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The response properties of mechanosensitive neurons innervating the temporomandibular joint (TMJ neurons) in the rabbit trigeminal ganglion were investigated. Three types of discharge patterns were found: a slowly adapting type (39%), a slowly adapting type with spontaneous discharges (59%), and a rapidly adapting type (2%).

In the present study, we examined the applicability of tonometer to evaluate the hardness of human gingival tissue. For this purpose, induction-based impact method for measuring intraocular pressure was applied. The measurement was made on the young male subjects (n = 7, aver. 24.8 years) who had clinically healthy gingival tissue. The labial surfaces of attached gingival site between teeth were selected as examination. The gingival pressure ranged between 18 and 77 (n = 70, mean ± SD; 44.4 ± 8.1 mmHg). The results indicated that tonometric measurement of the gingival tissue could give quantitative information of the gingival inflammation.

The purpose of this retrospective study was to investigate the factors that affected the usage of removable partial dentures (RPDs) and the patients’ satisfaction with their RPDs 5 years after insertion. Sixty-seven patients treated with 90 RPDs that were inserted at the Tohoku University Hospital between 1996 and 2001 participated in this study. The usage rate and 12 factors that might affect usage were examined, and 15 factors regarding satisfaction were evaluated. Statistically significant associations were found between denture usage and patient’s age, location of edentulous area, pain, color of artificial teeth, and arrangement. These findings suggest that the acceptance of RPDs among patients was related to factors such as patient’s age, oral status, and satisfaction.

Porphyromonas gingivalis and Mogibacterium timidum were more frequently detected in subgingival microflora of periodontitis than that of healthy subjects. However, few have been investigated to quantify these bacteria in subgingival microflora. This study aimed to quantify P. gingivalis and M. timidum , as well as other 11 bacteria, e.g., Tannerella forsythia and Eubacterium saphenum , in subgingival plaque, and to evaluate their relationship with periodontitis. Subgingival plaque was obtained from 12 periodontally healthy (mean 26.4 years) and 28 periodontitis (mean 62.4 years) subjects. Total and target bacteria were quantified by real-time polymerase chain reaction (PCR) using universal and species-specific primers, respectively. The proportion of obligate anaerobes, including P. gingivalis , T. forsythia , and E. saphenum , was higher in periodontitis subjects than in healthy subjects. These results suggest an environmental shift in subgingival area toward more suitable for obligate anaerobes in periodontitis subjects.

Oral Veillonella is one of the predominant hydrogen sulfide (H_2S)- producing bacteria in the tongue coating. Metabolic properties of the H_2S production, however, have not been known well. Therefore, this study was aimed to determine the metabolic substrates of the H_2S production and examine whether environmental pH affects the H_2S production. Veillonella atypica ATCC17744, Veillonella dispar ATCC17748, and Veillonella parvula ATCC10740 grew anaerobically in tryptone-yeast extract medium containing 1.8% sodium lactate at pH 7, and all the Veillonella species produced higher amounts of H_2S in the presence of 1 mM cysteine or glutathione, when compared with that in the absence of these sulfur compounds. These sulfur compounds, however, did not stimulate bacterial growth. The cell suspensions of these bacteria were able to produce H_2S from 1 mM cysteine or glutathione. The amounts of H_2S produced from cysteine and glutathione were the highest at pH 6–7 and pH 8, respectively. These results indicate that oral Veillonella species utilized cysteine and glutathione as substrates for H_2S production, and that their H_2S production was efficient around neutral pH, suggesting a high oral malodor level between meals when environmental pH in the oral cavity is expected to be around neutral.

Oral epithelium is endowed with innate immune receptors for bacterial components, which play important roles in host defense against bacterial infection. We examined the expression of various Toll-like receptors (TLRs), NOD1 and NOD2 in oral epithelial cells, and the production of β-defensin 2 and peptidoglycan recognition proteins (PGRPs) upon stimulation with their respective chemically synthesized ligands. We found a clear expression of TLR4 as well as TLR2, and a strong expression of NOD1 and NOD2 in normal oral epithelial tissues by immunohistochemical analysis. In the inflamed oral epithelium, cell-surface localizations of TLR2 and TLR4 were more clearly observed than in the healthy tissue. We also showed that oral epithelial cells in culture constitutively expressed TLR3 and TLR7 in addition to TLR2, TLR4, NOD1, and NOD2, and stimulation with synthetic ligands for these receptors (TLR2 agonistic lipopeptide, TLR3 agonistic poly I:C, TLR4 agonistic lipid A, TLR7 agonistic single-stranded RNA, NOD1 agonistic iE-DAP and NOD2 agonistic muramyldipeptide) markedly up-regulated the expression of antibacterial factors, such as β-defensin 2 and PGRPs, but not the proinflammatory cytokines. These findings indicate that these molecules in oral epithelial cells are functional receptors that induce antibacterial responses without excessive inflammatory responses.

