Porphyromonus gingivalis is a major pathogen of chronic periodontitis. An outer membrane protein with a molecular mass of 40-kDa (40k-OMP) is a highly immunogenic surface protein produced by P. gingivalis. In this study, to develop an effective vaccine against P. gingivalis infection, we assessed T helper (Th) cell responses in systemic and mucosal compartments after 40k-OMP was administered transcutaneously. When CD4⁺ T cells isolated from the spleens of mice immunized with 40k-OMP alone or 40k-OMP plus cholera toxin were restimulated with 40k-OMP in vitro, significant levels of proliferative responses were induced. In contrast, only low levels of CD4⁺ T cell proliferation were induced in cervical lymph nodes. Analysis of Th1 [interferon (IFN)-γ] and Th2 [interleukin (IL)-4, IL-5, and IL-6] cytokine responses showed that 40k-OMP-specific Th cells from the spleen produced significant levels of IL-4, IL-5, and IL-6 but did not trigger changes in IFN-γ production. These results suggest that transcutaneous administration of 40k-OMP can elicit 40k-OMP-specific Th2-type cytokine responses in systemic, but not mucosal, lymphoid tissues.

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The aim of this study was to determine the amount of Ca diffusion through radicular dentin from 4 calcium-hydroxide-based materials placed in root canals following different treatments. The materials studied were (U) Ultradent-Ultracal XS, (D) Diadent-Vitapex, (R) Roeko Calcium Hydroxide Plus points, and (M) Merck-pure calcium hydroxide. Ninety freshly extracted human teeth were decrowned to a standard length of 14 mm, instrumented, irrigated with 5.25% NaOCl and divided into 5 groups. Group 1 was divided into 4 subgroups that received one of the following treatments prior to obturation with U : (a) ultrasound, (b) 50% citric acid, (c) ultrasound and citric acid, and (d) no treatment. Groups 2, 3, and 4 were similarly treated with D, R and M, respectively. Group 5 acted as the control group and was divided into two subgroups : (a) biomechanical preparation only and (b) no preparation. Ca diffused (mg/dl) in water through dentin as a function of time (1, 3, 5 and 16d) and was measured by spectrophotometry. Ca diffusion (mean±SD.) through dentin from different materials as a function of different treatments and time covered a wide range (6.37-35.99). For all groups and time intervals, the amount of Ca diffused from different materials was the following : (U) 27.75±14.28, (D) 21.42±12.20, (R) 14.55±12.54, and (M) 26.74±14.14. From day 1 to day 16, there was a steady release of Ca from U, D, and M but not from R. Ultrasound and citric acid treatment yielded the highest (significant at p<0.0001) Ca diffusion (40.57±18.79) with R, followed by M (34.82±27.99), D (20.18±6.66) and U (18.32±6.21) at day 1. The highest diffusion of Ca ions for all materials occurred after the use of ultrasonic cavitation with citric acid irrigation. This study found Ca diffusion through dentin is influenced both by the nature of the material and type of treatment.

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The labial surface of the upper central incisor has mesial and distal marginal ridges, and these vary in form and development. We measured the height of the labial marginal ridges of the upper central incisors, which had double-shovel (DS) and no double-shovel (NDS) on the outer enamel surface (OES) and dentino-enamel junction (DEJ) using a 3D scanner. Enamel thickness of the labial surface was also measured in these specimens. Mesiodistal and buccolingual diameters on both OES and DEJ were measured for the comparison of OES and DEJ structures. We obtained the following results ; 1. On the DEJ, DS incisors had more sharp and clear ridges than on the OES. 2. The mesial marginal ridge (MMR) was significantly higher than the distal marginal ridge (DMR) on both OES and DEJ of DS incisors. 3. There were no significant differences of the enamel thicknesses at the three points of the labial surface, such as mesial and distal marginal ridges and the central ridge. 4. The enamel thickness of the DS was significantly thicker than that of the normal incisor at the center of the labial surface, the average of which was 0.91 mm in DS and 0.73 in NDS incisors. 5. No significant differences of both mesiodistal and buccolingual diameters of OES and DEJ were found between averages of NDS group and DS group. 6. Both mesiodistal diameter and buccolingual diameter on OES had a strong correlation to the corresponding diameters on DEJ. The enamel substance at the central labial surface of the DS was significantly thicker than that of the NDS, and marginal ridges in DS observed in OES were clearer and more developed in the DEJ, which was an anatomical base for crown development.

