inseparable from the meniscofemoral portion of the lateral capsule proximal to

the fabella.18,37 The lateral gastrocnemius tendon is rarely avulsed in posterolateral knee

injuries.33,40 Therefore, it has been included in surgical reconstructions such as advancement

procedures,3 and also as a referencing structure for identifying other posterolateral knee

structure attachment sites.28 According to LaPrade et al. the average attachment of the lateral

gastrocnemius tendon is 13.8 mm (range, 11.3 to 16.4) posterior to the fibular collateral

ligament attachment on the femur.9 The distance from the lateral gastrocnemius tendon

femoral attachment to the popliteal tendon femoral attachment is about 28.4 mm (23.1 to 36.3

mm).18

Oblique Popliteal Ligament (OPL)

The OPL originates from the posterior surface of tibial head and blends with fibers from

the semimembranosus tendon. It courses through the upper margin of the intercondylar fossa

and the posterior surface of the femur with eventual blending into the posterior capsule. It has

an arch-shaped structure within the posterolateral capsule. It has a length of 45 ± 4 mm and

width of 15 ± 4 mm.17 According to the Osti M et al. cadaveric study, this structure is present

in 36.6% of knees.17

Meniscofibular Ligament

Natsis et al. evaluated 21 unpaired cadaveric knee joints and found a 100% incidence of

a meniscofibular ligament (MFL).41 The MFL directed backwards, outwards, and inferiorly

anchored to the head of the fibula with the knee fibrous capsule attaching just proximal to the

fibular head. It has a mean thickness 3.84 mm (range 2.6-6.1 mm).42 The MFL reinforces the

lateral coronary ligament. With knee motion, the MFL was tense during knee extension and

external rotation of the tibia.41 The MFL could therefore play a role in protecting the lateral

meniscus from potential ruptures during terminal knee extension.41

Vascular Supply to the PCL and PLC

The vascular supply to the PCL comes from the middle genicular artery, a branch of the

popliteal artery. The thin synovial sheath vessels that surround the cruciate ligaments are also

seen in the fat pad, and are major vascular contributors.43 These end arteries appear to branch

from the middle genicular artery.44 The middle geniculate artery and the small branches off of

the popliteal artery also supply the posterior capsular region.44, 45 These capsular vessels then

supply distal portions of the PCL.46

The vascular supply to the PLC also comes from branches of the popliteal artery. The

lateral superior geniculate artery is divided into three branches. The articular branch supplies

the lateral collateral ligament and the lateral region of the knee. This branch anastomoses with
the ascending branch of the lateral inferior geniculate artery that runs anteriorly, deep to the

lateral collateral ligament.29, 45 Additional contributions come from the posterior tibial

recurrent artery that divides into smaller branches to supply the popliteus muscle, the tibial

condyle, and the joint area superior to the fibular head.45

Innervation to the PCL and PLC

The PCL and PLC have many types of innervation including named and unnamed nerves,

free nerve endings, and mechanoreceptors. The popliteal plexus, formed by the posterior

articular nerve (tibial n.) and the terminal portions of the obturator nerve, supplies the PCL and

its synovial sleeve, the outer part of the lateral meniscus and the posterolateral part of the

capsule.47,48 The superior part of the lateral capsule is supplied by the terminal portion of the

nerve to the vastus lateralis, and the inferior part of the lateral capsule is innervated by the

lateral articular nerve.48,49 Free nerve-endings, which are widely distributed throughout most

of the articular tissues, are non-adapting pain receptors that respond to mechanical

deformation or inflammatory mediators.49,50 Mechanoreceptors found within the capsule,

meniscus, and ligaments play an important role in proprioception.47,50 Ruffini corpuscles (type

I, pressure receptors), Pacinian corpuscles (type II, velocity receptors), free nerve endings (type

IV, pain receptors), and Golgi-tendon organ apparatus have all been identified within these

tissues.50,51 Thus, injury to the PCL or PLC not only creates a mechanical disturbance but also a

neurologic one by severing the afferent signals to the central nervous system.8
Biomechanics of the PCL

Over the past 30 years, many authors have studied the biomechanical role of the PCL.

Studies have included: cadaveric sectioning studies, comparison studies with PCL-deficiency in

one knee and a normal contralateral knee, as well as contact pressure studies and kinematic

analysis.

