ABSTRACT
BACKGROUND: Preservation of the Anterior Cruciate Ligament (ACL) remnant is important from the biological point of view as it enhances revascularization, and preserves the proprioceptive function of the graft construct. Additionally, it may have a useful biomechanical function. Double bundle ACL reconstruction has been shown to better replicate the native ACL anatomy and results in better restoration of the rotational stability than single bundle reconstruction. METHODS: We used the far anteromedial (FAM) portal for creation of the femoral tunnels, with a special technique for its preoperative localization using three dimensional (3D) CT. The central anteromedial (AM) portal was used to make a longitudinal slit in the ACL remnant to allow visualization of the tips of the guide pins during anatomical creation of the tibial tunnels within the native ACL tibial foot print. The use of curved hemostat allow retrieval of the wire loop from the apertures of the femoral tunnels through the longitudinal slit in the ACL remnant thereby, guarding against impingement of the reconstruction graft against the ACL remnant as well as the roof of the intercondylar notch. CONCLUSION: Our technique allows for anatomical double bundle reconstruction of the ACL while maximally preserving the ACL remnant without the use of intra-operative image intensifier.
ABSTRACT
OBJECTIVE: miRNAs, which are non-coding RNAs, play a role in the pathogenesis of disease including OA. miRNA (miR)-34a is induced by p53, subsequently leading to cell apoptosis, which is one of the major factors in the pathogenesis of OA. The purpose of this study is to investigate the effect of silencing miR-34a on IL-1ß-induced chondrocyte apoptosis in a rat OA model in vitro. METHODS: Locked nucleotide analogue (LNA)-modified miR-34a-specific anti-sense was transfected into rat chondrocyte monolayer culture. After that, IL-1ß was added to the chondrocytes to create an OA model in vitro. The effect of silencing miR-34a on the prevention of chondrocyte apoptosis was analysed by assessment of the expression levels of Col2a1 and iNOS, also through assessment of cell viability and TUNEL staining. RESULTS: The expression of miR-34a was significantly up-regulated by IL-1ß. Silencing of miR-34a significantly prevented IL-1ß-induced down-regulation of Col2a1, as well as IL-1ß-induced up-regulation of iNOS. Finally, MiR-34a inhibitor could also reduce TUNEL-positive cells. CONCLUSION: Silencing of miR-34a by LNA-modified anti-sense could effectively reduce rat chondrocyte apoptosis induced by IL-1ß. This present study revealed that silencing of miR-34a might develop a novel intervention for OA treatment through the prevention of cartilage degradation.
