Anatomy, Bony Pelvis and Lower Limb, Knee Posterior Cruciate Ligament

Article Author:
Chandler Cox
Article Editor:
Bruno Bordoni
12/6/2018 6:05:27 PM
PubMed Link:
Anatomy, Bony Pelvis and Lower Limb, Knee Posterior Cruciate Ligament


The posterior cruciate ligament (PCL) is one of two cruciate ligaments of the knee that acts to restrict posterior tibial translation relative to the femur. It is the functional counterpart of the anterior cruciate ligament (ACL), which prevents excessive anterior tibial translation relative to the femur. Both cruciate ligaments are static stabilizers of the knee that help it move throughout a full range of motion. The PCL also acts secondarily to resist varus, valgus, and external rotation moments about the knee.[1]

PCL is the largest and strongest knee ligament, consisting of two bundles: anterolateral bundle (ALB) and posteromedial bundle (PMB). PCL trauma accounts for 3% of the lesions occurring in the knee; 95% of lesions involve other ligaments of the knee. The usual dynamics of an injury to the PCL is a posteriorly directed force to the knee in the flexed position.

The most commonly used test for an assessment of ligament mechanics is the posterior drawer test; the latter has a very high sensitivity and specificity, 90% and 99% respectively.

Structure and Function

The PCL is an intra-articular structure, but it is also considered extra-synovial, as it is covered by synovium within the knee. The PCL, with a thickness nearly twice that of the ACL, originates from the anterolateral margin of the medial condyle of the femur and the intercondylar notch roof, and inserts along the posterior aspect of the tibial plateau. Two ligamentous bundles comprise the PCL: the anterolateral bundle (ALB) and posteromedial bundle (PMB). The location of their attachments can easily identify these bundles to the femur as opposed to their tibial attachments that are much more compact and difficult to differentiate. The femoral attachment of the ALB, estimated to range from 112 to 118 mm in area, is much larger than the size of its tibial attachment, estimated at around 88 mm. The tibial attachment of the ALB is bordered medially and posteriorly by the PMB, with a horizontal bony prominence known as the 'bundle ridge' separating the two. Overall, the PMB is smaller than the ALB. The femoral attachment of the PMB is estimated to range from 60 to 90 mm in area, while the tibial attachment measures approximately 105 mm along the posteromedial aspect of the ALB.[1][2]

Classically, the ALB and the PMB are thought to have independent functions, with the ALB primarily functioning in flexion and the PMB in extension. However, recent biomechanical studies have found that changes in orientation during knee flexion and extension prevent either bundle from exhibiting a complete dominance in the overall function of the PCL in restraining posterior tibial motion. Recent studies have also identified the PCL as a secondary restraint to both internal and external rotation, particularly between 90 and 120 degrees of flexion.[1][2]


The posterior cruciate ligament appears around week 8 of development of the human embryo, with the ACL developing soon afterward. Maturation of the synovial joint of the knee continues during development and into early postnatal life.[3]

Blood Supply and Lymphatics

The blood supply of the PCL primarily comes from the middle geniculate artery, a branch of the popliteal artery. The terminal branches of the middle geniculate artery form a periligamentous network with the synovial fold covering the PCL. Blood vessels in this periligamentous network penetrate the PCL in a horizontal direction and anastomose with a longitudinally oriented intraligamentous network. The blood vessels within the ligament are located in the loose connective tissue situated between the dense connective tissue of the longitudinal ligament fiber bundles. The blood supply in the PCL is not homogeneous, however. Both fibrocartilaginous entheses at either attachment site of the PCL are devoid of blood vessels. Another avascular area has also been identified in the central portion of the middle third of the PCL. Lymphatic drainage of the PCL follows a similar distribution as the blood supply since lymphatics accompany most of the smaller vessels.[4]


The PCL receives nerve supply from the posterior articular nerve, a branch of the tibial nerve, that penetrates the posterior capsule to reach the PCL. Four types of receptors have been identified in the PCL: Ruffini slow adapting M-receptors, Pacinian fast adapting M-receptors, Golgi-like tendon receptors, and pain receptors. Afferent feedback to the central nervous system is believed to assist in proprioception and stabilization of the knee.[5]


The mechanoreceptors of the posterior ligament influence the musculature that acts on the knee. This mechanoreceptor activity contributes to better neuromuscular coordination during the phases of the gait cycle.

