We consider that CT is a useful aid in periodontal examination and diagnosis, and in the prediction and evaluation of periodontal treatment outcomes.

The results of the present study indicate that butyric acid alters the expression of adhesion molecules by Ca9-22 cells. The elucidation of the mechanism of action of butyric acid on the periodontium may help to clarify several aspects of the onset and progression of periodontal disease.

In vitro studies suggest that enamel matrix derivative (EMD) affects the early stages of osteogenic maturation by stimulating bone cell proliferation. In the present study, we evaluated the effects of EMD and beta-tricalcium phosphate (beta-TCP) on bone augmentation within a titanium cap in rabbit calvaria, using 14 adult male Japanese white rabbits. The calvarium was exposed, a circular groove prepared, the marrow penetrated, and a standard hemispherical titanium cap placed in the groove. The cap was filled with a mixture of beta-TCP and EMD at the experimental site, and was filled with beta-TCP alone at the control site. At 1 and 3 months after cap implantation, animals were euthanized, and histological sections prepared. The sections were stained with basic fuchsin and methylene blue, and were examined using light microscopy. At 1 month, EMD tended to increase the amount of bone, but there was no significant difference in the amount of new tissue and mineralized bone between the experimental and control sites. The present findings indicate that the present mixture of EMD and beta-TCP does not accelerate bone formation, compared with beta-TCP alone.

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BackgroundNicotine use is one of the most important risk factors for the development of cardiovascular and periodontal diseases. Numerous reports have suggested the possible contribution of disturbed lipid metabolism for the development of both disease groups. Despite these observations, little is known about the relationship between tobacco smoking and the development of these diseases. Our previous microarray data revealed that nicotine induced low-density lipoprotein receptor (LDLR) expression in oral epithelial cells (OECs). The aim of the present study was to confirm nicotine-mediated LDLR induction and to elucidate the signaling mechanisms leading to the augmented expression of LDLR in OECs.Methods and ResultsLDLR and nicotinic acetylcholine receptor (nAChR) subunit expression was detected by real-time PCR. The production of LDLR was demonstrated by immunofluorescence staining. nAChR-mediated LDLR induction was examined by pre-incubation of the cells with its specific inhibitor, α-bungarotoxin (α-BTX). The functional importance of transcription factor specific protein 1 (Sp1) was examined by luciferase assay, mithramycin pre-incubation or by small interfering RNA (siRNA) transfection. The specific binding of Sp1 to R3 region of LDLR 5’-untranslated region was demonstrated with electrophoretic mobility shift assay (EMSA) and streptavidin-agarose precipitation assay followed by western blotting. The results confirmed that nicotine induced LDLR expression at the transcriptional level. Nicotine was sensed by nAChR and the signal was transduced by Sp1 which bound to the R3 region of LDLR gene. Augmented production of LDLR in the gingival epithelial cells was further demonstrated by immunofluorescence staining using the gingival tissues obtained from the smoking patients. ConclusionsTaken together, the results suggested that nicotine might contribute to the development of both cardiovascular and periodontal diseases by inducing the LDLR in OECs thereby disturbing lipid metabolism.