Posterior Tibial Translation

In vitro studies reaffirm the role the PCL has in preventing posterior tibial translation,

however, controversy still exists as to the relative translational stability provided by the PCL at

varying angles of knee flexion. Kumagai et al. conducted translational measurements in the

anterior to posterior plane on five cadaveric specimens before and after PCL sectioning. 52 They

found no difference in posterior translation at angles less than 25o of knee flexion, while

displacement increased significantly between 25o to 90o of flexion, averaging >10mm of

posterior translation at 90o of flexion.52 In contrast, Li et al. examined 8 cadaveric knees and

found that in PCL deficient knees, posterior tibial translation only occurred above 60 o; this was

reaffirmed by Pearsall et al. where 8 cadaveric knees were examined with strain gauges in

either meniscus to measure strain in the menisci in varying degrees of flexion in the PCL intact,

ruptured, and reconstructive states.53,54 They found that in scenarios where the PCL was cut,

the total anterior-posterior translation was >18 mm and was statistically significant compared

to the intact and reconstructive PCL states at knee flexion angles of 60o and 90o.54
 However, other authors have shown increased posterior tibial displacement in PCL

deficient knees throughout the arc of motion (0-120o).25,55–58 Gollehon et al. tested the static

stability of the PCL and the PLC structures in a sectioning study of 17 human cadaveric knee at

knee flexion angles between 0o to 90o.25 They found that at all angles of flexion, the PCL was

the principle restraint to posterior translation and that at all angles tested, isolated sectioning

of the PCL did not affect varus or external rotation stability.25 Similarly, Li et al. examined 12

fresh frozen cadaveric knees using a robotic testing system and applied a 130 Newton

posteriorly-directed load at 30o increments between 0o and 150o; they found statistically

significant posterior tibial translation at all knee flexion angles except 150 o, indicating the role

of the PCL in posterior stability except for at extreme flexion angles.55 Hagemeister et al.

reaffirmed the importance of the PCL in providing posterior stability at low flexion angles when

they looked at 5 pairs of fresh frozen cadaveric knees with a mean age of 73.2 years and used

electromagnetic sensors to effectively examine the translation caused by sectioning of the PCL

and posterolateral corner structures.56 Statistically significant differences in anterior-posterior

translation existed at all 15o intervals measured from 0o to 75o.56 Grood et al. also looked at the

effect of tibial translation at low flexion angles of the knee using 15 whole lower limb cadavers

and found that sectioning of the PCL did produce posterior tibial sag even at full extension;

however, the posterior translation was most apparent at 90 o of flexion (the highest flexion

angle they measured) where it averaged 11.4 mm of posterior displacement.57 Finally, Hoher

et al. examined 8 cadaveric knees using a universal force-moment sensor (UFS) testing system

to apply a 110 Newton load to the knee at 0o/30o/60o/75o/90o.58 They found that with the
application of the load, even at full extension there was a difference in posterior tibial

translation of 3.0 mm, which progressively increased to 14.1 mm at 90o of knee flexion.58

In addition, in vivo studies examining the posterior tibial translation of PCL deficient

knees also exist. Castle et al. examined posterior tibial translation at varying degrees of knee

flexion in 10 patients with unilateral PCL deficiency using lateral radiographs.59 They found

that at knee flexion angles between 70o to 90o, the mean displacement of the tibia posteriorly

was 7.4 mm, while knee flexion angles between 30o to 50o resulted in a mean displacement of

just 2.1 mm.59 Furthermore, displacement at lower flexion angles was not uniform.

Assimilation of the data available in all of these studies would suggest that the PCL is the

primary restraint to posterior translation of the knee and that although it likely has an effect

throughout the functional arc of motion, its effect is likely greatest at high angles of knee

flexion (60o - 120o).

Rotational & Medial/Lateral Stability

The role that the PCL plays in providing rotational stability to the knee is still unclear.

