The anterior cruciate ligament (ACL) is a band of dense connective tissue which courses from the femur to the tibia. The ACL is a key structure in the knee joint, as it resists anterior tibial translation and rotational loads. When the knee is extended, the ACL has a mean length of 32 mm and a width of 7-12 mm. There are two components of the ACL, the anteromedial bundle (AMB) and the posterolateral bundle (PLB). They are not isometric with the main change being lengthening of the AMB and shortening of the PLB during flexion. The ACL has a microstructure of collagen bundles of multiple types (mostly type I) and a matrix made of a network of proteins, glycoproteins, elastic systems, and glycosaminoglycans with multiple functional interactions. The complex ultrastructural organization and abundant elastic system of the ACL allow it to withstand multiaxial stresses and varying tensile strains. The ACL is innervated by posterior articular branches of the tibial nerve and is vascularized by branches of the middle genicular artery.

The use of a QT graft in ACL reconstruction leads to equal or better functional outcomes than does the use of an HT graft, without affecting morbidity.

Anterior cruciate ligament (ACL) reconstruction has the best chance for success when the graft undergoes extensive biologic remodeling and incorporation after implantation. There are many factors that can lead to graft failure and possible revision surgery. These include patient selection; surgical technique such as graft placement and tensioning; the use of allograft versus autograft; mechanical factors such as secondary restraint laxity; lack of a correct, carefully controlled post-operative rehabilitation program; and biological factors. When a patient presents with knee instability following ligament reconstruction and there is no history of a new trauma or identifiable technical error, biological failure should be considered. However, the biologic response of the grafted tissue is closely linked to the mechanical and biochemical environment into which the graft is placed. Thus, the "biological failure" of the ACL graft is a complex pathological entity whose cause is not fully understood. Failure may be initiated by early extensive graft necrosis, disturbances in revascularization, problems in cell repopulation and proliferation, and as well difficulties in the ligamentization process. However, further study of the biological characterization of a failed graft placed in a correct mechanical environment is warranted.

Inaugural traumatic patellar dislocation is most often due to trauma sustained during physical or sports activity. Two-thirds of acute patellar dislocations occur in young active patients (less than 20 years old). Non-contact knee sprain in flexion and valgus is the leading mechanism in patellar dislocation, accounting for as many as 93% of all cases. The strong displacement of the patella tears the medial stabilizing structures, and notably the medial patellofemoral ligament (MPFL), which is almost always injured in acute patellar dislocation, most frequently at its femoral attachment. Lateral patellar glide can be assessed with the knee in extension or 20° flexion. Displacement by more than 50% of the patellar width is considered abnormal and may induce apprehension. Plain X-ray and CT are mandatory to diagnose bony risk factors for patellar dislocation, such as trochlear dysplasia or increased tibial tubercle-trochlear groove distance (TT-TG), and plan correction. MRI gives information on cartilage and capsulo-ligamentous status for treatment planning: free bodies or osteochondral fracture have to be treated surgically. If patellar dislocation occurs in an anatomically normal knee and osteochondral fracture is ruled out on MRI, non-operative treatment is usually recommended.

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