The most commonly used grafts are the patellar tendon graft with bone blocks at both sides, the hamstrings tendon graft, and the quadriceps tendon graft. Allografts and synthetic grafts have also been used; however, these should not be considered the first choice for athletes. Several issues have been considered important, initiating a discussion on ways to improve the ACL reconstruction technique, aiming toward a more anatomic approach [13, 14]. The discussion is mainly focused either on the choice of graft or on tunnel position, which are the main considerations in an anatomic ACL reconstruction. In the first aspect, bone-patellar tendon-bone and hamstring graft (either single-bundle [SB] or double-bundle [DB] graft) are the most commonly used; they have comparable properties to the native tissue, and their effectiveness has been proven [14–16]. The second concept regarding where to place the femoral and tibial tunnels has been well discussed. Most recent evidence suggests positioning of the graft at the anatomic insertions of the native ACL [17, 18]. A more detailed description of the anatomy of the ACL has been helpful in an attempt to replicate the exact anatomy and behavior of the ACL (Fig. 15.2).

The MCL consists of three units, named the superficial MCL (s-MCL), the deep MCL (d-MCL) or medial capsular ligament, and the posterior oblique ligament (POL) [20]. The s-MCL is a broad ligament that attaches at the medial femoral epicondyle and inserts just below the pes anserinus, 4–5 cm distal from the joint line that is taut during flexion and lax during full extension. Just deep into the s-MCL lies the d-MCL which is a confluence of the meniscofemoral, meniscocapsular, and meniscotibial ligaments. Posterior to the MCL is the posteromedial corner (PMC), made up of a condensation of the capsule forming the POL that is tight in extension [20, 21].

The MCL, and more specifically the s-MCL, provides 78% of the valgus restraining force of the knee. In extension, the ACL and PMC (POL, medial meniscus, and semimembranosus) also contribute to valgus stress, and the MCL provides 57% of the restraining force against valgus stress [22–24]. In general, an isolated MCL tear leads to valgus laxity in flexion, while additional injury to the secondary valgus restraints (PMC or ACL) leads to increased laxity in extension.

The mechanism of injury includes either contact valgus stress on the knee such as after a lateral blow to the lower thigh or upper leg or noncontact valgus stress with or without a rotational component, for example, during cutting maneuvers when an athlete plants his/her foot and then forcefully shifts directions [23]. There is pain and swelling at the site of MCL, but not knee joint swelling. If this occurs other concomitant ligamentous injuries may be suspected (ACL, PCL). The ability to walk may be impaired. Valgus stress testing at 0–30° of knee flexion estimates the amount of laxity (Fig. 15.3). At 30° of knee flexion, a grade I injury is <5 mm of medial joint opening, grade II is 5–10 mm of laxity, and grade III is >10 mm. Any laxity at 0° is indicative of associated injuries such as a cruciate tear or a posteromedial capsular injury. The location of the MCL injury refers to femoral avulsion, tibial avulsion, or midsubstance tear. Complete tibial-sided MCL tears (tears that involve both the deep and the superficial components) often do not heal. Plain radiographs may show a bony avulsion or an osteochondral fragment that could alter the treatment plan. MRI often provides significant data that assist in treatment of an MCL injury: the severity and location of the MCL tear and any associated cruciate ligament, meniscal, or capsular damage.

Treatment recommendations are based on the severity, location, and chronicity of the MCL injury, as well as concomitant knee injuries.

The PCL originates on the posterior surface of the tibia and passes superiorly and anteromedially to insert on the lateral wall of the medial femoral condyle. It has an average width of 13 mm and length of 38 mm, and it is fan-shaped, being narrowest in the midportion and fanning out superiorly and, in a lesser extent, inferiorly. The PCL consists of a larger anterior band which is taut in flexion and relaxed in extension and a smaller posterior band which is taut in extension and relaxed in flexion.

