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Background: Resin-based materials are the popular restorative material in dentistry. The majority of these materials are light cured with a major disadvantage: marginal leakage. Objective: To evaluate the gap width of different resin-based materials at the cervical dentin when achieved mechanical force. Methods: Class II cavities were prepared on extracted premolar teeth with the gingival margin 1 mm below the Cementoenamel Junction (CEJ). In the first three experimental groups, three different lining materials (flowable resin composite, bulk-fill flowable resin composite, and resin-modified glass ionomer cement) were placed at the cervical dentin with a thickness of 1 mm. The rest of the cavities were restored with conventional resin composite. The other two groups were restored with conventional resin composite (control) or high viscosity bulk-fill resin composite, respectively. All groups were thermocycled and underwent vacuum pressure 2.6 KPa for 30 min in a Scanning Electron Microscope (SEM). Results: There was no gap formation at the cervical dentin on the external surface when restored with high-viscosity bulk fill resin composite. Almost all gaps occurred at the interface between restorative materials and the hybrid layer. The flowable bulk fill resin composite showed a significantly smaller gap width on both the external and internal surfaces compared to the other groups (p< 0.05). The resin-modified glass ionomer cement showed the largest gaps in the cervical dentin (p < 0.05). Conclusion: The different types of resin-based materials demonstrated a different failure of gap width under mechanical force. It clearly occurred at the restorative material-hybrid layer interface.

Streptococcus mutanspredominantly creates an acidic environment in an oral cavity. This results in dental demineralization and carious lesions. The probiotics are beneficial microorganisms that modulate the bacterial balance in the digestive system. Prebiotics are defined as nondigestible oligosaccharides that are utilized for the selective stimulation of the beneficial microorganisms. The objective of this study was to evaluate the efficacy of the prebiotics, galactooligosaccharides (GOS) and fructooligosaccharides (FOS), for enhancing the probioticLactobacillus acidophilusATCC 4356, for inhibitingStreptococcus mutans(A32-2) for the prevention of dental caries. The growth rate of theS. mutanssignificantly decreased when cocultured withL. acidophilusin the GOS-supplemented medium at 3%, 4%, and 5%. In the FOS-supplemented medium, the growth rate ofS. mutanssignificantly decreased in all concentrations when cocultured withL. acidophilus. There was no significant difference in the growth rate ofL. acidophilusin all concentrations of either GOS or FOS. It can be concluded that the growth rate ofS. mutanswas significantly retarded when cocultured withL. acidophilusand the proper concentration of prebiotics. These prebiotics have potential for a clinical application to activate the function of the naturally intraoralL. acidophilusto inhibitS. mutans.

Purpose. To investigate the efficiency of natural astaxanthin that has been extracted from Xanthophyllomyces dendrorhous in inhibiting the proliferation and viability of colorectal adenocarcinoma cell line (Caco-2; colon cancer cells). Methodology. Caco-2 cells and normal human oralkeratinocytes (NOKs) were treated with different concentrations of extracted astaxanthin, ranging from 0.075 to 10 mg ml−1, for 24, 48 and 72 h. The number of cells was determined via MTS assay and the proliferating cells were investigated by bromodeoxyuridine (BrdU) assay. Results/Key findings. Of the Caco-2 cells, 30–50 % remained viable, while the NOKs showed 110–120 % survival when treated with 5 mg ml−1 astaxanthin. The Caco-2 cells showed distinct structural shrinkage when treated with the same concentration of astaxanthin. Fluorescent labelling of the DNA of the proliferative cells with BrdU showed a significant decrease in the number of the proliferative Caco-2 cells when the concentration of astaxanthin was increased to 5 mg ml−1. Conclusion. The natural astaxanthin from X. dendrorhous, at an appropriate concentration, is effective in terminating the viability of, or retarding the proliferative activity of, Caco-2 cells, without harmful effects on NOKs.

Dental materials have been continuously developing over a long period of time. Every effort has been made to develop the physical and mechanical properties of the materials to mimic the natural tooth substances. However, that has not yet been achieved, making it necessary to apply conservative dental treatments. Conservative treatments are procedures which minimize the amount of defective tooth structure removed while maximizing the remaining amount of intact tooth structure, and defining the margin of the restoration at the supragingival level. In a substantially destructed tooth, the direct restoration, which is the most conservative restoration, has the limitations on the retention or creation of the proper contour of the restoration. The indirectly partial coverage restoration has recently gained in popularity. This treatment preserves the tooth structure while allowing reconstruction of the destructed structure to enable correct and proper tooth functioning and also provides a satisfactory cosmetic appearance. The purpose of this paper is to review and compare the various conservative techniques of partial coverage restorations and the full coverage treatment with crowns.

