Mie Kuroiwa

Brushing-lnduced Effects with and without a Non-Fluoride Abrasive Dentifrice on Remineralization of Enamel Surfaces Etched with Phosphoric Acid

The remineralization of acid-etched enamel after brushing with and without a non-fluoride abrasive dentifrice was investigated using scanning electron microscopy after sodium hypochlorite (NaOCl) or ethylenediamine tetra-acetic acid treatment, of the specimens. Ground enamel pieces were etched with 30% phosphoric acid for 60 s and attached to resin plates. They were exposed to the oral environment of 4 subjects for 8 weeks and brushed for 1 min daily. Paste and brushing caused the acid-etched enamel to erode selectively, i.e., deep grooves were formed in the prism peripheral regions, while projections of the prism bodies showing a relatively low density of crystallites were retained. Brushing without dentifrice, on the other hand, caused about 0.5 micron thick pellicle with tag-like structures to cover the etched enamel. Fine mineral granules, presumably derived from saliva and minute fragments of etched crystallites, were precipitated on the enamel surface as a thin layer with the pellicle. These results indicate that daily brushing without dentifrice induces the remineralization of acid-etched enamel by depositing salivary components, while paste brushing will lead to abrasion of the weakened enamel.

Role of CXC chemokines in the enhancement of LPS-induced neutrophil accumulation in the lung of mice by dexamethasone.

Lipopolysaccharide (LPS)-induced multiple organ injury was mediated in part by a transcription factor, nuclear factor-kappaB (NF-kappaB). Mice were pretreated with dexamethasone (DEX), an inhibitor of NF-kappaB activation, to elucidate its effects on LPS-induced early responses in vivo. Early responses measured 1 h after intraperitoneal LPS administration at a dose of 1 mg/kg were (1) neutrophil accumulation in the tissues, (2) neutrophil degranulation, and (3) protein and mRNA expressions of tumor necrosis factor-alpha (TNF-alpha) and ELR(+) CXC chemokines [macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (KC)]. Treatment with DEX before LPS administration suppressed NF-kappaB activation and plasma TNF-alpha levels almost to undetectable levels, but enhanced neutrophil accumulation and augmented MIP-2 levels in the lung. The suppression of plasma TNF-alpha levels by pretreatment with an anti-TNF-alpha antibody did not enhance LPS-induced neutrophil accumulation in the lung. These results demonstrate that the enhancement of LPS-induced neutrophil accumulation by DEX might be mediated by MIP-2 and not by TNF-alpha.

Three-Dimensional Observations of Accessory Canals in Mature and Developing Rat Molar Teeth

The structure, distribution and formation of accessory canals in the developing and mature molar teeth of rat mandibular jaws were investigated with scanning electron microscopy and with three-dimensional image analysis using serial light-microscopic sections. In the initial stage of the accessory canal formation, most of the canals appeared in the gaps of the epithelial root sheaths formed by their approaching each other in the initial stage of the root formation. However, some of the canals appeared in the slits which may be formed by the destruction of the epithelial root sheath in the root apex regions. When the gaps and slits were invaded by blood vessels, the regions surrounding the vessels did not mineralize but became accessory canals. Usually, an accessory canal with one blood vessel connected the periodontal ligament to the dental pulp; however, in some cases, the canals were broken off midway following the destruction of the vessels.