Faculty of Dentistry

Permanent URI for this communityhttps://hdl.handle.net/1807/16909

Internationally known for its academic achievements in both clinical and research, the Faculty of Dentistry at the University of Toronto is the champion of dental school in Canada. Since founded in 1875 by the Royal College of Dental Surgeons of Ontario, the Faculty has continuously educated top-notch specialists in Orthodontics, Paediatric, Dentistry, Periodontology, Endodontics, Prosthodontics, and many more disciplines. One of the major commitments of the faculty is to dental research as no such research is carried out by private industry or government bodies. On the same page, the faculty also takes on a multi-disciplinary approach as it participates in a number of inter-faculty programs.

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The 22nd annual meeting of the European Tissue Repair Society (ETRS) in Athens, Greece
(BioMed Central, 2013-02-01) Hinz, Boris ; Ulrich, Magda ; Beele, Hilde ; Kletsas, Dimitris
The 22nd Annual Meeting of the European Tissue Repair Society, Athens, Greece, October 4 to 5, 2012 informed about pathophysiological mechanisms in tissue repair and on the development of clinical treatments of chronic wounds, fibrosis, and cancer, considering recent advances in molecular biology and biotechnology.
A Microcomputed Tomographic Evaluation of Root Canal Morphology of Maxillary Second Premolars in a Pakistani Cohort
(2021-05-31) Alkahtany, Mazen F.; Ali, Saqib; Khabeer, Abdul; Shah, Shafqat A.; Almadi, Khalid H.; Abdulwahed, Abdulaziz; Farooq, Imran; Vohra, Fahim; Abduljabbar, Tariq
This study aimed to investigate variations in the root canal morphology of maxillary second premolar (MSP) teeth using microcomputed tomography (micro-CT). Sixty (N = 60) human extracted MSPs were collected and prepared for micro-CT scanning. The duration for scanning a single sample ranged between 30 and 40 min and a three-dimensional (3-D) image was obtained for all the MSPs. The images were evaluated by a single observer who recorded the canal morphology type, number of roots, canal orifices, apical foramina(s), apical delta(s), and accessory canals. The root canal configuration was categorized in agreement with Vertucci’s classification, and any configuration not in agreement with Vertucci’s classification was reported as an “additional canal configuration”. Descriptive statistics (such as mean percentages) were calculated using SPSS software. The most common types agreeing with Vertucci’s classification (in order of highest to lowest incidence) were types I, III, V, VII, II, and VI. The teeth also exhibited four additional configurations that were different from Vertucci’s classification: types 2-3, 1-2-3, 2-1-2-1, and 1-2-1-3. A single root was found in 96.7% and the majority of the samples demonstrated two canals (73.3%). Further, 80% of the teeth showed one canal orifice. The number of apical foramina’s in the teeth was variable, with 56.7% having solitary apical foramen. The accessory canal was found in 33.3%, and apical delta was found in only 20% of the samples. Variable morphology of the MSPs was detected in our study. The canal configuration most prevalent was type 1; however, the results also revealed some additional canal types.
The Actin Binding Protein Adseverin Regulates Osteoclastogenesis
(Public Library of Science (PLoS), 2014-10-02) Hassanpour, Siavash ; Jiang, Hongwei ; Wang, Yongqiang ; Kuiper, Johannes W. P. ; Glogauer, Michael
Adseverin (Ads), a member of the Gelsolin superfamily of actin binding proteins, regulates the actin cytoskeleton architecture by severing and capping existing filamentous actin (F-actin) strands and nucleating the assembly of new F-actin filaments. Ads has been implicated in cellular secretion, exocytosis and has also been shown to regulate chondrogenesis and megakaryoblastic leukemia cell differentiation. Here we report for the first time that Ads is involved in regulating osteoclastogenesis (OCG). Ads is induced during OCG downstream of RANK-ligand (RANKL) stimulation and is highly expressed in mature osteoclasts. The D5 isoform of Ads is not involved in regulating OCG, as its expression is not induced in response to RANKL. Three clonal Ads knockdown RAW264.7 (RAW) macrophage cell lines with varying degrees of Ads expression and OCG deficiency were generated. The most drastic OCG defect was noted in the clonal cell line with the greatest degree of Ads knockdown as indicated by a lack of TRAcP staining and multinucleation. RNAi mediated knockdown of Ads in osteoclast precursors resulted in distinct morphological changes characterized by altered F-actin distribution and increased filopodia formation. Ads knockdown precursor cells experienced enhanced migration while fusion of knockdown precursors cells was limited. Transient reintroduction of de novo Ads back into the knockdown system was capable of rescuing TRAcP expression but not osteoclast multinucleation most likely due to the transient nature of Ads expression. This preliminary study allows us to conclude that Ads is a RANKL induced early regulator of OCG with a potential role in pre-osteoclast differentiation and fusion.