Many reports exist throughout the literature that show isolated sectioning of the PCL does not

significantly affect tibial external rotation. Gollehon et al. sectioned the PCL in 17 cadaveric

specimens and showed that external rotation or varus stress did not increase at any position of

knee flexion.25 Nielsen et al. evaluated 25 osteoligamentous intact cadaveric knees and

performed sectioning of the PCL along with the medial and lateral structures. 60 They found

that axial rotatory instability was only detectable when the PCL lesion was combined with

either a medial or lateral side ligamentous injury; furthermore, a reverse pivot shift was only
elicited when the PCL/LCL/popliteus tendon were sectioned.60 Finally, Kaneda et al. looked at

15 cadaveric fresh frozen knees and performed sequential sectioning of the PCL, LCL, and

posterolateral structures and found that in isolated sectioning of the PCL, there was no increase

in tibial external rotation; however, they did find that isolated sectioning of just the

anterolateral bundle of the PCL shifted the axis of external rotation of the knee. 61

This is in contrast to four other studies, all which showed that isolated sectioning of the

PCL does lead to increased tibial rotation. Li et al. examined 8 cadaveric knees using a robotic

testing system with applied simulated quadriceps and hamstring loads (400N and 200N,

respectively) at knee flexion angles from 0-120o and found that at angles above 60o significant

external tibial rotation occurred.53 Harner et al. performed an investigation using 10 cadaveric

knee specimens where simulated popliteus muscle contraction was performed in both the

presence and absence of the PCL.62 They found that simulated popliteus muscle contraction

resulted in an internal tibial rotation of 2o and 4o at 60o and 90o of knee flexion, regardless of

whether or not the PCL was intact.62 Gupte et al. used 8 cadaveric knees to evaluate the role

of the meniscofemoral ligaments in providing sagittal plane and rotational stability in the

posterior cruciate ligament-deficient knee.63 They found that although isolated sectioning of

the PCL does increase rotational instability between 60o to 90o, further sectioning of the

meniscofemoral ligaments still does not lead to increased rotational instability.63 Finally,

Ogata et al. performed sequential sectioning of the PCL and collateral ligaments and found

increasing posterior sag and internal rotation of the tibia with increasing degrees of knee

flexion in specimens in which only the PCL was deficient.64

 Additionally, three in vivo studies examined the varus/valgus and rotational stability

provided by the PCL. Fontbote et al. examined 10 patients with unilateral grade II (6-10 mm

posterior displacement) PCL insufficiency and found objective clinical and radiographic

evidence of posterior tibial displacement; however, although differences in gait and vertical

landing existed, they concluded that minimal biomechanical and neuromuscular differences

were found between PCL intact and insufficient knees.65 Hooper et al. examined 9 patients

with PCL deficiency compared to a control group in walking, ascending and descending stairs.66

They found a direct correlation between subjective patient outcome measures (Flandry) and

higher peak knee extensor torque during stance phase.66 Finally, Jonsson and Karrholm looked

at 8 patients with unilateral PCL deficiency and performed radiostereometric measurements in

patients performing a step-up test while a posterior stress test was applied to the tibia at 30 o of

flexion; this study was unable to show any kinematic differences in the knee during the step-up

test.67 In addition, this study suggested that of the 8 patients with known isolated PCL

deficiency, 6 of them were found to show abnormalities in the other ligaments of the knee. 67

In conclusion, the role the PCL plays in the rotational control of the knee is still unclear,

with many contradictory studies published in the literature. It may act as a secondary stabilizer

to rotational forces when other ligaments are compromised and other ligaments may provide

control to rotation when the PCL is deficient. Further work both in the in vivo and

biomechanical arenas may provide further insight into the exact role the PCL plays in providing

rotational stability to the knee.

Morphological/Meniscal/Chondral Degeneration

Hamada et al. looked at 61 patients with acute, isolated PCL tears characterized as grade

2+ or higher and found that 28% of these patients had meniscal tears (with the anterior horn of

the lateral meniscus being the most common site of pathology) and 52% of these patients had

chondral injuries (most commonly in the medial femoral condyle).68 They recommended for

the clinician to have a high index of suspicion for concomitant pathology in the menisci or

cartilage when evaluating patients with presumed isolated, high grade PCL injuries.

Shelbourne et al. examined the natural history of the isolated PCL deficient knees in 68

patients with a mean age at the time of injury of 25.2 years, and obtained subjective, objective,

functional, and radiographic data at a mean of 5.4 years post-injury.69 They found no

difference in subjective knee scores and the amount of time from the initial injury;

furthermore, laxity did not increase with time and laxity did not correlate with radiographic

changes.69 In addition, regardless of laxity, 50% of this cohort return to sport at the same level

or higher.69 Radiographic interpretation suggested that medial tibiofemoral compartment

arthrosis was more prevalent in the PCL injured knee compared to the contralateral (normal)

knee; however, this did not quite reach statistical significance in this series (p = 0.077).69

Shelbourne et al. most recently provided longer term follow-up (minimum 10 years) in their

