Morphology of the proximal femur differs widely with age and sex: relevance to design and selection of femoral prostheses.

The ability of uncemented femoral stems to osseointegrate properly depends largely on their fit in the proximal femur. We evaluated the topography of the proximal femur and determined differences based on age and sex. Retrospectively, anteroposterior radiographs from 312 (168 male, 144 female) pre-operative total hip arthroplasty (THA) patients (age of 21-85 years) were collected.

Revision for stiffness following TKA: a predictable procedure?

Background: Stiffness is a known complication following total knee arthroplasty. Multiple options are available to address this problem but revision TKA has been reported to be an effective treatment especially in the presence of technical issues such as oversized or loose components. However, it is not clearly known what factors may affect the outcome of revision TKA for stiffness.

Primary total hip arthroplasty with an uncemented femoral component five- to nine-year results.

This study reports the outcome of total hip arthroplasty with use of an uncemented, tapered stem with a 5- to 9-year follow-up. The first 200 consecutive patients (214 hips) undergoing total hip arthroplasty with the Accolade TMZF stem (Stryker Orthopaedics, Mahwah, NJ) were enrolled prospectively. Follow-up for these patients averaged 7.

Stiffness after revision total knee arthroplasty.

Stiffness after a revision total knee arthroplasty (TKA) is a disabling complication that has largely been overlooked in the literature. This study attempts to define the prevalence of stiffness after revision TKA and to determine the risk factors that may lead to its development. Thirty-two knees (4.

TRAF6 autoubiquitination-independent activation of the NFkappaB and MAPK pathways in response to IL-1 and RANKL.

The adapter protein TRAF6 is critical for mediating signal transduction from members of the IL-1R/TLR and TNFR superfamilies. The TRAF6 RING finger domain functions as an ubiquitin E3 ligase capable of generating non-degradative K63-linked ubiquitin chains. It is believed that these chains serve as docking sites for formation of signaling complexes, and that K63-linked autoubiquitination of TRAF6 is essential for formation and activation of a complex involving the kinase TAK1 and its adapters, TAB1 and TAB2.

TRAF6 is a T cell-intrinsic negative regulator required for the maintenance of immune homeostasis.

TRAF6 has a key role in the regulation of innate immune responses by mediating signals from both TNF receptor and interleukin-1 receptor/Toll-like receptor superfamilies. Here we show that T cell-specific deletion of TRAF6 unexpectedly results in multiorgan inflammatory disease. TRAF6-deficient T cells exhibit hyperactivation of the phosphatidylinositol 3-kinase (PI3K)-Akt pathway compared with wild-type T cells and, as a result, become resistant to suppression by CD4+ CD25+ regulatory T cells.