Actin polymerization stabilizes α4β1 integrin anchors that mediate monocyte adhesion
(Rockefeller University Press, 2012-04-02) Rullo, Jacob ; Becker, Henry ; Hyduk, Sharon J. ; Wong, Janice C. ; Digby, Genevieve ; Arora, Pamma D. ; Cano, Adrianet Puig ; Hartwig, John ; McCulloch, Christopher A. ; Cybulsky, Myron I.
Leukocytes arrested on inflamed endothelium via integrins are subjected to force imparted by flowing blood. How leukocytes respond to this force and resist detachment is poorly understood. Live-cell imaging with Lifeact-transfected U937 cells revealed that force triggers actin polymerization at upstream α4β1 integrin adhesion sites and the adjacent cortical cytoskeleton. Scanning electron microscopy revealed that this culminates in the formation of structures that anchor monocyte adhesion. Inhibition of actin polymerization resulted in cell deformation, displacement, and detachment. Transfection of dominant-negative constructs and inhibition of function or expression revealed key signaling steps required for upstream actin polymerization and adhesion stabilization. These included activation of Rap1, phosphoinositide 3-kinase γ isoform, and Rac but not Cdc42. Thus, rapid signaling and structural adaptations enable leukocytes to stabilize adhesion and resist detachment forces.
Activation of antibacterial autophagy by NADPH oxidases
(National Academy of Sciences, 2009-04-14) Huanga, Ju; Canadiena, Veronica; Lama, Grace Y.; Steinberga, Benjamin E.; Dinauer, Mary C.; Magalhaes, Marco A. O.; Glogauer, Michael; Grinstein, Sergio
Autophagy plays an important role in immunity to microbial pathogens. The autophagy system can target bacteria in phagosomes, promoting phagosome maturation and preventing pathogen escape into the cytosol. Recently, Toll-like receptor (TLR) signaling from phagosomes was found to initiate their targeting by the autophagy system, but the mechanism by which TLR signaling activates autophagy is unclear. Here we show that autophagy targeting of phagosomes is not exclusive to those containing TLR ligands. Engagement of either TLRs or the Fcγ receptors (FcγRs) during phagocytosis induced recruitment of the autophagy protein LC3 to phagosomes with similar kinetics. Both receptors are known to activate the NOX2 NADPH oxidase, which plays a central role in microbial killing by phagocytes through the generation of reactive oxygen species (ROS). We found that NOX2-generated ROS are necessary for LC3 recruitment to phagosomes. Antibacterial autophagy in human epithelial cells, which do not express NOX2, was also dependent on ROS generation. These data reveal a coupling of oxidative and nonoxidative killing activities of the NOX2 NADPH oxidase in phagocytes through autophagy. Furthermore, our results suggest a general role for members of the NOX family in regulating autophagy.
Aquaporin 9 phosphorylation mediates membrane localization and neutrophil polarization.
(Society for Leukocyte Biology, 2011-11) Karlsson, T ; Glogauer, Michael ; Ellen, EP ; Loitto, VM ; Magnusson, KE ; es, MA Magalhã
Neutrophils are of prime importance in the host innate defence against invading microorganisms by employing two primary mechanisms, locomotion towards and phagocytosis of the prey. Recent research points to pivotal roles for water channels known as aquaporins in cell motility. Here, we focused on the role of aquaporin 9 (AQP9) in chemoattractant-induced polarization and migration of primary mouse neutrophils and neutrophil-like HL60 cells. We found that AQP9 is phosphorylated downstream of the fMLF receptor or PMA stimulation in primary human neutrophils. The dynamics of AQP9 was assessed using GFP-tagged AQP9 constructs and other fluorescent markers through various live-cell imaging techniques. Expression of wild-type or the phosphomimic S11D AQP9 changed cell volume regulation as a response to hyperosmotic changes and enhanced neutrophil polarization and chemotaxis. Wt AQP9 and S11D AQP9 displayed a very dynamic distribution at the cell membrane, whereas the phosphorylation-deficient S11A AQP9 failed to localize to the plasma membrane. Furthermore, we found that Rac1 regulated the translocation of AQP9 to the plasma membrane. Our results show that AQP9 plays an active role in neutrophil volume regulation and migration. The display of AQP9 at the plasma membrane depends on AQP9 phosphorylation, which appeared to be regulated through a Rac1-dependent pathway.
