Th), trabecular separation (Tb.Sp), trabecular number (Tb.N) and specific bone surface (BS/BV). Only small differences between IPL and CTan were found for BV/TV. For Tb.Th, Tb.Sp and BS/BV high correlations (R2 ≥ 0.99) were observed between the two software packages, but important relative offsets were observed. For microCT scans, the offsets were relative constant, e.g., around 15% for Tb.Th. However, for the HR-pQCT scans the mean relative offsets ranged over the different bone samples (e.g., for Tb.Th from 14.5% to 19.8%). For Tb.N, poor correlations (0.43 ≤ R2 ≤ 0.81) for all tested cases were observed. We conclude that trabecular bone microstructural parameters obtained with IPL and CTan cannot be directly compared except for BV/TV. For Tb.Th, Tb.Sp and BS/BV, correction factors can be determined, but these depend on both the image voxel size and specific anatomic location. The two software packages did not produce consistent data on Tb.N. The development of a universal standard seems desirable.Endochondral ossification is the major process of long bone formation, and chondrogenesis is the final step of this process. Several studies have indicated that bone morphogenetic proteins (BMPs) are required for chondrogenesis and regulate multiple growth plate features. Abnormal BMP pathways lead to growth plate defects, resulting in osteochondrodysplasia. The SPARC-related modular calcium binding 2 (SMOC2) gene encodes an extracellular protein that is considered to be an antagonist of BMP signaling. In this study, we generated a mouse model by knocking-in the SMOC2 mutation (c.1076 T > G), which showed short-limbed dwarfism, reduced, disorganized, and hypocellular proliferative zones and expanded hypertrophic zones in tibial growth plates. To determine the underlying pathophysiological mechanism of SMOC2 mutation, we used knock-in mice to investigate the interaction between SMOC2 and the BMP-SMAD1/5/9 signaling pathway in vivo and in vitro. Eventually, we found that mutant SMOC2 could not bind to COL9A1 and HSPG. Furthermore, mutant SMOC2 inhibited BMP signaling by competitively binding to BMPR1B, which lead to defects in growth plates and short-limbed dwarfism in knock-in mice.It has been assumed that the secondary cartilage in the temporomandibular joint (TMJ), which is the most complex and mystery joint and expands rapidly after birth, is formed by periochondrium-derived chondrocytes. The TMJ condyle has rich attachment sites of tendon, which is thought to be solely responsible for joint movement with a distinct cell lineage. Here, we used a Scx-Cre ERT2 mouse line (the tracing line for progenitor and mature tendon cells) to track the fate of tendon cells during TMJ postnatal growth. Our data showed a progressive differentiation of Scx lineage cells started at tendon and the fibrous layer, to cells at the prechondroblasts (Sox9 -/Col I +), and then to cells at the chondrocytic layer (Sox9 +/Col I -). Importantly, the Scx + chondrocytes remained as "permanent" chondrocytes to maintain cartilage mass with no further cell trandifferentiation to bone cells. This notion was substantiated in an assessment of these cells in Dmp1 -null mice (a hypophosphatemic rickets model), where there was a significant increase in the number of Scx lineage cells in response to hypophosphatemia. In addition, we showed the origin of disc, which is derived from Scx + cells. Thus, we propose Scx lineage cells play an important role in TMJ postnatal growth by forming the disc and a new subset of Scx + chondrocytes that do not undergo osteogenesis as the Scx - chondrocytes and are sensitive to the level of phosphorous.Repair or regeneration of load-bearing bones has long been an incentive for the tissue engineering community to develop a plethora of synthetic bone scaffolds. Despite the key role of physical forces and the mechanical environment in bone regeneration, the mechanotransduction concept has rarely been incorporated in structural design of bone tissue scaffolds, particularly those made of bioactive materials such as hydrogels and bioceramics. Herein, we introduce a modular design strategy to fabricate a load bearing device that can support a wide range of hydrogel- and ceramic-based scaffolds against complex in-vivo loading conditions to induce desirable mechanical strains for bone regeneration within the scaffolds. The device is comprised of a fenestrated polymeric shell and ceramic structural pillars arranged in a sophisticated configuration to provide ample internal space for the scaffold, also enabling it to purposely regulate the levels of strains and stresses within the scaffolds. Utilizing this top-down design approach, we demonstrate that the failure load of alginate hydrogels increases 3200-fold in compression, 300-fold in shear and 75-fold in impact, achieving the values that enable them to withstand physiological loads in weight-bearing sites, while allowing generation of osteoinductive strains (i.e., 0.2-0.4%) in the hydrogel. This modular design approach opens a broad range of opportunities to utilize various bioactive but mechanically weak scaffolds for the treatment of load-bearing defects and exploiting mechanobiology strategies to improve bone regeneration.A class of phenolic-chitosan quaternary ammonium derivatives have been designed and synthesized.  https://www.selleckchem.com/products/zeocin.html  Three chitosan derivatives possess effective structure of hydroxycinnamic acid have been obtained through chemical modification to get chitosan derivatives owning high antioxidant activity and antitumor activity. In this study, the scavenging ability of DPPH, hydroxyl (•OH), and superoxide (O2•-) free radical and reducing power have been tested to evaluate the antioxidant activity of the synthesized chitosan derivatives. Base on the value of IC50, the chitosan derivatives have the best inhibitory property of 0.019 mg/mL (DPPH), 0.016 mg/mL (•OH), and 0.008 (O2•-), respectively; and the chitosan derivatives with conjugate structure of ferulic acid and sinapic acid (4b and 4c) show promising antitumor activity toward A549 cells with the IC50 of 0.046 and 0.052 mg/mL. These data indicate that the chitosan derivatives with phenolic group give much stronger antioxidant activity and antitumor activity. On the other hand, the synthesized chitosan derivatives show no cytotoxicity for L929 cells at the testing concentrations.