Kokubyo Gakkai zasshi. The Journal of the Stomatological Society, Japan最新文献

The effects of oral commensal streptococci (Streptococcus sanguinis, Streptococcus gordonii, Streptococcus mitis, and Streptococcus salivarius) on biofilm formation by cariogenic mutans streptococci (Streptococcus mutans and Streptococcus sobrinus) were investigated. Cell suspensions were cultured on 96-well microtiter plates coated with or without salivary components (SC), and in flow cell systems coated with SC in tryptic soy broth including 0.25% sucrose without dextrose (TSB). The resultant biofilm formations were stained using safranin or a LIVE/DEAD BacLight Viability Kit, and examined with absorbance at 492 nm or using confocal laser scanning microscopy. Mutans streptococci and S. sanguinis biofilms were formed significantly on the polystyrene surfaces in TSB. Further, in combination cultures, S. sanguinis formed a sufficient biofilm when cultured with S. mutans. However, when S. sanguinis was cultured with S. sobrinus, biofilm formation was slightly inhibited. S. gordonii also inhibited biofilm formation in the culture with S. sobrinus, but not when cultured with S. mutans. S. mitis and S. salivarius collapsed the biofilm morphology and inhibited volume development in some conditions when cultured with S. mutans or S. sobrinus. Biofilm formation by mutans streptococci was challenged and collapsed on the whole by culturing with each of the other oral streptococci. These results indicate that co-culturing of multiple species of mutans streptococci and other oral streptococci has physical effects related to previous attachment and colonization on the surface, as well as biological effects to regulate biofilm formation.

Decrease of the alveolar ridge after tooth extraction causes difficulties in prosthodontic treatment, especially in implant supported prostheses. Statins, which are inhibitors of cholesterol synthesis and therapeutic drugs for hypercholestemia, stimulate BMP-2 expression in osteoblasts. The purpose of the present study was to examine how local application of simvastatin, one of the statins, to the tooth socket after tooth extraction affects alveolar bone. A mixture of lactic acid/glycolic acid copolymer (PLGA), alpha-tricalcium phosphate (alpha-TCP), calcium carbonate was prepared as a carrier for simvastatin. Ninety-six male Wistar rats, 10 weeks old, were used. After right mandibular incisor extraction, they were divided into eight groups and tooth sockets were treated differently: no treatment (control), PLGA carrier only, or PLGA containing 0.1, 0.25, 0.5, 1.0, 2.0, and 4.0 mg simvastatin, respectively. They were sacrificed at 4 and 8 weeks. Bone mineral content (BMC) of the alveolar ridge was measured with dual-energy X-ray absorptiometry and histological analyses were performed. All groups treated with simvastatin showed higher BMC compared to the control group and PLGA carrier group at 4 and 8 weeks. Histological analyses revealed that the thickness of cortical bone of the statin group increased compared to the control group at 4 and 8 weeks; however, newly-formed bone in the tooth socket of the statin group was less than in those of the control group and PLGA carrier group. The results of this study show that local application of simvastatin may enhance bone formation and preserve the alveolar ridge after tooth extraction.

In this study, we prepared four types of 10-mm-diameter, 10-mm-long, large, columnar, bone powder-impregnated, porous apatite blocks, which did or did not have a single nutrient channel of 1, 2, or 3 mm in diameter in the long-axis direction. We implanted them in the subcutaneous tissue of adult dogs for 4, 8, or 16 weeks, and examined the status of bone formation in each block. As a result, bone formation started with the differentiation of osteoblasts along the wall of macro-pores within an area of dense multinucleated cells, and the area of bone formation consisting of bone along the pore wall and bone marrow in the pores gradually expanded around the block in a ring fashion and inward or outward. In apatite blocks with a 2- or 3-mm nutrient channel, bone formation also proceeded along the channel in the block. At 16 weeks after implantation, even in the middle level, almost the entire porous apatite block with a 3-mm channel became the area of bone formation. However, in other apatite blocks, there remained an area without bone formation; in particular, in blocks without a nutrient channel or with a 1-mm nutrient channel, there remained an area slightly over 4 mm in diameter without bone formation at the middle level. These findings indicate the importance of the nutrient channel for good bone formation in large blocks.

The purpose of this study was to elucidate the state of preparation of the dental healthcare system for a large-scale disaster in terms of health-related crisis management by public health centers (PHCs). Questionnaires were sent by e-mail to 549 PHCs. The response rate was 51.4%. The results showed that the percentage of preparedness for a large-scale disaster was only 26.2% and the dental healthcare system has not been constructed nationwide, especially among PHCs located in areas with smaller populations. The main reasons given for why such a dental healthcare system has not been effectively established were related to lack of concern about such a crisis and a sense that the situation is not critical. Nevertheless, PHCs have made progress in assigning dentists and dental hygienists to the dental healthcare system in preparation for a large-scale disaster.

Smoking has various influences on oral mucosa, including color change. We quantitatively analyzed color changes of oral mucosa by smoking. To examine the influence of smoking over a wider age range, we measured the color of oral mucosa of 62 nonsmokers and 56 smokers (age 30-83 years). We measured color with a colorimeter by a perpendicular course, illuminating the measuring sites from a distance of 1 meter by artificial sunlight. Before measuring, we used standard white for calibration. We used the CIE L * a * b * colorimetric system for the color specification. The measured sites were the lips, gingiva, tongue and buccal mucosa. Before colorimetry, we examined the precision and repeatability of colorimeter, but the change was small. Moreover, we similarly examined the sex difference and age difference, but there was no significant difference. This study was approved by the Tokyo Medical and Dental University ethics screening committee. Among nonsmokers and smokers, a statistical difference was recognized in lips L *, a *, gingiva L *, a *, and buccal mucosa L *, b *. Smoking decreased the luminosity of the lips, gingiva, buccal mucosa and caused a blue coloration of gingiva and buccal mucosa.

It is widely accepted that the sympathetic nerve activity might participate in some mechanisms underlying neuropathic pain which sometimes develops after nerve injuries. Many chemical substances have been proposed to induce pain sensation. Bradykinin (BK) is the most potent in exciting nociceptors and in sensitizing them to thermal and mechanical stimuli. We investigated modulatory effects of sympathetic agents on BK actions in primary afferent dorsal root ganglion (DRG) cells. The present electrophysiological experiments by using the patch clamp technique were conducted to examine the effects of noradrenaline (NA) on BK responses and to determine the sites and mechanism of interaction between them. 1. Small (diameter, 20-35 μm) DRG neurons responded to BK with inducing inward currents (BK-responses), but no BK responses could be evoked in DRG neurons larger than 35 μm . 2. NA at 10 μm augmented the BK responses in amplitude compared to the control response. 3. Clonidine at 1 μm augmented the BK responses in amplitude, but isoproterenol at 1 μm failed to augment the BK responses. 4. After pretreatment with yohimbine, the BK responses were not changed by NA. It is concluded that NA-induced augmentation of the BK actions occurred by activating alpha 2-adrenergic receptor. Furthermore, this experimental system is a useful model in order to study the cellular mechanisms of neuropathic pain.