Artificial Enamel Wear after Prolonged Chewing Simulation against Monolithic Y-TZP Crowns
(2018) Vedana, Deborah; Vedana, Leonardo; Martins, Emerson Alves; Brodersen, Peter; De Souza, Grace M.
The axonal repellent, Slit2, inhibits directional migration of circulating neutrophils.
(Society for Leukocyte Biology, 2009-12) Tole, S ; Mukovozov, IM ; Huang, YW ; Magalhaes, MA ; Yan, M ; Crow, MR ; Liu, GW ; Sun, CX ; Durocher, Y ; Glogauer, Michael ; Robinson, Lisa A
In inflammatory diseases circulating neutrophils are recruited to sites of injury. Attractant signals are provided by many different chemotactic molecules, such that blockade of one may not effectively prevent neutrophil recruitment. The Slit family of secreted proteins, and their transmembrane receptor, Roundabout (Robo), repel axonal migration during central nervous system development. Emerging evidence shows that by inhibiting the activation of Rho-family GTPases, Slit2/Robo also inhibit migration of other cell types towards a variety of chemotactic factors, in vitro and in vivo. The role of Slit2 in inflammation, however, has been largely unexplored. We isolated primary neutrophils from human peripheral blood and mouse bone marrow, and detected Robo-1 expression. Using video-microscopic live cell tracking, we found that Slit2 selectively impaired directional migration, but not random movement, of neutrophils towards formyl-methionyl-leucyl-phenylalanine (fMLP). Slit2 also inhibited neutrophil migration towards other chemoattractants, namely C5a and interleukin (IL)-8. Slit2 inhibited neutrophil chemotaxis by preventing chemoattractant-induced actin barbed end formation and cell polarization. Slit2 mediated these effects by suppressing inducible activation of Cdc42 and Rac2, but did not impair activation of other major kinase pathways involved in neutrophil migration. We further tested the effects of Slit2 in vivo using mouse models of peritoneal inflammation induced by sodium periodate, C5a, and macrophage inflammatory protein-2 (MIP-2). In all instances, Slit2 effectively reduced neutrophil recruitment (p < 0.01). Collectively, these data demonstrate that Slit2 potently inhibits chemotaxis, but not random motion, of circulating neutrophils, and point to Slit2 as a potential new therapeutic for preventing localized inflammation.
Bone sialoprotein does not interact with pro-gelatinase A (MMP-2) or mediate MMP-2 activation
(BioMed Central, 2009-04-22) Hwang, Queena ; Cheifetz, Sela ; Overall, Christopher M. ; McCulloch, Christopher A. ; Sodek, Jaro
Background A recent model for activation of the zymogen form of matrix metalloproteinase 2 (MMP-2, also known as gelatinase A) has suggested that interactions between the SIBLING protein bone sialoprotein (BSP) and MMP-2 leads to conformational change in MMP-2 that initiates the conversion of the pro-enzyme into a catalytically active form. This model is particularly relevant to cancer cell metastasis to bone since BSP, bound to the αvβ3 integrin through its arginine-glycine-aspartic acid motif, could recruit MMP-2 to the cell surface. Methods We critically assessed the relationship between BSP and proMMP-2 and its activation using various forms of recombinant and purified BSP and MMP-2. Gelatinase and collagenase assays, fluorescence binding assays, real-time PCR, cell culture and pull-down assays were employed to test the model. Results Studies with a fluorogenic substrate for MMP-2 showed no activation of proMMP-2 by BSP. Binding and pull-down assays demonstrated no interaction between MMP-2 and BSP. While BSP-mediated invasiveness has been shown to depend on its integrin-binding RGD sequence, analysis of proMMP-2 activation and the level of membrane type 1 (MT1)-MMP in cells grown on a BSP substratum showed that the BSP-αvβ3 integrin interaction does not induce the expression of MT1-MMP. Conclusion These studies do not support a role for BSP in promoting metastasis through interactions with pro-MMP-2.