Surgical Considerations

In isolated PCL injuries, the recommendation for surgery is only for acute injuries with severe posterior tibial subluxation and instability. Surgical reconstruction is also recommended when there is damage to other structures in the knee in addition to the PCL. Such cases require surgery within two weeks of the injury to allow for best anatomical ligament repair of the PCL and to reduce capsular scarring. There is no gold standard approach to PCL reconstruction and debate exists on the best graft source, placement of tibial and femoral tunnels, number of graft bundles, and the amount of graft tension. There are several allografts and autologous tissues used for PCL reconstruction. The most common allograft tissue is the Achilles tendon. With allograft reconstruction, surgical time decreases and there exists a small risk of iatrogenic trauma to the harvest site. As far as autologous tissue grafts are concerned, bone-patellar tendon-bone is most common. The bone plugs allow for sufficient fixation of the tissue, but there is the risk of harvest site morbidity.[6]

Recent literature has investigated whether a single or double bundle approach to PCL reconstruction using either a tibial inlay or tunnel method results in better outcomes. A double-bundle procedure allows for the reconstruction of both the anterolateral and posteromedial bundles of the PCL, which has been shown to restore normal knee kinematics across a full range of motion. Comparatively, a single bundle approach only focuses on reconstructing the bigger and stronger anterolateral bundle and has been shown to primarily restore normal knee kinematics through 0-60 degrees of knee flexion. However, there has been no literature proving superior functional outcomes of one surgical approach over the other.[6]

There are two methods used by orthopedic surgeons to place the graft with the goal being to recreate the optimal biomechanical restraint of the PCL. The tunnel method is an arthroscopic procedure in which the graft is placed in an acute angular turn. This placement of the graft in this method can potentially elongate and thin the graft over time due. The tibial inlay approach places the graft near the trough at the tibial insertion of the PCL and avoids having to place the graft in the acute angular turn used in the tunnel method, but the tibial inlay approach is an open procedure. Additional research may determine if there are better functional, long-term outcomes for one approach over the other.[6]

Like any surgery, PCL reconstruction is associated with potential complications including fracture, neurovascular injury to the popliteal artery, deep vein thrombosis, residual laxity, and loss of range of motion. Although reduction of posterior tibial laxity associated with PCL injury is the goal of surgery, residual laxity is the most common problem following surgery. This can be due to an additional undiagnosed PLC or soft tissue injury. Range of motion limitations following surgery are typically due to limitations in knee flexion that can be addressed with physical therapy. In more serious cases, the range of motion limitations could be due to improper placement of the graft or excessive tension placed on the graft.[6]

Clinical Significance

Injury to the PCL rarely occurs independently of other knee injuries. ACL, medial collateral ligament (MCL), and posterolateral corner (PLC) injuries are all commonly seen with PCL injuries. While not as common as ACL injuries, there is a 2-3% prevalence of PCL injuries in athletic knee injuries and up to a 40% incidence in trauma patients with a knee effusion. Mechanisms of PCL injury include hyperextension, posteriorly directed force to the proximal tibia on a flexed knee, forced hyperflexion of the knee, rotation combined with varus or valgus force, and knee dislocation. The mechanism of injury can also often give clues as to whether there is damage to related structures. ACL rupture is commonly seen in hyperextension injuries, and rotational injuries with varus or valgus stress typically involve multiple ligaments and meniscal or chondral injury.[2][6]

Patients who suffer an isolated PCL injury seldom report a popping or tearing sound or sensation that is commonly seend with ACL and MCL injuries. More frequently, patients will complain of vague, non-specific symptoms, such as general knee discomfort. Unless there is a concomitant injury to other supporting structures of the knee, patients with PCL injuries rarely report feeling gross instability. Acutely after the injury, patients may complain of knee swelling, stiffness, pain in the posterior aspect of the knee, or pain with deep knee flexion. Patients with a chronic PCL injury may present with vague anterior knee pain, difficulty going up or down stairs or pain with sprinting or deceleration.[2][6][7]