2013 paper published in the American Journal of Sports Medicine (AJSM). 70 Here they had

subjective and objective outcomes data on 44 patients at a mean follow up of 14.3 years (range

10-21) from the time of injury.70 Although radiographic changes and progressive degeneration
of the knee was seen in 41% of patients, patients maintained quadriceps strength compared to

the contralateral side (97% of normal), and had subjective knee scores in the form of

International Knee Documentation Committee (IKDC) and modified Cincinnati Knee Rating

System (CKRS) Scores of 73.4 and 81.3, respectively.70

Parolie et al. treated 25 patients with isolated PCL tears without surgical reconstruction

and followed them for a mean of 6.2 years (range 2.2 to 16 years); they found that although

36% had radiographic changes, 80% of patients were satisfied with their knees and 84% had

returned to their previous sport.71 In their study, quadriceps strength seemed to correlate

with patient satisfaction.71 They concluded that the majority of athletes with PCL deficient

knees who maintain strength in their quadriceps can predictably return to sports without

disability.

Keller et al. examined 40 patients with isolated PCL injuries (75% were sports related)

that were treated nonoperatively at a mean of 6 years from the initial injury. 72 On the

modified Noyes knee questionnaire, 65% of patients noted limitations in their activities and

49% noted that their knee had not fully recovered despite adequate rehabilitation. 72 In

contrast to other studies, they did find a correlation between the length of time since the injury

and worse knee score and progression of radiographic degenerative changes.72 Furthermore,

90% of patients complained of activity associated knee pain and 43% had pain with basic

activities such as walking - despite having strength measurements essentially the same as the

contralateral, uninjured extremity.72

 Boynton et al. examined 38 patients with isolated PCL injuries both subjectively

(questionnaire) and objectively (physical exam and radiographs of both knees) at a mean

follow-up of 13.4 years (range 5 - 38 years).73 They found that 21% of patients had to have

additional surgery for meniscal pathology and that those patients had statistically significant

worse subjective scores than those without meniscal pathology.73 In addition, 81% of patients

with normal menisci had at least occasional knee pain and 56% had occasional swelling.73

Radiographic examination did demonstrate articular degeneration which seemed to increase

with time from the injury.73 They concluded that a bimodal distribution of patients exists, with

some having significant symptoms and radiographic degeneration and others remaining

essentially asymptomatic with no loss of function.

Strobel et al. published their series of 181 patients with a known PCL injury that had

undergone arthroscopy to assess chondral damage.74 They found that patients with a

duration of PCL-deficiency greater than 5 years had an incidence of nearly 78% for lesions of

the medial femoral condyle and nearly 47% had chondral damage of the patella. 74

Furthermore, they also found that degenerative changes in the medial femoral condyle set in

fairly quickly with a 3-fold increase in the number of lesions within the first year of becoming

PCL-deficient; they also found that medial degeneration increased significantly with the

presence of a combined PCL/PLC injury.74 They recommended that the early and continuous

increase in both medial compartment and patellofemoral degeneration be taken into account

when counseling patients about options for conservative versus reconstructive treatments.
 Assimilation of the literature on both acute and chronic PCL tears would suggest that

clinicians examining the acute, high-grade PCL tear should have a high index of suspicion for

concurrent diagnosis of lateral meniscus tear or medial femoral condyle chondral injury and

that failure to diagnose these conditions may miss an opportunity for potentially natural history

altering intervention. Furthermore, deficiency of the PCL may lead to ultrastructural changes in

other knee ligaments as they are required to assume additional roles as posterior stabilizers.

Predictable sequences of degeneration occur in both the medial and patellofemoral

compartments with untreated PCL-deficiency. In regards to the outcomes of nonoperative

treatment, the literature is mixed with some series providing very compelling evidence for

nonoperative treatment of PCL-deficiency with high subjective outcomes and return to sport,

and other series showing activity associated knee pain in 90% of patients with PCL-deficiency.

We believe that patients with PCL-deficiency should be evaluated for concomitant injuries and

counseled about the natural history of nonsurgical treatment so that the patient can make an

informed decision regarding their care.

