Effect of additional distal femoral resection on flexion deformity in posterior-stabilized total knee arthroplasty.

PURPOSE: Flexion deformity after total knee arthroplasty (TKA) is associated with poor function and dissatisfaction and should, therefore, be avoided. In the case of preoperative flexion deformity, an increased distal resection of the femur may be necessary. The degree of resection required has only been determined for cruciate-retaining (CR) prostheses to date and varies considerably from study to study. Although, for many surgeons, the algorithm for the treatment of a flexion deformity includes the resection of the posterior cruciate ligament (PCL) before additional distal resection, the degree of resection necessary for posterior-stabilized (PS)-type prostheses is not known. METHODS: Fifty consecutive patients (50 knees) who were due to undergo navigated TKA were included in this prospective study. At the end of the operation, the flexion deformity resulting from different sizes of distal femoral augmentations on the trial implants (0-8.5 mm) was determined using the navigation system. RESULTS: A linear relationship of 2.2° ± 0.3° flexion deformity per mm distal femoral augmentation was found. This was not dependent on age, sex, the preoperative coronal alignment, or the preoperative flexion deformity. CONCLUSIONS: In conclusion, after the removal of posterior osteophytes and posterior capsule release, around 5 mm of the distal femur must be further resected in the case of 10° flexion deformity and 9 mm in the case of 20° flexion deformity. LEVEL OF EVIDENCE: II (Prospective cohort study).

Thirty-eight-negative kinase 1 mediates trauma-induced intestinal injury and multi-organ failure.

Dysregulated intestinal epithelial apoptosis initiates gut injury, alters the intestinal barrier, and can facilitate bacterial translocation leading to a systemic inflammatory response syndrome (SIRS) and/or multi-organ dysfunction syndrome (MODS). A variety of gastrointestinal disorders, including inflammatory bowel disease, have been linked to intestinal apoptosis. Similarly, intestinal hyperpermeability and gut failure occur in critically ill patients, putting the gut at the center of SIRS pathology. Regulation of apoptosis and immune-modulatory functions have been ascribed to Thirty-eight-negative kinase 1 (TNK1), whose activity is regulated merely by expression. We investigated the effect of TNK1 on intestinal integrity and its role in MODS. TNK1 expression induced crypt-specific apoptosis, leading to bacterial translocation, subsequent septic shock, and early death. Mechanistically, TNK1 expression in vivo resulted in STAT3 phosphorylation, nuclear translocation of p65, and release of IL-6 and TNF-α. A TNF-α neutralizing antibody partially blocked development of intestinal damage. Conversely, gut-specific deletion of TNK1 protected the intestinal mucosa from experimental colitis and prevented cytokine release in the gut. Finally, TNK1 was found to be deregulated in the gut in murine and porcine trauma models and human inflammatory bowel disease. Thus, TNK1 might be a target during MODS to prevent damage in several organs, notably the gut.