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Measuring the ACL's footprint by 3D MR imaging or open cadaveric dissection has strong agreement and can be used interchangeably. 3D MR imaging has the potential to allow surgeons to: (1) tailor ACL reconstruction technique or graft choice based on ACL footprint size, (2) plan for selective bundle ACL reconstruction for partial tears, and (3) preoperatively template tunnel position according to the patient's individual anatomy.

Despite contemporary techniques and a concerted effort to perform anatomic ACL reconstruction by 4 experienced sports orthopaedic surgeons, the position of the femoral footprint was significantly different between the native and reconstructed ACLs. Furthermore, each surgeon used a different technique, but all had comparable errors in their tunnel placements.

Oral contraceptive pill use yielded statistically significant decreases in anterior translation of the tibia as compared with nonusers. The OCP may have a role to play in the prevention of ACL injuries by prophylactically targeting 1 of the variables responsible for the increased ACL injury rates in women.

Current commercially available transtibial femoral offset guides cannot reach the center of the ACL's femoral footprint and therefore should not be used. Alternative techniques, such as referencing from the ADC through an anteromedial (AM) portal, are recommended.

In the adult skeleton, cells of the immune system interact with those of the skeleton during all phases of bone repair to influence the outcome. Mast cells are immune cells best known for their pathologic role in allergy, and may be involved in chronic inflammatory and fibrotic disorders. Potential roles for mast cells in tissue homeostasis, vascularization and repair remain enigmatic. Previous studies in combined mast cell- and Kit-deficient KitW-sh/W-sh mice (KitW-sh) implicated mast cells in bone repair but KitW-sh mice suffer from additional Kit-dependent hematopoietic and non- hematopoietic deficiencies that could have confounded the outcome. The goal of the current study was to compare bone repair in normal wild type (WT) and Cpa3Cre/+ mice, which lack mast cells in the absence of any other hematopoietic or non- hematopoietic deficiencies. Repair of a femoral window defect was characterized using micro CT imaging and histological analyses from the early inflammatory phase, through soft and hard callus formation, and finally the remodeling phase. The data indicate 1) mast cells appear in healing bone of WT mice but not Cpa3Cre/+ mice, beginning 14 days after surgery; 2) re-vascularization of repair tissue and deposition of mineralized bone was delayed and dis-organised in Cpa3Cre/+ mice compared with WT mice; 3) the defects in Cpa3Cre/+ mice were associated with little change in anabolic activity and biphasic alterations in osteoclast and macrophage activity. The outcome at 56 days postoperative was complete bridging of the defect in most WT mice and fibrous mal-union in most Cpa3Cre/+ mice. The results indicate that mast cells promote bone healing, possibly by recruiting vascular endothelial cells during the inflammatory phase and coordinating anabolic and catabolic activity during tissue remodeling. Taken together the data indicate that mast cells have a positive impact on bone repair.

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