The physical exam is essentialy in diagnosing and determining the severity of a PCL injury. Assessment of range of motion in the affected knee should be performed, and patients may present with a 10-20 degree lack of knee flexion compared to the uninvolved side. This motion loss is commonly attributed to the tibia shifting posteriorly earlier during knee flexion and thus reaching a range of motion endpoint sooner due to the loss of normal restraint to posterior displacement that the PCL provides. Range of motion is also potentially limited by knee effusion and pain. The posterior drawer test is the most common clinical exam used to assess PCL function. The test is performed with patient supine while flexing the hip 45 degrees and the knee 90 degrees. It is essential to keep the tibia held in a neutral position with the foot flat on the exam table as this decreases the likelihood of a false negative test for PCL injury by minimizing the tension through the PLC and allowing maximal posterior tibial subluxation. A posteriorly directed force should be applied to the tibia with the examiner’s thumbs while their fingers are wrapped around the tibia assessing for hamstring muscle activation. The goal of the posterior drawer test is to evaluate the amount of posterior translation or step off at the medial joint line. On a normal resting knee, the tibia lies approximately 0-2 mm anterior to femoral condyles. Any posterior tibial translation that is 3 mm or greater is indicative of a positive posterior drawer test and PCL injury. Recent studies have also found that posterior tibial translation greater than 10 mm is suggestive of additional trauma to the PLC. The sensitivity and specificity of the posterior drawer test have been reported to be 90% and 99% respectively, with a +LR of 90 and a -LR of 0.10.[2][6][7]

In patients with an isolated PCL injury, non-operative management is often recommended. Surgery should be considered immediately over non-operative management if other ligamentous structures are damaged, and there is increased rotation instability of the knee. Surgical intervention can also be an option with PCL injuries when conservative, non-operative management has failed, or there increased osteoarthritic changes in the PCL-deficient knee present. During acute management of an isolated PCL injury, rehabilitation should focus on reducing knee joint effusion, restoring range of motion, and regaining muscle strength, especially of the quadriceps. Mild tears generally have a rapid recovery, with patients able to return to full activity within two to four weeks of injury. More severe ligamentous tears may require a period of immobilization and partial weight bearing before beginning physical therapy. These patients should be able to return to full activity within three months of injury. Those that continue to have pain and are unable to resume a pre-injury level of function may require surgical intervention.[2][6][7]

  • (Move Mouse on Image to Enlarge)
    • Image 1921 Not availableImage 1921 Not available
      Contribute By Gray's Anatomy Plates


[1] Logterman SL,Wydra FB,Frank RM, Posterior Cruciate Ligament: Anatomy and Biomechanics. Current reviews in musculoskeletal medicine. 2018 Sep     [PubMed PMID: 29855794]
[2] LaPrade CM,Civitarese DM,Rasmussen MT,LaPrade RF, Emerging Updates on the Posterior Cruciate Ligament: A Review of the Current Literature. The American journal of sports medicine. 2015 Dec     [PubMed PMID: 25776184]
[3] Ratajczak W, Early development of the cruciate ligaments in staged human embryos. Folia morphologica. 2000     [PubMed PMID: 11107700]
[4] Petersen W,Tillmann B, Blood and lymph supply of the posterior cruciate ligament: a cadaver study. Knee surgery, sports traumatology, arthroscopy : official journal of the ESSKA. 1999     [PubMed PMID: 10024962]
[5] Çabuk H,Kuşku Çabuk F, Mechanoreceptors of the ligaments and tendons around the knee. Clinical anatomy (New York, N.Y.). 2016 Sep     [PubMed PMID: 27376635]
[6] Rosenthal MD,Rainey CE,Tognoni A,Worms R, Evaluation and management of posterior cruciate ligament injuries. Physical therapy in sport : official journal of the Association of Chartered Physiotherapists in Sports Medicine. 2012 Nov     [PubMed PMID: 23068893]
[7] Bedi A,Musahl V,Cowan JB, Management of Posterior Cruciate Ligament Injuries: An Evidence-Based Review. The Journal of the American Academy of Orthopaedic Surgeons. 2016 May     [PubMed PMID: 27097125]