Investigating the effect of autograft diameter for quadriceps and patellar tendons use in anterior cruciate ligament reconstruction: a biomechanical analysis using a simulated Lachman test

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.

Revision anterior cruciate ligament (ACL) reconstruction is poorly described because of its rare incidence and mainly small case series presented in the literature. The Danish ACL reconstruction registry has monitored the development in revision ACL reconstruction since 2005.

In this study, porcine bone-anterior cruciate ligament-bone (B-ACL-B) grafts were decellularized using one of three protocols incorporating surfactants lauryl sulfate (SDS), Triton X-100, and/or an organic solvent (tributyl phosphate (TnBP)). The effectiveness of Triton-SDS, Triton-Triton or Triton-TnBP treatments in removing cellular materials was determined and possible changes in biochemical composition and mechanical properties due to each treatment were investigated. Treatment with Triton-SDS was most effective at removing cell nuclei and intracellular protein (vimentin) from the ACL but affected both the collagen and glycosaminoglycan (GAG) components of the extracellular matrix while increasing the tensile stiffness of the ligament. Triton-Triton was the least effective of the three treatments in terms of cellular extraction, but did not significantly change the mechanical and biochemical properties of the ACL. Triton-TnBP matched the level of decellularization achieved by Triton-SDS in terms of visible cell nuclei; however, the extraction of intracellular vimentin was less consistent. TnBP treatment also slightly decreased the collagen content of the ACL but did not alter its mechanical properties. Overall, all three decellularization treatments maintained adequate mechanical and biochemical properties of B-ACL-B grafts to justify the further investigation of all three decellularization protocols. The selection of a superior treatment will depend on future studies of the propensity of treated tissues for repopulation by host ACL fibroblasts and, ultimately, on any immunogenic and/or remodeling host response induced in vivo.