Acute Anterior Cruciate Ligament Rupture: A Biological Approach through Primary Anterior Cruciate Ligament Repair, Augmentation with Bone Marrow Stimulation, and Growth Factor Injection


Introduction

Anterior cruciate ligament (ACL) injuries are common in recreational and competitive sporting activities. According to an ongoing study in the United States, an estimated 200,000 ACL reconstructions (ACLRs) are performed annually, and the incidence of ACL injury is roughly 1 in 3000 per year. The treatment of ACL injury is an area of considerable controversy, despite advances in sports medicine literature. The current gold standard for the treatment of acute ACL lesions is reconstruction with tendon graft, with a high success rate of 80%. Despite the good results, donor site morbidity, poor proprioception, and incomplete return to high-risk sports are potential pitfalls of this procedure. In addition, there is the risk of iatrogenic damage of the distal femoral or the proximal tibial growth plate, and subsequent growth disturbance and angular deformity in adolescents.

Considering the fact that ACL injury most commonly affects young people, leading to significant morbidity, other therapeutic options should be investigated to effectively address acute partial ACL lesions. In addition, developing a regenerative method for ACL repair would preserve the proprioceptive function and the architecture of the ligament insertion site.

Is Anterior Cruciate Ligament Repair Feasible?

Many authors in animal and in vitro studies investigated ACL biology and its healing response to injury. Rapid degeneration of ACL has been observed following acute rupture, which is associated with a significant increase in collagenase activity and a decrease in total collagen of the injured ligament. The poor healing abilities of ACL, when compared with the medial collateral ligament (MCL), are well known. The outgrowth of cells from ACL explants in vitro was slower than from MCL explants, as shown by the size of the surrounding clusters of cells, suggesting a lower proliferation and migration potential of ACL cells in comparison with MCL cells. In a rabbit model, a higher level of procollagen mRNA was consistently detected in normal MCL than in normal ACL, suggesting higher collagen synthetic activity in the MCL and possible differences in their healing capacities.

Comparing the healing response of ACL with other ligaments, the process of platelet fibrin clot formation of injured ACL is deranged/deficient. Without this clot, the wound remains opened and interferes with tissue remodeling and cellular migration, ultimately leading to nonhealing of the ruptured ligament. Presence of circulating plasmin in the joint space, which prematurely breaks down the fibrin clot, has been postulated to be the reason for lack of clot formation. Moreover, synovial fluid is also proven to inhibit ACL fibroblast proliferation and migration and thereby retard healing of tissue. Identification of strategies that could either form or aid in the formation of a scaffold between the tendon ends to address this problem has become an area of active research and investigation.

Primary Anterior Cruciate Ligament Repair—Healing Stimulation

The primary suture repair of the torn portions of the ACL was popularized in the 1950s. Long-term follow-up studies showed that these techniques presented failure rates up to 90% and were therefore abandoned. Despite these reports, recent investigations showed the possibility of ACL healing after primary suture of the ligament augmented with the use of growth factors and bone marrow–derived mesenchymal stem cells (MSCs). The potential advantages over ACLR technique are the preservation of the anatomy and kinematics of the ACL and knee proprioception, while donor site morbidity and muscular weakness are significantly reduced.

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