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The anterior cruciate ligament (ACL) fails to heal adequately after rupture, even after partial injuries or primary repair. This is vastly different from the extra-articular medial collateral ligament (MCL), which heals even without surgical intervention. The reasons for this involve cellular and structural factors. On a cellular level, ACL cells have decreased migration and different extracelluar matrix production profiles when compared with MCL cells; however, it is unlikely that these small differences are fully responsible for the stark dichotomy in healing response for the two ligaments. With regards to structural issues, recent experiments have shown a premature loss of the bridge between the ruptured ACL ends, and this structural defect is also likely a key factor in the failure of the ACL to heal. New approaches using a substitute bridge, or provisional scaffold, with implanted growth factors are being developed to stimulate the ACL to heal after primary repair. To lay the foundation for these new approaches, the four phases of the injury response in the ACL (inflammatory, epiligamentous regeneration, proliferative, and remodeling phases), and the differences in intrinsic ACL and MCL cellular response are reviewed in this article followed by a discussion of the manipulations currently being attempted to improve the healing response of the ACL, including hyaluronic acid, implanted growth factors, and tissue engineered scaffolds.