The posterior cruciate ligament (PCL) is an intra-articular structure, surrounded by synovial membrane, and it provides about 95 % of the total resistance to posterior translation of the tibia. Its tensile strength is nearly twice that of the ACL [1]. Different studies demonstrated that, just like the ACL, PCL is composed of two different bundles: anterolateral (AL) and posteromedial (PM), which have different functions during knee movement [2, 3]. PCL has been described to be from 32 to 38 mm long and to have a cross-sectional area of 11 mm [4]. Femoral insertion of the PCL is located on the lateral side of the medial femoral condyle, in an area which is much larger than the ligament’s thickness: AL bundle insertion starts from the medial intercondylar ridge, 13 mm posterior to the medial articular cartilage-intercondylar wall interface and 13 mm inferior to the articular cartilage-intercondylar roof interface [5]. PM bundle insertion is located 8 mm posterior to the medial articular cartilage-intercondylar wall interface and 20 mm inferior to the articular cartilage-intercondylar roof interface [5]. The tibial insertion is located posteriorly to the posterior horn of the medial meniscus, 10–15 mm below the articular surface, around 7 mm anteriorly to the posterior tibial cortex [6, 7]. Just anteriorly to the PCL passes Humphrey’s ligament (also called anterior meniscofemoral ligament), connecting the posterior horn of the lateral meniscus to the medial femoral condyle. The same structures are connected also by the posterior meniscofemoral ligament (Wrisberg’s ligament), which is located posterior to the PCL. These two ligaments may serve as a secondary stabilizer in a PCL-deficient knee [8]. PCL is mainly vascularized by the middle geniculate artery and innervated by articular branches of the tibial nerve [9].

PCL biomechanic has been a hard challenge for years. Different studies in the past have shown the AL bundle to be extended during knee flexion and laxed during knee extension, while the PM bundle to be extended during knee extension and laxed during knee flexion [10, 11]. This led to the idea that the two bundles had an independent function, with the AL working in flexion and the PM working in extension. New studies changed this kind of vision, which nowadays has been substituted with a more synergical one. During flexion, actually, it is true that the AL bundle becomes tighter, but it becomes also more vertically oriented, losing its ability to resist posterior tibial translation. The PM bundle, instead, during flexion becomes more horizontally oriented, acquiring ability in posterior stabilization [10–12]. It is nowadays clear that none of the two PCL bundles acts independently in restraining posterior tibial translation at any degree of knee flexion.

PCL injury is rarely an isolated lesion. It is more commonly associated with other lesions in patients with multiligamentous rupture.

The incidence of PCL rupture in literature goes from 1 to 44 % of all acute knee ligament injuries [13–17].

It was reported that up to 2 % of NFL professional players are found to have a PCL laxity, and they are usually unaware about this lesion [18].

The most frequent multiligamentous injuries involving the PCL are PCL-PLC (posterolateral corner), followed by PCL-ACL and PCL-PMC (posteromedial corner) [19].

The most common injury causes are high-energy trauma like road traffic accidents (dashboard injury and motorcycle accidents), which are responsible for about 45 % of PCL tears. The second most frequent cause of lesion is sports injuries (40 %), which are usually responsible for low-energy traumatic ruptures [20]. Different mechanisms of injury are described:

PCL tears are not always easy to discover, especially chronic lesions, because they can sometimes be asymptomatic.

Unlike ACL injuries, PCL isolated lesions usually cause a gradual and slow swelling over the first days, patients are usually able to bear weight on the injured knee, and especially for isolated tears, they rarely complain a sense of knee instability during daily life activities.

Patients with PCL injuries may complain generalized knee pain, not being able to identify the kind of problem and its location.

In patients with chronic PCL-deficient knees, pain with prolonged walking and descending stairs is the main issue and is localized to the medial side or patellofemoral joint [19].

A standard examination should be executed, with attention to eventual joint effusion, patient’s gait pattern, and extremity alignment.

There are specific tests for investigating PCL tears:

It is always mandatory to clinically evaluate every other ligamentous structure of the knee when a PCL tear is found (ACL, PLC, MCL, LCL).