We investigated the mechanism and impact of various inflammatory stimuli on dendritic cell (DC)-gingival fibroblast (GF) adhesion. Human immature (im) DCs were generated from monocytes by culturing with interleukin (IL)-4 and granulocyte macrophage-colony stimulating factor (GM-CSF). GFs were outgrown from the human gingival specimen. DCs were co-cultured with GFs with/without pretreatment with various stimuli. Adhered cells were measured by fluorometer. Expression of adhesion molecules was analyzed by flow cytometry. Pretreatment of GFs with tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and Escherichia coli ( Ec ) lipopolysaccharides (LPS) significantly increased the adhesion to imDCs and enhanced intercellular adhesion molecule (ICAM)-1 expression. A signifi-cantly increased DC-GF adhesion was also observed when imDCs were pretreated with Ec LPS, Porphyromonas gingivalis ( Pg ) fimbriae, and peptideglycan but not with Pg LPS. Expression of LFA-1 and Mac-1 on DCs was not altered by the pretreatment with these stimuli. However, LFA-1 and Mac-1 blockade of imDC signifi cantly reduced the adhesion to TNF-α-stimulated GFs. These results showed that inflammatory stimuli increased the imDC-GF adhesion via lymphocyte function- associated antigen (LFA)-1/Mac-1-ICAM-1 ligation. Adhesion of DC to GFs may be important not only for the localization of DCs in the inflammatory periodontal lesion, but also for the modulation of immune responses.

Anti-neutrophil cytoplasmic antibodies (ANCA) against proteinase 3 (PR3) have been detected under a wide range of inflammatory conditions, and the interaction of anti-PR3 antibodies (Abs) with leukocytes provoked cell activation. Flow cytometric analysis revealed an increase of CD14, various Toll-like receptors (TLRs), NOD1, and NOD2 expressions during the anti-PR3 priming in human monocytic THP-1 cells. Anti-RP3 Abs resulted in a markedly enhanced interleukin (IL)-8, tumor necrosis factor-α, and monocyte chemoattractant protein-1 liberation on chemically synthesized TLR2-agonistic lipopeptide (FSL-1), TLR3-agonistic Poly I:C, TLR4-agonistic lipid A, TLR7/8-agonistic ssPoly U, TLR9-agonistic bacterial CpG DNA, NOD1-agonistic FK156, and NOD2-agonistic muramyldipeptide in human monocytic THP-1 cells and human peripheral blood mononuclear cells. RNA interference assays revealed that anti-PR3 Abs primed THP-1 cells in a PR3- and protease-activated receptor-2-dependent manner. Furthermore, anti- PR3 Ab-mediated priming was significantly abolished by inhibition of phospholipase C and nuclear factor-κB. These results suggest that anti-PR3 Abs prime human monocytic cells to produce cytokines on stimulation with various microbial components by the up-regulation of the TLR and NOD signaling pathway, and that these mechanisms may actively participate in the inflammatory process in ANCArelated autoimmune diseases.

Recently, several studies have revealed that β-glucans in fungal cell wall components are known to modulate innate immunity. Water-insoluble α-glucans are synthesized from sucrose by glucosyltransferase-I of mutans streptococci and play an important role in the development of dental plaque. However, it remains unknown whether water-insoluble α-glucans also initiate these disease processes because of their innate immune response. In the present study, we showed that water-insoluble α-glucans synthesized by Streptococcus sobrinus activated mouse peritoneal exudate macrophages to produce proinflammatory cytokines. Furthermore, human monocytes stimulated by water-insoluble α-glucans produced TNF-α and IL-8, whereas human polymorphonuclear cells were activated by waterinsoluble α-glucans, resulting in chemotaxis and hydrogen peroxide production. The results demonstrated that water-soluble α-glucans modulate macrophage- and granulocyte-induced inflammatory immune responses, and suggest that inflammation induced by those α-glucans is associated with the development of periodontal diseases.

Biotin, a water-soluble vitamin of the B complex, functions as a cofactor of carboxylases that catalyze indispensable cellular metabolism. It was reported that the concentrations of biotin were significantly lower in sera of patients with chronic inflammatory diseases. However, the biological roles of biotin in inflammatory responses are unclear. In this study, we investigated the effects of biotin-deficiency on tumor necrosis factor (TNF)-α production in vivo and in vitro. Mice were fed a basal diet or a biotin-deficient diet for 8 weeks. After intravenous administration of lipopolysaccharide (LPS), serum TNF-α levels in biotin-deficient mice were significantly higher than those in biotin-sufficient mice. A murine macrophage-like cell line, J774.1, was cultured in biotin-sufficient or biotin-deficient medium. Biotindefi cient J774.1 cells produced TNF-α significantly higher than biotin-sufficient J774.1 cells in response to LPS and even without LPS stimulation. Moreover, biotin-supplementation inhibited TNF-α production of biotin-deficient cells. Addition of cyclic guanosine 5′-monophosphate (cGMP) significantly decreased TNF-α production of the biotin-deficient cells, indicating that up-regulation of TNF-α production was regulated by cGMP-dependent signaling pathways. In conclusion, these results suggest that biotin is critically involved in inflammatory diseases via the regulation of TNF-α production in vivo and in vitro.