Biomechanics of the PLC

Several biomechanical studies have been performed to try to better understand the

complexity of the lateral and posterolateral structures. The PLC structural function, like that of

the PCL, has been defined by selectively sectioning each structure and then performing further

analysis.5,25,26,29,75 Through these methods, the primary static stabilizers of the PLC have been

identified as the LCL, popliteofibular ligament, and the popliteal muscle tendon complex.
5,25,26,29,75
These structures primarily work to resist posterior translation, posterolateral tibial
rotation, external rotation, and varus rotation.29 The PLC structures along with the cruciate

ligaments work together to provide static and dynamic stability to the lateral knee. 25,26,75

Posterior translation is restrained by a dynamic interplay between the PCL and PLC. As

the knee goes from flexion to extension, the PLC becomes more important in posterior

stabilization. The converse has been reported as well, when the knee goes from full extension

to flexion, the PLC becomes lax, and past 90 degrees of flexion, the PCL is the primary restraint

to posterior tibial translation on the femur. Sectioning of the PLC increases posterior translation

of the lateral tibial plateau at 30° to 45°, but less so at 90° of knee flexion.29 Cutting both the

PLC and PCL increases posterior translation of both medial and lateral tibial plateaus at 30° and

90°.76 The posterolateral structures serve as secondary restraint to posterior translation as the

knee goes beyond 30° to 45° of knee flexion.

Posterolateral instability is defined as a coupled external rotation with posterior

translation. In the studies by Veltri, isolated PLC sectioning in an increased amount of

posterolateral instability.36 Combined sectioning of the LCL and the posterolateral part of the

capsule resulted in more posterolateral instability than did isolated cutting of either structure. 77

The PLC, therefore, provides a strong secondary stabilizer the posterolateral aspect of the knee.

External rotation stability has many smaller contributors: posterior joint capsule,

popliteus, and PFL. Sectioning these smaller components leads to increased external rotation of

the tibia with the knee closer to extension, maximal at 30 degrees, minimal at 90 degrees. 36, 78

Sectioning both the PLC and PCL leads to increased external rotation at all flexion angles. The

PLC provides greatest stability with the knee near full extension and acts as a secondary

stabilizer to external rotation with the knee in flexion. The popliteus tendon resisted excessive
external rotation of the tibia during knee flexion from 20° to 130°, and it resisted excessive

varus rotation of the tibia during flexion from 0° to 90°.79 The LCL acts as secondary stabilizer

to external rotation.

Varus rotation is primarily restrained by the LCL and secondarily restrained by the

popliteus muscle tendon complex. When the LCL is sectioned, varus rotation is increased from

0-30 degrees, with maximal displacement at 30 degrees.36, 37 If both LCL and PCL are sectioned,

then increased varus rotation is seen at all flexion angles, maximal at 60 degrees. The PLC

controls varus rotation when the knee is near full extension, and the PCL with the knee in

flexion.

Combined PCL and PLC Biomechanics

Sectioning of the PCL and PLC causes a further increase in varus and external rotation

laxity and a marked increase in posterior translation.36 If only the PLC is injured and the PCL is

intact, then an increased tibial rotation can be seen at 30 degrees of flexion, however not at 90

degrees. This is because the PCL becomes increasingly taut with increased knee flexion angles,

so as the knee flexes the PCL provides more resistance to translation and rotation.

In situ forces in the PCL increase from full extension to 90° of flexion. 58 These loads are

reduced with quadriceps loading and are increased with hamstring loading. The popliteus

muscle also reduces the in situ forces on the PCL.62 Harner et al. examined the effect of the

popliteus tendon in conjunction with the PCL in 10 cadaveric specimens, and concluded that the

popliteus muscle is an important stabilizer against posterior tibial translation in the PCL-

deficient knee.62 In situ forces on the posterolateral structures resulting from posterior tibial
loading are greatest at full extension; sectioning of the PCL increases posterolateral forces at all

angles of knee flexion.

Combined PLC and ACL Biomechanics

The functions of the PLC with respect to the anterior cruciate ligament (ACL) has also

been studied.36 Combined sectioning of the ACL and the PLC causes increased internal rotation

laxity at 30° and 60° of flexion.36 Isolated sectioning of the ACL or combined sectioning of the

LCL and the deep ligament complex did not increase internal rotation of the tibia. Veltri et al.

reported that sectioning of the ACL and PLC resulted in increased primary anterior and

posterior translation, increased coupled external rotation with a posterior force, increased

primary varus rotation, and increased primary internal rotation.36 LaPrade et al. measured the

forces across the native and reconstructed ACL after complete sectioning of the posterolateral

structures, and found there to be increased forces exerted with varus loading, and with coupled

varus and external rotation.80, 81

Joint Contact Pressures

Skyhar et al. looked at the contact pressures using pressure-sensitive film in 10

cadaveric knee with sequential sectioning of the PCL and posterolateral corner structures