CD109 Plays a Role in Osteoclastogenesis
(Public Library of Science (PLoS), 2013-04-12) Wang, Yongqiang ; Inger, Maayan ; Jiang, Hongwei ; Tenenbaum, Howard ; Glogauer, Michael
Osteoclasts are large multinucleated cells that arise from the fusion of cells from the monocyte/macrophage lineage. Osteoclastogenesis is mediated by macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-kB ligand (RANKL) and involves a complex multistep process that requires numerous other elements, many of which remain undefined. The primary aim of this project was to identify novel factors which regulate osteoclastogenesis. To carry out this investigation, microarray analysis was performed comparing two pre-osteoclast cell lines generated from RAW264.7 macrophages: one that has the capacity to fuse forming large multinucleated cells and one that does not fuse. It was found that CD109 was up-regulated by>17-fold in the osteoclast forming cell line when compared to the cell line that does not fuse, at day 2 of the differentiation process. Results obtained with microarray were confirmed by RT-qPCR and Western blot analyses in the two cell lines, in the parental RAW264.7 cell line, as well as primary murine monocytes from bone marrow. A significant increase of CD109 mRNA and protein expression during osteoclastogenesis occurred in all tested cell types. In order to characterize the role of CD109 in osteoclastogenesis, CD109 stable knockdown cell lines were established and fusion of osteoclast precursors into osteoclasts was assessed. It was found that CD109 knockdown cell lines were less capable of forming large multinucleated osteoclasts. It has been shown here that CD109 is expressed in monocytes undergoing RANKL-induced osteoclastogenesis. Moreover, when CD109 expression is suppressed in vitro, osteoclast formation decreases. This suggests that CD109 might be an important regulator of osteoclastogenesis. Further research is needed in order to characterize the role played by CD109 in regulation of osteoclast differentiation.
Collagen remodeling by phagocytosis is determined by collagen substrate topology and calcium-dependent interactions of gelsolin with nonmuscle myosin IIA in cell adhesions
(American Society for Cell Biology, 2013-03) Arora, P. D. ; Wang, Y. ; Bresnick, J. ; Dawson, J. ; Janmey, P. A. ; McCulloch, Christopher A.
We examine how collagen substrate topography, free intracellular calcium ion concentration ([Ca(2+)]i, and the association of gelsolin with nonmuscle myosin IIA (NMMIIA) at collagen adhesions are regulated to enable collagen phagocytosis. Fibroblasts plated on planar, collagen-coated substrates show minimal increase of [Ca(2+)]i, minimal colocalization of gelsolin and NMMIIA in focal adhesions, and minimal intracellular collagen degradation. In fibroblasts plated on collagen-coated latex beads there are large increases of [Ca(2+)]i, time- and Ca(2+)-dependent enrichment of NMMIIA and gelsolin at collagen adhesions, and abundant intracellular collagen degradation. NMMIIA knockdown retards gelsolin recruitment to adhesions and blocks collagen phagocytosis. Gelsolin exhibits tight, Ca(2+)-dependent binding to full-length NMMIIA. Gelsolin domains G4-G6 selectively require Ca(2+) to interact with NMMIIA, which is restricted to residues 1339-1899 of NMMIIA. We conclude that cell adhesion to collagen presented on beads activates Ca(2+) entry and promotes the formation of phagosomes enriched with NMMIIA and gelsolin. The Ca(2+) -dependent interaction of gelsolin and NMMIIA in turn enables actin remodeling and enhances collagen degradation by phagocytosis.
Comparative Temporospatial Expression Profiling of Murine Amelotin Protein during Amelogenesis.
