1,271 research outputs found
Osteoindctivization of dental implants and bone- defect-filling materials
No full texthttp://www.woodheadpublishing.com/en/book.aspx?bookID=159
Preprosthetic and maxillofacial surgery: Biomaterials, bone grafting and tissue engineering
No full text
The structure of articular cartilage
No full texthttp://www.woodheadpublishing.com/en/book.aspx?bookID=148
EB development and TJ formation.
No full text<p>(<b>A</b>) Schematic diagram of EB development. The development of EBs starts with the aggregation of ESCs into suspended spheroids of inner cell mass (ICM) and parallels the development of the mouse blastocyst ICM. By day 3 of culture, the outer cells differentiate into a circumferential epithelium known as the primitive endoderm (PrEn). The apical and basal domains of the PrEn face the exterior environment and interior ICM core of the EB respectively. The EBs at this point are called simple EBs. Progressively from day 4 onwards, the PrEn basally secretes key ECM components Laminins and Collagen IV to form a basement membrane (BM). The PrEn also further differentiates in the visceral endoderm (VEn). In conjunction with this, the interior ICM differentiates into the epiblast. By day 5 or 6, the epiblast in contact with the BM in turn differentiates into the primitive ectoderm (PrEc) or epiblast epithelium. The rest of the epiblast not in contact with the BM will undergo apoptosis. The apoptotic bodies are removed by autophagy-initiated phagocytosis, leaving a progressively enlarging lumen or Proamniotic-like cavity (PAC) surrounded by the apical domain of the PrEc and the basal BM. EBs at this stage are called cystic EBs and equivalent to the egg cylinder stage of the mouse peri-implantation embryo just before gastrulation. (<b>B</b>) Immunofluorescence staining of ZO-1 and ZO-2 in Day-5 or -6 EB cryosections. WT (panels a and e), ZO-1<sup>-/-</sup> (panels b and f), ZO-2<sup>-/-</sup> (panels c and g) and ZO-1<sup>-/-</sup> ZO-2<sup>-/-</sup> (panels d and h) EBs were stained with antibodies to ZO-1 (panels a-d, green color) or ZO-2 (panels e-h, green color). Nuclei are labeled with DAPI (blue color). Magnification of image in insets. ExEn is indicated here as ‘en’. (<b>C</b>) Transmission electron micrographs. TJ complex at the apico-lateral membrane of Day-9 EB ExEn was visualized by TEM as electron-dense material (indicated by arrows in magnification of inset) in WT (panels a and e), ZO-1<sup>-/-</sup> (panels b and f) and ZO-2<sup>-/-</sup> (panels c and g) EBs. This was absent in ZO-1<sup>-/-</sup> ZO-2<sup>-/-</sup> EBs (panels d and h, arrowheads in magnification of inset). (<b>D</b>) Immunofluorescence staining of Cldn-6 in Day-9 EB cryosections. WT, ZO-1<sup>-/-</sup>, ZO-2<sup>-/-</sup> and ZO-1<sup>-/-</sup> ZO-2<sup>-/-</sup> EBs were stained with antibodies to Cldn-6 (panels a–d, green color). Nuclei are labeled with DAPI (blue color). Magnification of image in insets. ExEn is indicated here as ‘en’.</p
Differential effects of dexamethasone on the chondrogenesis of mesenchymal stromal cells: Influence of microenvironment, tissue origin and growth factor
No full textnchymal stromal cells (MSCs), which reside within various tissues, are utilized in the engineering of cartilage tissue. Dexamethasone (DEX) – a synthetic glucocorticoid – is almost invariably applied to potentiate the growth-factor-induced chondrogenesis of MSCs in vitro, albeit that this effect has been experimentally demonstrated only for transforming-growth-factor-beta (TGF-β)-stimulated bone-marrow-derived MSCs. Clinically, systemic glucocorticoid therapy is associated with untoward side effects (e.g., bone loss and increased susceptibility to infection). Hence, the use of these agents should be avoided or limited. We hypothesize that the influence of DEX on the chondrogenesis of MSCs depends upon their tissue origin and microenvironment [absence or presence of an extracellular matrix (ECM)], as well as upon the nature of the growth factor. We investigated its effects upon the TGF-β1- and bone-morphogenetic-protein 2 (BMP-2)-induced chondrogenesis of MSCs as a function of tissue source (bone marrow vs. synovium) and microenvironment [cell aggregates (no ECM) vs. explants (presence of a natural ECM)]. In aggregates of bone-marrow-derived MSCs, DEX enhanced TGF-β1-induced chondrogenesis by an up-regulation of cartilaginous genes, but had little influence on the BMP-2-induced response. In aggregates of synovial MSCs, DEX exerted no remarkable effect on either TGF-β1- or BMP-2-induced chondrogenesis. In synovial explants, DEX inhibited BMP-2-induced chondrogenesis almost completely, but had little impact on the TGF-β1-induced response. Our data reveal that steroids are not indispensable for the chondrogenesis of MSCs in vitro. Their influence is context dependent (tissue source of the MSCs, their microenvironment and the nature of the growth-factor). This finding has important implications for MSC based approaches to cartilage repair
Cartilage, bone and synovial histomorphometry in animal models of osteoarthritis
No full texthttp://www.ncbi.nlm.nih.gov/pubmed/2086401
EB ExEn differentiation is not affected by ZO-1 and/or ZO-2 deletion.
No full text<p>(<b>A</b>) Semi-quantitative RT-PCR of Day-4 EB. Reverse transcribed cDNA was amplified with specific GATA-4 and -6 primer sets at optimized cycle numbers (indicated on right side of panels). GAPDH amplification served as a control for equal RNA input. (<b>B</b>) Immunofluorescence staining of EB ExEn. Fixed and permeabilized EB cryosections were treated with antibodies immunoreactive to Dab2 (panels a-d) and Keratin-8 (Troma-1) (panels e-h) and visualized (red color). Nuclei are labeled with DAPI (blue color). Magnification of image in insets. ExEn is indicated here as ‘en’.</p
Controlled enzymatic matrix degradation for integrative cartilage repair: effects on viable cell density and proteoglycan deposition.
No full text- …