(posterolateral capsule, popliteus muscle and tendon, and the lateral collateral ligament). 82

They found a mean pressure increase of 52% in the medial compartment, regardless of the

angle of knee flexion in specimens with isolated PCL deficiency.82 Furthermore, pressure
increases were noted in the patellofemoral compartment from an intact state measurement of

23.2 Pascals to measurements of 28.0 and 34.8 Pascals with subsequent sectioning of the PCL

and posterolateral corner, respectively (p < 0.05).82 In the study by MacDonald et al., 9 fresh

frozen cadavers under the age of 45 years were used to study the biomechanical changes that

occur in the absence of the PCL under physiologic loads.83 Using pressure sensitive film

inserted into the medial and lateral compartments at various angles of knee flexion, they

showed significant posterior subluxation of the tibia at 60o of flexion in the PCL deficient

specimen. This resulted in increased contact pressure and pressure concentration in the medial

compartment.83 Combined sectioning of the PCL and PLC, increases Intra-articular pressure in

the patellofemoral and medial compartments, therefore, forming the basis for the

development of degenerative changes in patients with chronic deficiencies.

Relevance

Although the biomechanical function of the PCL is known to be primary as a restraint to

posterior tibial translation, the true clinical relevance lies in the assessment of whether or not

operative reconstruction will allow for more predictable improvement in criteria such as return

to sport/normal activity, as well as whether residual posterior laxity will negatively affect

subjective and functional outcomes. Definitive answers to these questions will improve

surgeon-patient communication, allowing patients to make well-informed decisions regarding

their care.

The overall function of the combined structures of the PLC is to reduce anteroposterior

translation of the tibia in extension and to decrease external and varus rotation forces across
the cruciate ligaments. Knowing that complete sectioning of the posterolateral structures

increases the forces exerted on the native cruciate ligaments and on ACL and PCL grafts, 80, 81

we must strive to restore native PLC anatomy when a reconstruction is necessary. Restoring the

native PLC anatomy will not only protect the cruciate ligaments from failure, but will have the

added benefit of preventing early degenerative changes.

Future Directions

Future experimental designs will likely focus on using advanced motion analysis and

computer programs to further analyze the role of the PCL and the PLC in both the athlete and

non-athlete. Furthermore, a sports specific analysis may also lend further insight into the exact

functional role the PCL and PCL play within the demands of each sport.

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Figure 1: Sagittal view MRI illustrating The PCL ligament
 AL

PM

Figure 2: Arthroscopic photo depicting the AL (Anterolateral Bundle) and PM (Posteromedial Bundle)
of the PCL in an ACL deficient knee at 90 degrees of knee flexion. The AL bundle is steeper (more
vertical) and tighter in flexion, as demonstrated here.
Figure 3A and B: Anatomy of the PCL insertion. A, Outline of the anterolateral bundle
(AL) and posteromedial bundle (PM) of the PCL tibial insertion. B, Femoral origin.
(Cosgarea, Posterior Cruciate Ligament Injury: Evaluation and Management: JAAOS
Sept/Oct 2001 Vol 9 no 5 297-307 Permission requested- pending)
Figure 4: Tibial view of meniscal attachments in relation to the cruciate ligaments. From Netter, Atlas
of Human Anatomy Plate 478 (Elsevier)
Figure 5 A and B: A) Anterior view of PCL demonstrating 2 bundles of the PCL with the anterior
meniscofemoral ligament (aMFL). B) Posterior view of the knee demonstrating 2 bundles of the PCL
with the posterior meniscofemoral ligament (pMFL). (Anderson et al. Arthroscopically Pertinent
Anatomy of the Anterolateral and Posteromedial Bundles of the Posterior Cruciate Ligament J Bone
Joint Surg Am, 2012 Nov 07; 94 (21): 1936 -1945.) permission pending
Figure 6: Anatomy of the lateral side of the knee shown in transverse section, viewed from above. (R.
Seebacher et al.: Journal of Bone and Joint Surgery, 64A:536-541, 1982 (7). Permission pending
Figure 7: Lateral Collateral Ligament when visualized from the posterior aspect of the knee. (From
Netter, Atlas of Human Anatomy Plate 479 (Elsevier)
Figure 8: MRI depiction of intact Lateral Collateral Ligament (LCL)