Biology of Graft Incorporation

Introduction The bony insertion of the anterior cruciate ligament (ACL) is comprised of four distinct zones: ligamentous tissue, noncalcified fibrocartilage, calcified fibrocartilage, and bone. This “enthesis” is responsible for effectively transmitting the forces from the elastic ligament to the stiff bone. Despite its well organized structure, the enthesis has limited vascularity and thereby poor healing capacity(16, 40). As a result, primary repair of a torn ACL has been shown to be ineffective in restoring knee kinematics and stability, and reconstruction of the ligament (with autogenous or allogenous tissue) has become the standard of care. Although the outcomes following ACL reconstruction are generally good, there remains a 7-10 % overall re-rupture rate which warrants further evaluation(11). Technical errors (most frequently malposition of the femoral tunnel) are the most common cause of graft failure(18). However, 3 27% of ACL reruptures are considered “biologic” graft failures, which occur due to inappropriate graft ligamentization and inadequate graftto-bone tunnel healing(18). In the early post-operative phase, the primary strength of an ACL graft is afforded by the means of femoral and tibial fixation. However, long-term stability and the ultimate success of ACL reconstruction are dependent mainly on the secondary mechanical properties of the graft – instilled through the remodeling and graft-to-bone incorporation processes28. The purpose of this review is to discuss the important aspects of graft-to-bone healing and highlight their clinical relevance in anatomic ACL reconstruction.