Regenerative Repair of Bone Defects with Osteoinductive Hydroxyapatite Fabricated to Match the Defect and Implanted with CAD, CAM, and Computer-Assisted Surgery Systems

Regenerative repair of large bone defects currently remains a challenging issue during surgery, owing to the limited regenerative ability of the bone. To address this issue, we attempted a precise repair of a bone defect using computer-aided procedures. Using pelvic computed tomography (CT) images of beagle dogs, virtual tumors were created in the pelvis using computer-aided design (CAD), and a bone resection following the margins of the bone tumor was performed on the CAD image. Hydroxyapatite (HA) implants to fill the bone defects and implants for shape evaluation of bone resection sites were designed and produced by computer-aided manufacturing and three-dimensional printing. Subsequently, using a computer navigation system, iliac bone defects were created in beagle dogs as preoperatively planned on CAD, filled with HA implants shaped to fit the bone defect sites, and coated with a recombinant human bone morphogenetic protein (rhBMP)-2-containing dough bone-forming material. Postoperative CT revealed that the new bone was formed around the implant over time. Anatomical healthy bone repair was confirmed to be completed 12 weeks after the surgery. These results demonstrate potential novel technology for efficacious and accurate repair of large bone defects without bone grafting

Estrogen Prevents Bone Loss via Estrogen Receptor α and Induction of Fas Ligand in Osteoclasts

SummaryEstrogen prevents osteoporotic bone loss by attenuating bone resorption; however, the molecular basis for this is unknown. Here, we report a critical role for the osteoclastic estrogen receptor α (ERα) in mediating estrogen-dependent bone maintenance in female mice. We selectively ablated ERα in differentiated osteoclasts (ERαΔOc/ΔOc) and found that ERαΔOc/ΔOc females, but not males, exhibited trabecular bone loss, similar to the osteoporotic bone phenotype in postmenopausal women. Further, we show that estrogen induced apoptosis and upregulation of Fas ligand (FasL) expression in osteoclasts of the trabecular bones of WT but not ERαΔOc/ΔOc mice. The expression of ERα was also required for the induction of apoptosis by tamoxifen and estrogen in cultured osteoclasts. Our results support a model in which estrogen regulates the life span of mature osteoclasts via the induction of the Fas/FasL system, thereby providing an explanation for the osteoprotective function of estrogen as well as SERMs

Blocking of tumor necrosis factor activity promotes natural repair of osteochondral defects in rabbit knee

Background and purpose Osteochondral defects have a limited capacity for repair. We therefore investigated the effects of tumor necrosis factor (TNF) signal blockade by etanercept (human recombinant soluble TNF receptor) on the repair of osteochondral defects in rabbit knees

Individuality and reproducibility in high-speed motion of volleyball spike jumps by phase-matching and averaging

Pour l'analyse des traumatismes du genou en volleyball, un système a été développé pour obtenir des représentations en forme d'onde du mouvement très rapide des sauts de smash

Cooperative Inhibition of Bone Morphogenetic Protein Signaling by Smurf1 and Inhibitory Smads

Smad ubiquitin regulatory factor (Smurf) 1 binds to receptor-regulated Smads for bone morphogenetic proteins (BMPs) Smad1/5 and promotes their degradation. In addition, Smurf1 associates with transforming growth factor-β type I receptor through the inhibitory Smad (I-Smad) Smad7 and induces their degradation. Herein, we examined whether Smurf1 negatively regulates BMP signaling together with the I-Smads Smad6/7. Smurf1 and Smad6 cooperatively induced secondary axes in Xenopus embryos. Using a BMP-responsive promoter-reporter construct in mammalian cells, we found that Smurf1 cooperated with I-Smad in inhibiting BMP signaling and that the inhibitory activity of Smurf1 was not necessarily correlated with its ability to bind to Smad1/5 directly. Smurf1 bound to BMP type I receptors via I-Smads and induced ubiquitination and degradation of these receptors. Moreover, Smurf1 associated with Smad1/5 indirectly through I-Smads and induced their ubiquitination and degradation. Smurf1 thus controls BMP signaling with and without I-Smads through multiple mechanisms