Objective: Testing of methods to enhance the shear bond strength (SBS) between orthodontic metal brackets and amalgam by sandblasting and different primers. Materials And Methods: Three hundred samples of amalgam restorations (KerrAlloy®) were prepared in self-cured acrylic blocks, polished, and divided into two groups: nonsandblasted and sandblasted. Each group was divided into five subgroups with different primers used in surface treatment methods, with a control group of bonded brackets on human mandibular incisors. Following the surface treatments, mandibular incisor brackets (Unitek®) were bonded on the amalgam with adhesive resin (Transbond XT®). The SBS of the samples was tested. The adhesive remnant index (ARI) and failure modes were then determined under a stereo-microscope. Two-way analysis of variance, Chi-square, and Kruskal–Wallis tests were performed to calculate the correlations between and among the SBS and ARI values, the failure modes, and surface roughness results. Results: There were statistically significant differences of SBS among the different adhesive primers and sandblasting methods (P < 0.05). The sandblasted amalgam with Assure Plus® showed the highest SBS (P < 0.001). Samples mainly showed an ARI score = 1 and mix-mode failure. There was a statistically significant difference of surface roughness between nonsandblasted amalgam and sandblasted amalgam (P < 0.05), but no significant differences among priming agents (P > 0.05). Conclusions: Using adhesive primers with sandblasting together effectively enhances the SBS between orthodontic metal brackets and amalgam. The two primers with the ingredient methacryloxydecyl dihydrogen phosphate (MDP) monomer, Alloy Primer® and Assure Plus®, were the most effective. Including sandblasting in the treatment is essential to achieve the bonding strength required.

Bone formation is controlled by osteoblasts, but the signaling proteins that control osteoblast differentiation and function are still unclear. We examined if the dynamin GTPase, which is associated with actin remodeling and migration in other cells, plays a role in osteoblast differentiation and migration. Dynamin mRNA was expressed in primary osteoblasts throughout differentiation (0-21 days). However, alkaline phosphatase (ALP) activity, a marker of osteoblast differentiation, was decreased in osteoblasts over-expressing dynamin. Conversely, ALP activity was increased following shRNA-mediated knockdown of dynamin and in osteoblasts treated with the dynamin inhibitor, dynasore. Dynasore also reduced c-fos and osterix expression, markers of early osteoblasts, suggesting a role for dynamin in pre-osteoblast to osteoblast differentiation. Since dynamin GTPase activity is regulated by tyrosine phosphorylation, we examined the mechanism of dynamin dephosphorylation in osteoblasts. Dynamin formed a protein complex with the tyrosine phosphatase PTP-PEST and inhibition of phosphatase activity increased the level of phosphorylated dynamin. Further, PTP-PEST blocked the Src-mediated increase in the phosphorylation and GTPase activity of wild-type dynamin but not the phosphorylation mutant dynY231F/Y597F. Although ALP activity was increased in osteoblasts expressing GTPase-defective dynK44A, and to a lesser extent dynY231F/Y597F, osteoblast migration was significantly inhibited by dynK44A and dynY231F/Y597F. These studies demonstrate a novel role for dynamin GTPase activity and phosphorylation in osteoblast differentiation and migration, which may be important for bone formation.

The gram-negative anaerobe Porphyromonas gingivalis colonizes the gingival crevice and is etiologically associated with periodontal disease that can lead to alveolar bone damage and resorption, promoting tooth loss. Although susceptible to antibiotics, P. gingivalis can evade antibiotic killing by residing within gingival keratinocytes. This provides a reservoir of organisms that may recolonize the gingival crevice once antibiotic therapy is complete. Polymersomes are nanosized amphiphilic block copolymer vesicles that can encapsulate drugs. Cells internalize polymersomes by endocytosis into early endosomes, where they are disassembled by the low pH, causing intracellular release of their drug load. In this study, polymersomes were used as vehicles to deliver antibiotics in an attempt to kill intracellular P. gingivalis within monolayers of keratinocytes and organotypic oral mucosal models. Polymersome-encapsulated metronidazole or doxycycline, free metronidazole, or doxycycline, or polymersomes alone as controls, were used, and the number of surviving intracellular P. gingivalis was quantified after host cell lysis. Polymersome-encapsulated metronidazole or doxycycline significantly (P

Bone homeostasis is maintained by the balance between bone resorption by osteoclasts and bone formation by osteoblasts. Dysregulation in the activity of the bone cells can lead to osteoporosis, a disease characterized by low bone mass and an increase in bone fragility and risk of fracture. Kalirin is a novel GTP-exchange factor protein that has been shown to play a role in cytoskeletal remodeling and dendritic spine formation in neurons. We examined Kalirin expression in skeletal tissue and found that it was expressed in osteoclasts and osteoblasts. Furthermore, micro-CT analyses of the distal femur of global Kalirin knockout (Kal-KO) mice revealed significantly reduced trabecular and cortical bone parameters in Kal-KO mice, compared to WT mice, with significantly reduced bone mass in 8, 14 and 36 week-old female Kal-KO mice. Male mice also exhibited a decrease in bone parameters but not to the level seen in female mice. Histomorphometric analyses also revealed decreased bone formation rate in 14 week-old female Kal-KO mice, as well as decreased osteoblast number/bone surface and increased osteoclast surface/bone surface. Consistent with our in vivo findings, the bone resorbing activity and differentiation of Kal-KO osteoclasts was increased in vitro. Although alkaline phosphatase activity by Kal-KO osteoblasts was increased in vitro, Kal-KO osteoblasts showed decreased mineralizing activity, as well as decreased secretion of OPG, which was inversely correlated with ERK activity. Taken together, our findings suggest that deletion of Kalirin directly affects osteoclast and osteoblast activity, leading to decreased OPG secretion by osteoblasts which is likely to alter the RANKL/OPG ratio and promote osteoclastogenesis. Therefore, Kalirin may play a role in paracrine and/or endocrine signaling events that control skeletal bone remodeling and the maintenance of bone mass.