Download A Tissue Regeneration Approach to Bone and Cartilage Repair by Hala Zreiqat, Colin R. Dunstan, Vicki Rosen PDF

By Hala Zreiqat, Colin R. Dunstan, Vicki Rosen

Reviewing exhaustively the present cutting-edge of tissue engineering techniques for regenerating bones and joints by utilizing biomaterials, development components and stem cells, besides an research of the interactions among biomaterials, bone cells, development components and further stem cells and the way jointly skeletal tissues may be optimised, this e-book serves to focus on the significance of biomaterials composition, floor topography, architectural and mechanical homes in supplying help for tissue regeneration.

Maximizing reader insights into the significance of the interaction of those attributes with bone cells (osteoblasts, osteocytes and osteoclasts) and cartilage cells (chondrocytes), this e-book additionally presents an in depth reference as to how key signalling pathways are activated. The contribution of progress elements to force tissue regeneration and stem mobilephone recruitment is mentioned in addition to a overview the aptitude and demanding situations of grownup or embryonic mesenchymal stem cells to extra increase the formation of latest bone and cartilage tissues.

This booklet serves to illustrate the interconnectedness of biomaterials, bone/cartilage cells, development components and stem cells in identifying the regenerative technique and therefore the medical outcome.

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Extra resources for A Tissue Regeneration Approach to Bone and Cartilage Repair

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2005), increases the expression of a number of genes, including a sufficient increase in RANKL production by the cells to support osteoclast formation and activity (Wijenayaka et al. 2011). In these experiments, an increased rate of osteocyte apoptosis was not observed, suggesting that viable osteocytes may also initiate osteoclastogenesis and progress osteoclastic bone resorption. It is noteworthy that as an osteoclast tunnels through the bone matrix, it would encounter an osteocyte cell process every 2–3 μm in three dimensions, providing ample opportunity for intercellular contact (Atkins and Findlay 2012).

In vivo studies also demonstrated that BMP-2 induced expression of several Wnt ligands and their receptors, and activated β-catenin-mediated T cell factor (TCF)dependent transcriptional activity. Mice expressing conditional β-catenin null alleles displayed inhibition of BMP-induced chondrogenesis and osteogenesis (Chen et al. 2007). These findings suggest that BMP-2-induced bone formation may be mediated by canonical Wnt/β-catenin signaling. In contrast, other reports showed that BMPs induced Sost expression in Saos-2 osteosarcoma cells (Yu et al.

2011), at least in mice. Increased RANKL expression in association with osteocyte apoptosis is consistent with the extensive bone resorption, which was observed several days after induction of osteocyte ablation in mice, in association with dramatically increased RANKL expression in the bone (Tatsumi et al. 2007). We have also shown that exposure of osteocytes to exogenous sclerostin, a protein whose expression is largely confined to osteocytes (Poole et al. 2005), increases the expression of a number of genes, including a sufficient increase in RANKL production by the cells to support osteoclast formation and activity (Wijenayaka et al.

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