Introduction
The dense connective tissue band known as the anterior cruciate ligament (ACL) extends from the femur to the tibia. Since it can withstand loads on the anterior tibia during rotation and translation, the ACL is an important component of the knee joint.
Attachments
Origin
It originates from the intercondylar notch at the posteromedial corner of the medial portion of the lateral femoral condyle. The ACL’s femoral connection is located much posterior to the femoral shaft’s longitudinal axis on the medial surface of the lateral condyle’s posterior half. The interdigitation of collagen fibers and hard bone through the transitional zone of fibrocartilage and mineralized fibrocartilage is what actually causes the attachment.
Orientation
It extends medially, inferiorly, and anteriorly.
Insertion
Anterior to the tibia’s intercondyloid eminence, where it merges with the medial meniscus’s anterior horn. The tibial attachment lies in a fossa that is lateral to the anterior spinal column and extends from 11 mm in width to 17 mm in the AP plane.
Nerve Supply
The posterior articular branches of the tibial nerve send nerve fibers to the ACL. These fibers migrate through the posterior joint capsule and travel anteriorly to the infrapatellar fat pad alongside the synovial and periligamentous vessels that surround the ligament. The majority of the fibers have a vasomotor activity and are connected to the endoligamentous vasculature.
The receptors for the above-mentioned nerve fibers are as follows:
The femoral section of the ligament, where the deformations are the most severe, has the majority of the Ruffini receptors, which are sensitive to stretching.
The femoral and tibial ends of the ACL include Vater-Pacini receptors, which are sensitive to quick movements.
Near the ACL’s attachment points and at its surface, below the synovial membrane, are tension receptors resembling those in the Golgi.
By releasing neuropeptides with vasoactive properties, free-nerve endings can perform the function of nociceptors as well as operate as local effectors. They may therefore have a modulatory influence on late graft remodeling or normal tissue homeostasis.
The afferent arc for alerting knee postural changes is provided by the mechanoreceptors (Ruffini, Pacini, and Golgi-like receptors) mentioned above, which have a proprioceptive role. Ligament deformations affect how muscle spindles are produced by the fusimotor system. As a result, a phenomenon known as the “ACL reflex” occurs when afferent nerve fibers in the proximal section of the ACL are activated, which modulates motor activity in the muscles around the knee. When group II or III fibers are stimulated, these muscle reactions are brought on (i.e. mechanoreceptors). The ACL reflex plays a crucial role in maintaining muscle programming and is necessary for optimal knee function.
Blood Supply
The middle geniculate artery is where the cruciate ligaments receive the majority of their blood supply. The lateral and medial inferior geniculate arteries have branches that supply blood to the distal portions of both cruciate ligaments. The inferior and intermediate arteries’ terminal branches form a periligamentous network around the ligament, which is encased in a synovial fold. Blood vessels enter the ligament horizontally from the synovial sheath and anastomose with a longitudinally oriented intraligamentous vascular network. In the ligaments, the blood vessel density is not uniform. The fibrocartilage of the anterior section of the ACL, where the ligament meets the anterior rim of the intercondylar fossa, contains an avascular zone.
Constituents
The ACL has a matrix comprised of a network of proteins, glycoproteins, elastic systems, and glycosaminoglycans with complex functional connections, as well as a microstructure made of collagen bundles of various types (mainly type I).
Bundles
The ACL consists of two parts: the smaller anteromedial bundle (AMB) and the bigger posterolateral bundle (PLB), which are named for the locations of their insertions into the tibial plateau.
The posterolateral bundle is constrictive during extension, and the anteromedial bundle is constrictive in flexion. Both bundles are parallel while the joint is in extension; however, when the joint is flexed, the femoral insertion point of the posterolateral bundle shifts anteriorly, both bundles are crossed, and the anteromedial bundle tightens while the posterolateral bundle loosens.
When the knee is in extension, the large posterolateral bundle provides resistance to the anterior translation of the tibia during the Lachmans Test. The anterior medial bundle resists anterior translation of the tibia during the anterior drawer test while the knee is flexed.
The posterolateral bundle rupture results in increased hyperextension, anterior translation (extended knee), external and internal rotation (extended knee), and increases in external rotation with the knee in mid-flexion; the anteromedial bundle rupture results in anterolateral instability with increased anterior translation in flexion, minimally increased hyperextension and minimally increased rotational instability.
Function/Action
Approximately 85% of the overall restraining force against anterior translation is provided by the ACL. Additionally, it reduces excessive varus and valgus strains as well as medial and lateral tibial rotation. The ACL checks extension and hyperextension to a lesser extent. The ACL controls joint kinematics by directing the knee’s immediate centre of rotation along with the posterior cruciate ligament (PCL). The posterolateral bundle tends to maintain the knee towards full extension, especially against rotatory stresses, while the anteromedial bundle is the main constraint against anterior tibial translation.
