Biology of anterior cruciate ligament injury and repair: Kappa delta ann doner vaughn award paper 2013.

Anterior cruciate ligament (ACL) injuries are currently treated by removing the injured ligament and replacing it with a tendon graft. Recent studies have examined alternative treatment methods, including repair and regeneration of the injured ligament. In order to make such an approach feasible, a basic understanding of ACL biology and its response to injury is needed.

Platelets and plasma proteins are both required to stimulate collagen gene expression by anterior cruciate ligament cells in three-dimensional culture.

Collagen-platelet (PL)-rich plasma composites have shown in vivo potential to stimulate anterior cruciate ligament (ACL) healing at early time points in large animal models. However, little is known about the cellular mechanisms by which the plasma component of these composites may stimulate healing. We hypothesized that the components of PL-rich plasma (PRP), namely the PLs and PL-poor plasma (PPP), would independently significantly influence ACL cell viability and metabolic activity, including collagen gene expression.

Interspecies variation in the fibroblast distribution of the anterior cruciate ligament.

Background: The future of the treatment of a ruptured anterior cruciate ligament is likely to involve cell-based therapies. These therapies are intrinsically dependent on the cellular distributions in the ligament. Thus, when selecting an animal model for testing of these new treatment methods, it is important to select a model that has similar cellular distributions to that of the normal human anterior cruciate ligament.

Enhanced repair of the anterior cruciate ligament by in situ gene transfer: evaluation in an in vitro model.

The inability of the ruptured anterior cruciate ligament (ACL) of the knee joint to heal spontaneously presents numerous clinical problems. Here we describe a novel, gene-based approach to augment ACL healing. It is based upon the migration of cells from the ruptured ends of the ligament into a collagen hydrogel laden with recombinant adenovirus.

The death of articular chondrocytes after intra-articular fracture in humans.

Background: In this study, we wished to determine whether chondrocyte death occurs after intra-articular fracture and might thus contribute to the development of posttraumatic arthritis.

Methods: Articular fracture fragments were obtained from 30 patients and the terminal deoxynucleotide transferase-mediated dUTP nick-end labeling assay was used to identify dead or dying cells.

Results: Dead or dying cells were identified in all fracture fragments, with an average rate of cell death of 35%.

Cell outgrowth from the human ACL in vitro: regional variation and response to TGF-beta1.

One of the new methods being developed to stimulate healing of the human anterior cruciate ligament (ACL) after rupture is the implantation of a biodegradable scaffold which the host cells invade, populate and remodel. One of the cellular behaviors critical to the success of this method is cell outgrowth from the ligament remnants onto an adjacent scaffold. As morphological differences have been previously reported in the proximal and distal human ACL, the primary aim of this study was to determine if the cells from the proximal and distal ACL had different outgrowth behaviors as well.