(Karger, 2012-05) Somogyi-Ganss, E ; Nakayama, Y ; Iwasaki, K ; Nakano, Y ; Stolf, Diana ; McKee, MD ; Ganss, B
Tooth enamel is formed in a typical biomineralization process under the guidance of specific organic components. Amelotin (AMTN) is a recently identified, secreted protein that is transcribed predominantly during the maturation stage of enamel formation, but its protein expression profile throughout amelogenesis has not been described in detail. The main objective of this study was to define the spatiotemporal expression profile of AMTN during tooth development in comparison with other known enamel proteins. A peptide antibody against AMTN was raised in rabbits, affinity purified and used for immunohistochemical analyses on sagittal and transverse paraffin sections of decalcified mouse hemimandibles. The localization of AMTN was compared to that of known enamel proteins amelogenin, ameloblastin, enamelin, odontogenic ameloblast-associated/amyloid in Pindborg tumors and kallikrein 4. Three-dimensional images of AMTN localization in molars at selected ages were reconstructed from serial stained sections, and transmission electron microscopy was used for ultrastructural localization of AMTN. AMTN was detected in ameloblasts of molars in a transient fashion, declining at the time of tooth eruption. Prominent expression in maturation stage ameloblasts of the continuously erupting incisor persisted into adulthood. In contrast, amelogenin, ameloblastin and enamelin were predominantly found during the early secretory stage, while odontogenic ameloblast-associated/amyloid in Pindborg tumors and kallikrein 4 expression in maturation stage ameloblasts paralleled that of AMTN. Secreted AMTN was detected at the interface between ameloblasts and the mineralized enamel. Recombinant AMTN protein did not mediate cell attachment in vitro. These results suggest a primary role for AMTN in the late stages of enamel mineralization.
Contrasting phagosome pH regulation and maturation in human M1 and M2 macrophages
(American Society for Cell Biology, 2014-11-01) Canton, Johnathan ; Khezri, Rojyar ; Glogauer, Michael ; Grinstein, Sergio
Macrophages respond to changes in environmental stimuli by assuming distinct functional phenotypes, a phenomenon referred to as macrophage polarization. We generated classically (M1) and alternatively (M2) polarized macrophages--two extremes of the polarization spectrum--to compare the properties of their phagosomes. Specifically, we analyzed the regulation of the luminal pH after particle engulfment. The phagosomes of M1 macrophages had a similar buffering power and proton (equivalent) leakage permeability but significantly reduced proton-pumping activity compared with M2 phagosomes. As a result, only the latter underwent a rapid and profound acidification. By contrast, M1 phagosomes displayed alkaline pH oscillations, which were caused by proton consumption upon dismutation of superoxide, followed by activation of a voltage- and Zn(2+)-sensitive permeation pathway, likely HV1 channels. The paucity of V-ATPases in M1 phagosomes was associated with, and likely caused by, delayed fusion with late endosomes and lysosomes. The delayed kinetics of maturation was, in turn, promoted by the failure of M1 phagosomes to acidify. Thus, in M1 cells, elimination of pathogens through deployment of the microbicidal NADPH oxidase is given priority at the expense of delayed acidification. By contrast, M2 phagosomes proceed to acidify immediately in order to clear apoptotic bodies rapidly and effectively.
Correlation between clinical performance and degree of conversion of resin cements: a literature review
(2015) De Souza, Grace; Braga, Roberto Ruggiero; Cesar, Paulo Francisco; Lopes, Guilherme Carpena
Resin-based cements have been frequently employed in clinical practice to lute indirect restorations. However, there are numerous factors that may compromise the clinical performance of those cements. The aim of this literature review is to present and discuss some of the clinical factors that may affect the performance of current resin-based luting systems. Resin cements may have three different curing mechanisms: chemical curing, photo curing or a combination of both. Chemically cured systems are recommended to be used under opaque or thick restorations, due to the reduced access of the light. Photo-cured cements are mainly indicated for translucent veneers, due to the possibility of light transmission through the restoration. Dual-cured are more versatile systems and, theoretically, can be used in either situation, since the presence of both curing mechanisms might guarantee a high degree of conversion (DC) under every condition. However, it has been demonstrated that clinical procedures and characteristics of the materials may have many different implications in the DC of currently available resin cements, affecting their mechanical properties, bond strength to the substrate and the esthetic results of the restoration. Factors such as curing mechanism, choice of adhesive system, indirect restorative material and light-curing device may affect the degree of conversion of the cement and, therefore, have an effect on the clinical performance of resin-based cements. Specific measures are to be taken to ensure a higher DC of the luting system to be used.
