Cortical control of gait in aging is bilateral, widespread, and dependent on the integrity of both gray and white matter.

1) Intra-articular fractures of the calcaneus are associated with severe long-term consequences for function and pain. The condition of the soft tissues is of paramount importance when determining the method of treatment,the timing of surgery, and the post-injury rehabilitation.2) Intra-articular fractures are difficult to fully evaluate with plain radiographs. Computed tomography may assist in assessing the fracture pattern and planning for surgery. The likelihood of a good to excellent outcome is increased when an anatomic reduction is obtained.3) The outcome after operative management is difficult to characterize and appears to be influenced by factors related to the fracture, the patient, and the experience of the institution where the patient obtains treatment.All these factors should be factors in the decision to operate, but no single factor reliably determines the most appropriate treatment.4) Open reduction and internal fixation through an extensile approach achieves acceptable results in carefully selected patients. The use of a limited exposure with minimally invasive techniques may decrease the incidence of wound complications. However, this option is technically demanding and the quality of the reduction achieved may be more difficult to obtain and determine intraoperatively. Open fractures should be promptly debrided. The choice of fixation after reduction is based on the surgeons assessment of the soft tissue and the risk of infection.5) Post-traumatic arthritis of the subtalar joint is a common complication. Successful salvage can be achieved with a subtalar arthrodesis. However, these results may be influenced by the institution at which the initial management was rendered.

The TAL could not be routinely identified at surgery and when used for cup orientation it was no more accurate for cup positioning than free-hand technique.

Interleukin-1 (IL-1) is a proinflammatory cytokine that has been implicated in wear-debris associated total joint replacement failure. We hypothesized that the absence of the IL-I type-1 receptor would mitigate the inflammatory response to titanium particles and decrease periprosthetic inflammatory tissue in a murine intramedullary rod model. Methods: An intramedullary rod with and without commercially pure titanium particles was placed in the femora of 24 wild type mice (WT) and 24 mice lacking a functional type-1 receptor to IL-1. Femora were analyzed histologically and by ELTSA.of organ culture explant supernatants. Results: The presence of titanium particles in WT mice stimulated increased expression of interleukin-6 (IL-6) and macrophage chemoattractant protein-1 (MCP-1) relative to rod only controls. In contrast, IL-6 and MCP-1 expression were diminished in IL-lrl-KO mice exposed to titanium particles. Additionally, the formation of a periprosthetic fibro-inflammatory membrane in IL-1 rl -KO mice was blunted at 2 weeks when compared to that in wild-type mice. Inflammatory changes and the quality of periprosthetic bone of IL-lrl-KO mice was similar to WT mice in response to titanium particles. Conclusions: These results implicate IL-I as an important modulator in the local inflammatory response to intramedullary titanium particles. MCP-1 appears to be significantly modulated in IL-lrl-KO mice in response to titanium particles. This may be responsible, in part, for the diminished periprosthetic membrane observed in IL-lrl-KO mice at 2 weeks. Expansion of this murine model of intramedullary particle-induced inflammation to other gene targets may contribute to a more mechanistic understanding of wear-debris associated prosthesis failure.

Wear debris from total joint replacement prostheses is implicated in periprosthetic osteolysis and implant loosening. The pathophysiology of this biological process remains unclear. Animal models of particle-induced osteolysis have proven useful in the study of specific tissue responses to wear debris. However, existing in vivo murine models of particle-mediated inflammation do not permit analysis of cortical bone degradation. This study describes a murine model of particle disease using an intramedullary rod in the mouse femur to parallel the clinical situation. The model consists of placing a 10-mm-long Kirschner wire retrograde in both femurs of C57b1/6 male mice via a medial parapatellar arthrotomy. Phagocytosable titanium particles were also implanted unilaterally to replicate generation of wear debris. Mice were sacrificed at 2, 10, and 26 weeks and whole femurs were cultured for 72 h. Levels of interleukin-6, monocyte chemotactic protein-1, and macrophage colony stimulating factor were assayed by ELISA. Transverse histological sections, at the level of the implant, were taken and stained with hematoxylin and eosin (H&E). Results demonstrated increased expression of proinflammatory mediators at 2 weeks in femora with rod and particles compared to femora with rods alone. Destruction of the endosteum was evident at 2, 10, and 26 weeks in the femora with titanium. This novel murine model of particle-induced intramedullary inflammation may facilitate cost-effective genetic studies and offers investigators a simple, clinically relevant intramedullary model to readily examine the pathogenesis of particle-mediated periprosthetic osteolysis.