The physicochemical and biomechanical profile of forsterite and its osteogenic potential of mesenchymal stromal cells.

It has been demonstrated that nanocrystalline forsterite powder synthesised using urea as a fuel in sol-gel combustion method had produced a pure forsterite (FU) and possessed superior bioactive characteristics such as bone apatite formation and antibacterial properties. In the present study, 3D-scaffold was fabricated using nanocrystalline forsterite powder in polymer sponge method. The FU scaffold was used in investigating the physicochemical, biomechanics, cell attachment, in vitro biocompatibility and osteogenic differentiation properties. For physicochemical characterisation, Fourier-transform infrared spectroscopy (FTIR), Energy dispersive X-ray (EDX), X-ray diffraction (XRD), Raman spectroscopy, X-ray photoemission spectrometer (XPS) and Brunauer-Emmett-Teller (BET) were used. FTIR, EDX, XRD peaks and Raman spectroscopy demonstrated correlating to FU. The XPS confirmed the surface chemistry associating to FU. The BET revealed FU scaffold surface area of 12.67 m2/g and total pore size of 0.03 cm3/g. Compressive strength of the FU scaffold was found to be 27.18 ± 13.4 MPa. The human bone marrow derived mesenchymal stromal cells (hBMSCs) characterisation prior to perform seeding on FU scaffold verified the stromal cell phenotypic and lineage commitments. SEM, confocal images and presto blue viability assay suggested good cell attachment and proliferation of hBMSCs on FU scaffold and comparable to a commercial bone substitutes (cBS). Osteogenic proteins and gene expression from day 7 onward indicated FU scaffold had a significant osteogenic potential (p<0.05), when compared with day 1 as well as between FU and cBS. These findings suggest that FU scaffold has a greater potential for use in orthopaedic and/or orthodontic applications.

Zinc and Metallothionein in the Development and Progression of Dental Caries.

Chronic oxidative stress and reactive oxygen species (ROS) in oral cavity as well as acidic pH on dental enamel surface due to the metabolic activities of bacterial plaque are the major contributors in the development and progression of dental caries. Along with other factors, deposition or dissolution Ca and Mg mostly determines the re- or demineralization of dental enamel. Zn plays an important role for both Ca and Mg bioavailability in oral cavity. Metallothionein (MT), a group of small molecular weight, cysteine-rich proteins (~ 7 kDa), is commonly induced by ROS, bacterial infection, and Zn. In the current review, we evaluated MT at the junction between the progression of dental caries and its etiologies that are common in MT biosynthesis.

AFM analysis of collagen fibrils in expanded scalp tissue after anisotropic tissue expansion.

Successful use of tissue expanders depends on the quality of expanded tissue. This study evaluates the impact of anisotropic self-inflating tissue expander (SITE) on the biomechanics of skin. Two different SITE were implanted subcutaneously on sheep scalps; SITE that requires 30days for maximum expansion (Group A; n=5), and SITE that requires 21days for maximum expansion (Group B; n=5). Control animals (n=5) were maintained without SITE implantation. Young's Modulus, D-periodicity, overlap and gap region length, diameter, and height difference between overlap and gap regions on collagen fibrils were analyzed using atomic force microscopy. Histology showed no significant differences in dermal thickness between control and expanded skin of groups A and B. Furthermore, most parameters of expanded skin were similar to controls (p>0.05). However, the height difference between overlap and gap regions was significantly smaller in group B compared to both control and group A (p<0.01). Strong correlation was observed between Young's Modulus of overlap and gap regions of the control and group A, but not group B. Results suggest that a relatively slower SITE can be useful in reconstructive surgery to maintain the biomechanical properties of expanded skin.

Cellular and Molecular Responses to Mechanical Expansion of Tissue.

The increased use of tissue expander in the past decades and its potential market values in near future give enough reasons to sum up the consequences of tissue expansion. Furthermore, the patients have the right to know underlying mechanisms of adaptation of inserted biomimetic, its bioinspired materials and probable complications. The mechanical strains during tissue expansion are related to several biological phenomena. Tissue remodeling during the expansion is highly regulated and depends on the signal transduction. Any alteration may lead to tumor formation, necrosis and/or apoptosis. In this review, stretch induced cell proliferation, apoptosis, the roles of growth factors, stretch induced ion channels, and roles of second messengers are organized. It is expected that readers from any background can understand and make a decision about tissue expansion.

Molecular Mechanisms of Stress-Responsive Changes in Collagen and Elastin Networks in Skin.

Collagen and elastin networks make up the majority of the extracellular matrix in many organs, such as the skin. The mechanisms which are involved in the maintenance of homeostatic equilibrium of these networks are numerous, involving the regulation of genetic expression, growth factor secretion, signalling pathways, secondary messaging systems, and ion channel activity. However, many factors are capable of disrupting these pathways, which leads to an imbalance of homeostatic equilibrium. Ultimately, this leads to changes in the physical nature of skin, both functionally and cosmetically. Although various factors have been identified, including carcinogenesis, ultraviolet exposure, and mechanical stretching of skin, it was discovered that many of them affect similar components of regulatory pathways, such as fibroblasts, lysyl oxidase, and fibronectin. Additionally, it was discovered that the various regulatory pathways intersect with each other at various stages instead of working independently of each other. This review paper proposes a model which elucidates how these molecular pathways intersect with one another, and how various internal and external factors can disrupt these pathways, ultimately leading to a disruption in collagen and elastin networks.