Culture of primary bovine chondrocytes on a continuously expanding surface inhibits dedifferentiation
(Mary Ann Liebert, 2012-12-18) Rosenzweig, D. H.; Matmati, M.; Khayat, G.; Chaudhry, S.; Hinz, Boris; Quinn, T. M.
Expansion of autologous chondrocytes in vitro is used to generate adequate populations for cell-based therapies. However, standard (SD) culture methods cause loss of chondrocyte phenotype and dedifferentiation to fibroblast-like cells. Here, we use a novel surface expansion culture system in an effort to inhibit chondrocyte dedifferentiation. A highly elastic silicone rubber culture surface was continuously stretched over a 13-day period to 600% of its initial surface area. This maintained cells at a high density while limiting contact inhibition and reducing the need for passaging. Gene expression analysis, biochemical assays, and immunofluorescence microscopy of follow-on pellet cultures were used to characterize the results of continuous expansion (CE) culture versus SD cultures on rigid polystyrene. CE culture yielded cells with a more chondrocyte-like morphology and higher RNA-level expression of the chondrogenic markers collagen type II, aggrecan, and cartilage oligomeric matrix protein. Furthermore, the expression of collagen type I RNA and α-smooth muscle actin protein were significantly reduced, indicating suppression of fibroblastic features. Pellet cultures from CE chondrocytes contained more sulphated glycosaminoglycan and collagen type II than pellets from SD culture. Additional control cultures on static (unexpanded) silicone (SS culture) indicated that benefits of CE culture were partially due to features of the culture surface itself and partially due to the reduced passaging which that surface enabled through CE. Chondrocytes grown in CE culture may, therefore, be a superior source for cell-based therapies.
Dental 3D-Printing: Transferring Art from the Laboratories to the Clinics
(2021-01-04) Pillai, Sangeeth; Upadhyay, Akshaya; Khayambashi, Parisa; Farooq, Imran; Sabri, Hisham; Tarar, Maryam; Lee, Kyungjun T.; Harb, Ingrid; Zhou, Stephanie; Wang, Yifei; Tran, Simon D.
The rise of three-dimensional (3D) printing technology has changed the face of dentistry over the past decade. 3D printing is a versatile technique that allows the fabrication of fully automated, tailor-made treatment plans, thereby delivering personalized dental devices and aids to the patients. It is highly efficient, reproducible, and provides fast and accurate results in an affordable manner. With persistent efforts among dentists for refining their practice, dental clinics are now acclimatizing from conventional treatment methods to a fully digital workflow to treat their patients. Apart from its clinical success, 3D printing techniques are now employed in developing haptic simulators, precise models for dental education, including patient awareness. In this narrative review, we discuss the evolution and current trends in 3D printing applications among various areas of dentistry. We aim to focus on the process of the digital workflow used in the clinical diagnosis of different dental conditions and how they are transferred from laboratories to clinics. A brief outlook on the most recent manufacturing methods of 3D printed objects and their current and future implications are also discussed.
Dentin Bond Integrity of Filled and Unfilled Resin Adhesive Enhanced with Silica Nanoparticles—An SEM, EDX, Micro-Raman, FTIR and Micro-Tensile Bond Strength Study
(2021-03-30) Alhenaki, Aasem M.; Attar, Esra A.; Alshahrani, Abdullah; Farooq, Imran; Vohra, Fahim; Abduljabbar, Tariq
The objective of this study was to synthesize and assess unfilled and filled (silica nanoparticles) dentin adhesive polymer. Methods encompassing scanning electron microscopy (SEM)—namely, energy dispersive X-ray spectroscopy (EDX), micro-tensile bond strength (µTBS) test, Fourier transform infrared (FTIR), and micro-Raman spectroscopy—were utilized to investigate Si particles’ shape and incorporation, dentin bond toughness, degree of conversion (DC), and adhesive–dentin interaction. The Si particles were incorporated in the experimental adhesive (EA) at 0, 5, 10, and 15 wt. % to yield Si-EA-0% (negative control group), Si-EA-5%, Si-EA-10%, and Si-EA-15% groups, respectively. Teeth were set to form bonded samples using adhesives in four groups for µTBS testing, with and without aging. Si particles were spherical shaped and resin tags having standard penetrations were detected on SEM micrographs. The EDX analysis confirmed the occurrence of Si in the adhesive groups (maximum in the Si-EA-15% group). Micro-Raman spectroscopy revealed the presence of characteristic peaks at 638, 802, and 1300 cm⁻¹ for the Si particles. The µTBS test revealed the highest mean values for Si-EA-15% followed by Si-EA-10%. The greatest DC was appreciated for the control group trailed by the Si-EA-5% group. The addition of Si particles of 15 and 10 wt. % in dentin adhesive showed improved bond strength. The addition of 15 wt. % resulted in a bond strength that was superior to all other groups. The Si-EA-15% group demonstrated acceptable DC, suitable dentin interaction, and resin tag formation.
