The anterior cruciate ligament (ACL) is one of the two cruciate ligaments which stabilizes the knee joint by preventing excessive forward movements of the tibia or limiting rotational knee movements. It is one of the most commonly injured structures in sports medicine, and yet it, unfortunately, does not heal when damaged.[1] This article presents the anatomy and function of the ACL to help readers better understand the injury mechanism and reduce the risk of ACL damage. 

Structure

The ACL is a band of specialized connective tissue located in the knee joint that connects the femur and the tibia. They are predominantly made up of collagen fibers, which make up for 70% of its dry weight. Mostly type I collagen (90%) and a small amount of Type III collagen(10%).[1] Fibroblasts make up for the cellular components in them embedded in a matrix of elastin (<5%) and proteoglycans[2]. On the femoral side, the ACL attaches to the posterior aspect of the medial surface of the lateral femoral condyle, which is semi-circular in shape, measuring 20 mm by 10 mm. From the femoral attachment, the ACL descends and attaches to the site anterior and lateral to the medial intercondylar tubercle.[3][4] The ligament is the narrowest near the femoral attachment and fans out and widens as it proceeds to the tibial attachment, approximately 15mm anterior to the PCL, a broader and oval-shaped footprint measuring 10mm by 30mm.[5]

The ACL is composed of two bundles: the anteromedial (AMB) and the posterolateral (PLB). The AMB fascicles arise from the most posterior and proximal site of the femoral attachment and attach to the anteromedial portion of the tibial attachment. The PLB fascicles arise from the distal portion of the femoral attachment and attach to the posterolateral portion of the tibial attachment. The ACL is mostly composed of the PLB.[6] With knee motion, the length and orientation of the AMB and PLB bundles change. With knee flexion, the AMB lengthens and tightens while the PLB shortens and becomes lax. With knee extension, the PLB lengthens and tightens while the AMB remains tight but less so than the PLB.[7] The mean length of the ACL is 33 mm, and the mean mid-substance width is 11 mm.[8]

Function 

The ACL is a crucial element in stabilizing the knee joint. It primarily stabilizes the anterior tibial translation and plays a small role in resisting internal rotation and prevents any excessive movements. 

Anterior Tibial Translation

The ACL functions as the primary restriction to anterior tibial translation with respect to the femur. When the knee is extended, the anterior tibial translation is low (maximum 2 mm) and supports the knee while standing. With knee flexion, the anterior tibial translation can increase up to 3 mm while walking and up to approximately 6 mm under anterior load.[9] Patients with chronic ACL-deficient knees (grade 3 sprain) experience the anterior tibial movement relative to the femur that is about four times greater than those with healthy knees.[10] A study by Zantop et al. showed that the damaged ACL increased the anterior tibial translation by up to 10 to 15 mm at 30 degrees of flexion under the anterior load of 134 N.[11] In cadaveric knees with no active muscular forces, researchers observed that the highest increase in the anterior tibial translation was between 15 to 40 degrees of knee flexion. The ischio-crural muscle group, which includes the biceps femoris, the semitendinosus, and the semimembranosus, induces knee flexion by connecting the ischial tuberosity with the pes anserinus tibia and fibular head. At 90 degrees of knee flexion, the forces of the muscle group actively stabilize against the anterior tibial translation.[12] In cadaveric knees, the PLB plays an important role in stabilizing the anterior tibial translation at near-to-extension angles, whereas the AMB is more involved in stabilizing higher flexion angles.[13][14]

Internal rotation

The ACL also functions as the secondary restraint to internal rotation, especially when the joint is close to full extension. In a study by Fleming et al., an internal torque of the tibia between 0-10 Nm resulted in the ACL strain in vivo.[15] A study by Beynnon et al. demonstrated that an internal torque between 2 to 6 Nm resulted in the AMB strain when the knee was flexed at 90 degrees in vivo.[16] The ACL may also serve as the secondary restraint to external rotation and varus-valgus angulation.[1]

The knee starts to develop from a mesenchymal concentration at four weeks gestational age. A knee joint is identifiable starting at six weeks, and the ACL formation as a mesenchymal condensation in the fetal blastoma is observable between 6 to 7 gestational weeks. Both the posterior cruciate ligament (PCL) and ACL appear as well-oriented structures by nine weeks of gestation. The ACL initially begins as a ventral ligament but migrates posteriorly in the knee joint as the intercondylar space develops. The PCL does not move from its initial position. Both cruciate ligaments are intracapsular but extra-synovial.[17][1]

The middle genicular arterial (MCA) branches supply nutrients to the ACL.[1] The MCA branches arise from the anterolateral aspect of the popliteal artery located in the popliteal fossa and directly penetrate the posterior capsule.[7][18] The MCA generally originates at the level of the proximal femoral condyles and can be identified between the superior genicular artery and the sural artery.[19][1]

The lateral and medial inferior geniculate arterial branches vascularize the distal portions of the two cruciate ligaments.[20] The ACL is covered by a synovial sheath where the small branches of the inferior and middle geniculate arteries combine to form a periligamentous plexus. The periligamentous plexus horizontally penetrates the ACL to anastomose with a vertically oriented intraligamentous vascular network.[21]

The posterior articular branches of the tibial nerve are the major neural structure that innervates the ACL.[1] These nerves penetrate the posterior capsule and travel anteriorly with the synovial and periligamentous arterial branches toward the infrapatellar fat pad. Most of these nerve fibers have a vasomotor function, but some smaller myelinated and unmyelinated nerve fibers that lie among the ligament fascicles run independently of the vessels.[22]

A few neural mechanoreceptors are located within the ACL, and they are primarily Ruffini receptors, which function as stretch receptors, and free nerve-endings, which function as nociceptors. The free nerve-endings also function as local effectors and secrete neuropeptides with vasoactive function.[23] These receptors also play a significant role in proprioception as well.