Basic science of anterior cruciate ligament injury and repair

Abstract

Injury to the anterior cruciate ligament (ACL) is one of the most devastating and frequent injuries of the knee. Surgical reconstruction is the current standard of care for treatment of ACL injuries in active patients. The widespread adoption of ACL reconstruction over primary repair was based on early perception of the limited healing capacity of the ACL. Although the majority of ACL reconstruction surgeries successfully restore gross joint stability, post-traumatic osteoarthritis is commonplace following these injuries, even with ACL reconstruction. The development of new techniques to limit the long-term clinical sequelae associated with ACL reconstruction has been the main focus of research over the past decades. The improved knowledge of healing, along with recent advances in tissue engineering and regenerative medicine, has resulted in the discovery of novel biologically augmented ACL-repair techniques that have satisfactory outcomes in preclinical studies. This instructional review provides a summary of the latest advances made in ACL repair. Cite this article: Bone Joint Res 2014;3:20-31.

Keywords: Anterior cruciate ligament; Injury; Repair.

Fig. 1

Schematic showing the multi-planar loading mechanism of non-contact injury to the anterior cruciate ligament (Adapted and modified with permission from Levine et al).

Fig. 2

Diagrams showing the differences in intrinsic healing response of the anterior cruciate ligament (ACL; top) and medial collateral ligament (MCL; bottom), highlighting the lack of provisional scaffold (blood clot) formation within the ACL wound site as the key mechanism for ACL healing failure (reproduced with permission from Murray and Fleming).

Fig. 3

Representative photomicrographs of patellar ligament wounds (extra-articular, EA), untreated anterior cruciate ligament (ACL) wounds (intra-articular, IA) and treated ACL with collagen-platelet scaffold (IA Tx) at 21 days after injury (10x). Treated ACLs show similar distribution of protein presence as the patellar ligament. The untreated ACL wounds remain with almost no substratum (PDGF-A: platelet-derived growth factor; TGF-β: transforming growth factor; FGF: fibroblast growth factor) (adapted and modified with permission from Murray et al).

Fig. 4

Schematic of bio-enhanced anterior cruciate ligament (ACL) repair method (adapted and modified with permission from Murray and Fleming).

Fig. 5

Bar chart showing identical mechanical properties of bio-enhanced repaired anterior cruciate ligament (ACL) (Repair) compared with the surgically reconstructed samples (ACLR) (p > 0.6 for all comparisons), with significantly lower mechanical properties (*) within the untreated ACL rupture group (Tx) (reproduced with permission from Murray and Fleming).

Fig. 6

Photographs showing the distal femoral cartilage at one year after a) an untreated anterior cruciate ligament (ACL) rupture, b) after conventional ACL reconstruction, and c) bio-enhanced ACL repair. Note the damage to the medial femoral condyle in the untreated and ACL-reconstructed knee (black arrows). No damage to the medial femoral condyle in the bio-enhanced ACL-repair knee (white arrow) was observed (adapted and modified with permission from Murray and Fleming ).