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Mucous cysts are relatively common lesions in the oromaxillofacial region. A mucous cyst is composed of a mucoid substance and foamy mononuclear macrophages (mucinophages), with inflammatory cell infiltration and the overgrowth of blood vessels and fibrous tissue forming a mucoid granuloma. Although the mucoid substance characteristics and the inflammatory characteristics are thought to be important factors, details of the histopathogenesis in relation to the mucinophages remain unclear. Therefore, the present study was conducted to investigate the pathogenesis of mucous cysts with reference to the histochemical and immunohistochemical characteristics of thirteen cases and a review of the literature. Lectin histochemistry and immunohistochemistry showed that mucinophages gave a strong reaction to concanavalin A and lysozyme, and a weak or negative reaction to wheat germ agglutinin. In contrast, the mucoid substance, salivary ducts and acinar cells were strongly to weakly reactive to wheat germ agglutinin and weakly or negatively reactive to concanavalin A. The reactivity to the other lectins and salivary markers in mucous cysts was similar with those in the salivary gland tissues. These results suggested that mucoid degeneration resulted from phagocytosis by the mucinophages and that the mucoid substance in mucous cysts was derived from the saliva. The cell rate of CD68-positive mucinophages was higher in mucous cysts than in control tissues. The cell rates of panT-positive T-cells and panB-positive B-cells were lower in mucous cysts than in control tissues. In addition, the count of mast cells showing metachromasia with toluidine blue at pH 2.5 in mucous cysts was equal to that in control tissues. For immunoglobulin-producing plasma cells, the IgE positivity rate was higher in mucous cysts than in control tissues, whereas the IgA positivity rate was lower in mucous cysts than in control tissues. These results suggested that the accumulation of mucinophages, which had phagocytotic and antigen-presenting abilities, was mainly associated with the pathogenesis of the mucous cyst, in addition to a local T-cell-mediated cellular immune mechanism or to an acute allergic immunoresponse by IgE-producing cells and mast cells.

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The present study assesses the roles of the postnatal 55-kDa tumor necrosis factor (TNF) receptor (TNFR55)- or lymphotoxin-β receptor (LTβR)-mediated signals in the spleens of mice in terms of subsequent regulation of antigen-specific serum antibody responses after oral immunization. Inhibition of TNFR55-dependent signaling revealed significant reduction of germinal center (GC) formation in the spleen. Furthermore, when LTβR-dependent signaling was blocked, segregation of T and B cell areas was disrupted and the formation of GC and follicular dendritic cell (FDC) clusters was significantly reduced. TNFR55-Ig- or LTβR-Ig-treated mice with altered splenic microarchitecture continued to produce antigen-specific serum IgG and IgA antibody responses after oral immunization. However, the levels were significantly lower than those of control mice. These findings demonstrated that the splenic microarchitecture must be properly maintained for the induction of serum antibody responses after oral immunization.

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This article describes a case of oral involvement in chronic graft-versus-host disease (cGVHD) after hematopoietic cell transplantation. The patient suffered from painful oral ulcerations, especially on the tongue, lichenoid buccal mucosa lesions, and xerostomia. She also developed purpuric exanthema and scleroderma-like signs on her hands. Her history, in combination with clinical examination and histological findings of both lichenoid lesions and labial salivary glands, revealed cGVHD.

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