Imaging diagnostic exams should also be performed to complete the diagnosis:

The natural history of untreated isolated PCL tears is still unclear. Patients may clinically tolerate an isolated PCL-deficient knee and may not appreciate any disability initially; that is why there was a general consensus that isolated tears do well with conservative treatment. Prospective studies with 2–5 years of follow-up showed that the majority of the patients treated conservatively had good subjective results; half were able to return to their sport at the same or higher level [17, 26]. Nevertheless biomechanical studies showed that PCL deficiency results in altered loads and kinematics during functional activities [27–29]. Three specific phases have been described after PCL injuries. A survey of nonoperatively treated isolated PCL injuries at 15 and 25 years of follow-up shows a high incidence of arthrosis, especially in the medial and patellofemoral compartments as well as meniscal tear. At 15 years, 89 % had persistent pain and 50 % had chronic effusions [30]. At 25 years, almost all had degenerative changes [30]. The first is the adaptation stage which ranges from 3 to 18 months, the second is the functional tolerance stage that ranges from 15 to 20 years, and the final phase involves osteoarthritic degeneration and usually occurs after 25 years [30, 31]. The natural history of PCL-deficient knee is to develop overtime degenerative changes in the medial and patellofemoral compartments.

The goal of the rehabilitation program is to strengthen the musculature about the knee while minimizing forces across the patellofemoral and tibiofemoral compartments. In theory, quadriceps strengthening may compensate enough for loss of PCL [32]. Tibiofemoral compression forces are reduced with closed kinetic chain exercise; open kinetic chain quadriceps exercises exert an anterior pull on the tibia [33]. In our experience, acute grade I isolated PCL injuries are treated nonoperatively and could also be advocated for many grade II injuries. Individual treatment decision for an isolated grade II PCL injury is based on surgeon experience and patients factors and desires (usually high demanding athletes). Conservative management for grade I and II PCL injuries consist in pain relief, rest, ice, elevation regime, and immobilization of the knee with a brace locked in full extension 2–4 weeks, which will result in a decreased tension on the anterolateral bundle crutches and strengthening of the quadriceps muscle [34]. It is advisable to place within the brace a pad under the tibia to counter the force of gravity [35]. Conservative management of grade III PCL injuries could still be possible and is done by immobilizing the knee in full extension for 2–4 weeks. The patient is then allowed to progressive weight bearing with active, assisted range of motion exercises and quadriceps strengthening [20]. Return to sport is generally permitted when full quadriceps strength is regained, which usually takes 6–12 months. In spite of his rehabilitation program, progressive degeneration of the knee may be inevitable [30]. Nevertheless it is still not demonstrated whether the new advances in surgical reconstruction of PCL could change the natural history of this degenerative process.

Indications for surgical treatment of acute PCL injuries include insertion site avulsions with greater than grade I laxity, a decrease in tibial step of 8 mm or greater, and PCL tears combined with other structural injuries. Indications for surgical treatment of chronic PCL injuries are when an isolated PCL tear becomes symptomatic or when progressive functional instability develops. The symptoms are pain and swelling, but not instability as with the anterior cruciate-deficient knee. Initially the patient complains of patellofemoral pain, and then later on there is increased wear of the medial compartment.

The surgical timing should be considered in the context of the individual patient. Besides more than 50 % PCL injuries occur in multiple trauma patient [36], surgical timing is dependent upon vascular status, skin condition, systemic injuries, open versus closed knee injury, meniscus and cartilage, other orthopedic injuries, and the collateral/capsular ligaments involved. Multiple ligament knee injuries may require staged procedures (first acute capsular collateral structure repair and a delayed ACL/PCL reconstruction) [32].

Acute PCL reconstruction performed between 2 and 3 weeks post injury allows sealing of capsular tissues to permit an arthroscopic approach. Delayed PCL reconstruction may be indicated for patients below 60 years of age with persistent symptoms of pain and instability. These may help to rebalance pressure and shear forces within the knee, slowing progression of medial compartment degeneration, and the reduction of the posterior tibial translation restores the mechanical advantage of the quadriceps mechanism, thereby reducing patellofemoral contact forces as well [19]. Before performing a delayed PCL reconstruction, a thorough examination of the limb alignment and of the joint degeneration is mandatory. A long-standing weight-bearing x-ray AP (hip to ankle), lateral at 30° of knee flexion, and patellofemoral axial views are recommended. In case of a symptomatic varus malalignment a high tibial osteotomy should be performed first. In case of severe arthrosis a PCL reconstruction is not still indicated.