Dentin Bond Integrity of Hydroxyapatite Containing Resin Adhesive Enhanced with Graphene Oxide Nano-Particles—An SEM, EDX, Micro-Raman, and Microtensile Bond Strength Study
(2020-12-14) AlFawaz, Yasser F.; Almutairi, Basil; Kattan, Hiba F; Zafar, Muhammad S.; Farooq, Imran; Naseem, Mustafa; Vohra, Fahim; Abduljabbar, Tariq
The aim was to synthesize and characterize an adhesive incorporating HA and GO nanoparticles. Techniques including scanning electron microscopy (SEM) and energy dispersive X-ray spectroscopy (EDX), micro-tensile bond strength (μTBS), and micro-Raman spectroscopy were employed to investigate bond durability, presence of nanoparticles inside adhesive, and dentin interaction. Control experimental adhesive (CEA) was synthesized with 5 wt% HA. GO particles were fabricated and added to CEA at 0.5 wt% (HA-GO-0.5%) and 2 wt% GO (HA-GO-2%). Teeth were prepared to produce bonded specimens using the three adhesive bonding agents for assessment of μTBS, with and without thermocycling (TC). The adhesives were applied twice on the dentin with a micro-brush followed by air thinning and photo-polymerization. The HA and GO nanoparticles demonstrated uniform dispersion inside adhesive. Resin tags with varying depths were observed on SEM micrographs. The EDX mapping revealed the presence of carbon (C), calcium (Ca), and phosphorus (P) in the two GO adhesives. For both TC and NTC samples, HA-GO-2% had higher μTBS and durability, followed by HA-GO-0.5%. The representative micro-Raman spectra demonstrated D and G bands for nano-GO particles containing adhesives. HA-GO-2% group demonstrated uniform diffusion in adhesive, higher μTBS, adequate durability, and comparable resin tag development to controls.
Different Strategies to Bond Bis-GMA-based Resin Cement to Zirconia
(2016) Lopes, Guilherme Carpena; Spohr, Ana Maria; De Souza, Grace M
To evaluate the effect of different bonding strategies on short- and long-term bis-GMA-based resin cement bond strengths to zirconia.
Differential topical susceptibility to TGFβ in intact and injured regions of the epithelium: key role in myofibroblast transition
(American Society for Cell Biology, 2013-11-01) Speight, Pam ; Nakano, Hiroyasu ; Kelley, Thomas J. ; Hinz, Boris ; Kapusa, András
Induction of epithelial–myofibroblast transition (EMyT), a robust fibrogenic phenotype change hallmarked by α-smooth muscle actin (SMA) expression, requires transforming growth factor-β1 (TGFβ) and the absence/uncoupling of intracellular contacts. This suggests that an “injured” epithelium may be topically susceptible to TGFβ. To explore this concept, we use an epithelial wound model in which intact and contact-deprived regions of the same monolayer can be analyzed simultaneously. We show that TGFβ elicits dramatically different responses at these two loci. SMA expression and initially enhanced nuclear Smad3 accumulation followed by Smad3 mRNA and protein down-regulation occur exclusively at the wound. Mechanistically, three transcriptional coactivators whose localization is regulated by cell contact integrity are critical for these local effects. These are myocardin-related transcription factor (MRTF), the driver of the SMA promoter; β-catenin, which counteracts the known inhibitory effect of Smad3 on MRTF and maintains MRTF protein stability and mRNA expression in the wound; and TAZ, a Hippo effector and Smad3 retention factor. Remarkably, active TAZ stimulates the SMA and suppresses the Smad3 promoter, whereas TAZ silencing prevents wound-restricted expression of SMA and loss of Smad3. Such locus-specific reprogramming might play key roles in wound healing and the susceptibility of the injured epithelium to fibrogenesis.

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