The PCL is the strongest of the two cruciate ligaments in the knee and accounts for about 95% of the total restrain to posterior translation of the tibia in regard to the femur [40]. Secondary stabilizing functions are to restraint rotation when the knee is flexed, varus and valgus movement when the knee is extended, and restraint also overextension and hyperflexion [41, 42]. The main function of PCL (the resistance to posterior tibial translation) is also performed by other structures which are secondary stabilizers. These include the meniscofemoral ligaments and the posterolateral and posteromedial structures.

American football and football are among the most important sports activities leading to a PCL injury [43]. In football, the goalkeeper is most exposed to this type of injury [44]. The possible mechanisms of injury include:

Isolated PCL injuries are not uncommon and have been estimated from 7% up to 47%, although the injury is most commonly associated with other ligamentous injuries [44–46]. The most commonly injured structure along with a PCL injury is the posterolateral corner (PLC), resulting in posterolateral rotatory instability (PLRI) [47, 48]. Associated meniscal or cartilage lesions may be found along with either an isolated PCL injury [49, 50] or when other ligament injuries exist along with the PCL rupture [46].

Patients may present effusion, pain in the back of the knee, or pain with flexion beyond 90° or during kneeling. Instability is presented usually with combined PCL/PLC injuries rather than after an isolated PCL rupture. In general, the effusion and the pain are less than with an ACL injury. The clinical tests that indicate a PCL injury include:

The posterior translation is graded according to the amount of posterior subluxation of the tibia. Tibial translation between 1 and 5 mm is considered a grade I injury. A grade II injury exists when posterior tibial translation is between 5 and 10 mm, and a grade III injury is seen when the tibia translates greater than 10 mm posterior to the femoral condyles.

Other clinical tests include:

Instrumental devices such as the KT-1000 (MEDmetric) or rolimeter (AirCast) have been developed in order to accurately measure the posterior tibial translation [53] although these are less accurate for detecting PCL insufficiency than ACL deficiency [54].

Compared to the ACL, the PCL can heal spontaneously given its abundant blood supply from the branch of the middle genicular artery and the superficial synovial layer by which is covered [38, 55–57].

Nonoperative management with aggressive rehabilitation is proposed for acute grade I–II isolated PCL injuries. Conservative treatment includes a brace for 2–6 weeks and functional rehabilitation with special emphasis to quadriceps strengthening. On the other hand, surgery is recommended in patients with grade III injuries, symptomatic grade II injuries, chronic symptomatic isolated PCL lesions, and multi-ligament injuries. Arthroscopically assisted techniques are most commonly used to perform PCL reconstruction. The most commonly used grafts are patellar or quadriceps tendon autografts and Achilles tendon allografts for PCL reconstruction or hamstring tendons for PCL augmentation techniques.

For chronic posterior knee instability, some general rules for the PCL surgery are:

The principal factors to be considered before surgery include graft selection, one- or two-bundle technique, drilling of a tibial tunnel, or use of a tibial inlay fixation. Also other factors are treatment of combined instabilities and necessity to perform a high tibial valgus osteotomy (HTO) [59].

The lateral collateral ligament (LCL) is the primary static restraint to varus opening of the knee [60]. The LCL inserts at femur proximal and posterior to the lateral epicondyle in a small depression between the lateral epicondyle and the supracondylar process and distally at the fibular head 8 mm posterior to the most anterior aspect of the fibular head [61, 62]. The posterior lateral corner (PLC) of the knee consists of various anatomic structures that include the iliotibial tract, LCL, popliteus tendon complex (the muscle-tendon unit and the ligamentous connections from the tendon to the proximal fibula, tibia, and meniscus), popliteofibular ligament (PFL), the biceps tendon, and the posterolateral capsule [63, 64]. The primary function of the PLC is to resist varus rotation, external tibial rotation, and posterior tibial translation [60, 65]. It should be noted that the PLC, not the PCL, is the primary restraint to posterior tibial translation near full knee extension [65].