Background: Crown preparation of vital teeth involve the removal of a sound tooth structure, and when enamel removed this lead to exposed dentin with an increase in the number of open dentinal tubules also the diameter of dentinal tubules will increase, furthermore lead to increase movement of fluids inside the tubules all that causes post preparation sensitivity. The aim of this study is to evaluate the effect of desensitizing by Er:Cr:YSGG laser on shear bond strength of prepared tooth and resin cement. Materials and methods: Thirty sound maxillary premolars, grouped into three groups(n=10). Group A is the control group, group B irradiated by Er:Cr:YSGG laser with (0.25 W, 20 Hz, 10%water and air), group C irradiated by Er:Cr:YSGG laser with (0.5 W, 20 Hz, 10% water and air). Results: SEM examination showed complete occlusion of opened dentinal tubules after laser irradiation of both groups that irradiated with laser. Statistical analysis showed significant increase in surface roughness in group B and C. SBS was significantly increase in group B with no significant increase in group C. Conclusion: Er:Cr:YSGG laser can occlude open dentinal tubules without and adverse effect on the retention of the restoration, on the contrary it increase bonding strength. And this increasing was significant in group B with (0.25W, 20 Hz, 10 % water and air). suggestion: so the parameters used in group B (0.25 W, 20Hz, 10 % water and air) is recommended for desensitizing prepared tooth and induce enhancement to the bonding strength of resin to tooth surface.
ER Abbas, AA Jasim, Journal of Physical Education, 2023 - Cited by 1
Escherichia coli (E. coli) is a frequent gram-negative bacterium that causes nosocomial infections, affecting more than 100 million patients annually worldwide. Bacterial lipopolysaccharide (LPS) from E. coli binds to toll-like receptor 4 (TLR4) and its co-receptor’s cluster of differentiation protein 14 (CD14) and myeloid differentiation factor 2 (MD2), collectively known as the LPS receptor complex. LPCAT2 participates in lipid-raft assembly by phospholipid remodelling. Previous research has proven that LPCAT2 co-localises in lipid rafts with TLR4 and regulates macrophage inflammatory response. However, no published evidence exists of the influence of LPCAT2 on the gene expression of the LPS receptor complex induced by smooth or rough b
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