Based initially on epidemiological studies, an association between periodontitis and atherosclerosis has been suggested. In addition, several recent murine model studies have indicated that one periodontopathic bacterium, Porphyromonas gingivalis, can exacerbate heart lesion formation. This organism, as well as other suspected periodontopathogens, can also be demonstrated in human atheromas. Therefore, though not unequivocal, the present data from a variety of approaches are consistent with a role for periodontitis in cardiovascular disease. This review will discuss potential mechanisms which could explain a role for periodontitis in atherosclerosis. Both general inflammatory mechanisms as well as specific bacterial interactions with cardiac tissue, primarily mediated by Porphyromonas gingivalis, will be described. In addition, the complex nature of atherosclerosis suggests that it will be difficult to precisely define the relationship between these two diseases.

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The antiosteoporotic effect of organic germanium compound, poly-trans-(2-carboxyethyl)germaniumsesquioxide (Ge-132), was studied using ovariectomized rats maintained on a low calcium diet. Rats without ovariectomy and maintained on a normal commercial diet gave the highest femur transverse strength as well as the highest BMD or BMC, measured by peripheral quantitative computed tomography (pQCT) of the femur bone. A daily dose of 18 mg/kg gave the highest femur transverse strength among the dose schedules of 0, 0.5, 3.0, 18.0, and 108.0 mg/kg/day, after both 3 and 6 months in ovariectomized rats maintained on a low calcium diet. Morphological analysis of the femur, especially weight and outside diameter also supported that Ge-132 enhances the femur transverse strength. The pQCT measurements of the femur demonstrated that a high correlation existed between the transverse strength and total BMD or BMC.

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The present study, reports the chemical composition of hypoplastic primary teeth examined by electron probe microanalyzer comparing with the normal part in the same tooth; and reports the X-ray diffraction results of the hypoplastic dental enamel and the normal dental enamel, and comparing the crystalline structure between the two dental enamel together with that of the synthetic hydroxyapatite. The aim of this study was to find out any change of crystalline structure. Two exfoliated hypoplastic deciduous anterior teeth were used for the electron probe study. Each tooth was sliced into two parts along the defect lesion border in a labio-lingual direction. The normal part was used as control. Determinations of weight percentage (wt%) per mass volume were made in continuous scan for P, Al, Mg, Ca, Mn, Fe, Zn, Sr, Na, K and F, from the enamel edge of hypoplastic bottom to dentin-enamel junction. Four exfoliated hypoplastic deciduous anterior teeth and eight exfoliated normal deciduous anterior teeth were used for the X-ray diffraction study. We found by X-ray diffraction that the length of the a-axis of enamel crystallite and the d-spacing (corresponding 300) were increased in the defective enamel. These could be associated with the increased content of magnesium detected by electron probe. The present study demonstrated that there were both quantity and quality changes in the enamel hypoplasia lesion, which may increase the susceptibility of the defective teeth to caries.

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We examined the effect of sphingosine, the basic unit of sphingolipids, on GTPγS-stimulated [³H]inositol trisphosphate ([³H]InsP₃) formation in electrically permeabilized rat parotid acinar cells prelabeled with [³H]inositol. GTPγS-stimulated[³H] InsP₃ formation was inhibited by sphingosine in a concentration-dependent fashion. The [³H] InsP₃ formation evoked by NaF and AlCl₃ was also inhibited by sphingosine in a concentration-dependent manner. [³H]InsP₃ formation was also activated by 1.2μM Ca²⁺, but sphingosine failed to inhibit the Ca²⁺-induced [³H]InsP₃ formation. The protein kinase C inhibitor H-7 did not mimic the effect of sphingosine on GTPγS-induced [³H]InsP₃ formation. These results suggest that sphingosine inhibits phospholipase C activity coupled to GTP-binding protein. However, the effect of sphingosine is not due to the inhibition of protein kinase C.

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Stimulated-saliva, swabbing-plaque and brushing-plaque samples were successively collected from five volunteers four times over a seven-day period and the number of total streptococci (TS) and mutans streptococci (MS) in each sample were determined using selective media. The percentages of MS in TS (MS%) of the brushing-plaque and the stimulated saliva, but not the swabbing-plaque, were kept almost constant through a sampling period, and the ratio of mean MS% in both samples significantly varied among subjects. These findings suggest that plaque sample recovered by brushing treatment for 1 min is superior to stimulated whole saliva as a sampling material for assessment of individual caries risk.

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The purpose of this study was to identify the major candidate chromosome influencing susceptibility to dental caries in mice and to detect the region that contains it. Genetic factors affecting dental caries in mice were examined using two inbred strains of mice, C57BL/6J and C3H/HeJ, and these genetic crosses were inoculated with Streptococcus mutans serotype c (1.0 x 10⁹ CFU/mouse). The caries scores for C3H/HeJ and C57BL/6J were 3.1±2.6 and 39.8±12.6 (Mean±S.D.), respectively. The mean caries score of the F1 hybrids was 17.6 ±13.2 (Mean±S.D.) which was in the range 1 to 46. The caries scores of F2 [(C57BL x C3H) x (C57BL x C3H)] mice had an extensive range from 0 to 68. These findings suggested that some genes play roles in caries development.
Based on our results with the genetic crosses, we used F2 intercross mice to investigate candidate chromosomal linkages using DNA pooling methods and obtained a valuable linkage on chromosomes 2 and 17. Thus, we concluded that one of the candidate genes controlling the genetic difference for the dental caries promoting ability between C3H/HeJ and C57BL/6J might be located on chromosomes 2 and 17.

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Ets2 is a member of the Ets family of transcription factors that is involved in embryonic organ development. DMP1 is one of the chief non-collagenous proteins found in bone and mineralizing dentin. The DMP1 gene contains Ets binding sites in its regulatory sequences. Ets2 and DMP1 are co-expressed in certain tissues during tooth and craniofacial development. We therefore explored whether Ets2 regulates DMP1 expression. In the first approach, we determined the influence of elevated levels of Ets2 expression on DMP1 expression using Ets2-transfected MC3T3-E1 osteoblastic cells. The Ets2 expression vector is under the control of a mouse metallothionine promoter (mMT-1), which allows the controlled overexpression of Ets2 in the presence of Zn²⁺. DMP1 expression was elevated significantly in MC3T3-E1 cells induced to overexpress Ets2, indicating that the Ets2 transcription factor regulates DMP1 expression in these cells. In the second set of experiments, we examined DMP1 expression in E13.5 Ets2 overexpression transgenic mouse embryos, by in situ hybridization. DMP1 expression was observed in ectopic sites such as the Meckel's cartilage, where DMP1 is not expressed during normal development at any developmental stage, whereas Ets2 is expressed during this stage. The in vitro and in vivo data taken together, strongly suggest that DMP1 is a target for regulation by Ets2.

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Ameloblastomas originate from the odontogenic epithelium and are known as odontogenic tumors. Histopathologically, they are classified as follicular and plexiform patterns. However, there have been few reports concerning the morphological difference between these patterns. Cell adhesion and proliferation play important roles in maintaining tissues as well as in organ genesis and morphogenesis. To clarify the association of cell adhesion molecules and cell proliferation in the morphological difference between follicular and plexiform patterns of ameloblastomas, the expressions of E- and P-cadherins, alpha- and beta-catenins, integrin alpha3-betal (VLA-3) and proliferative cell nuclear antigen (PCNA) were examined by immunohistochemical analyses in 35 ameloblastomas. In the follicular pattern, the columnar and spindle cells showed 43.8% PCNA-positively. Those of the plexiform pattern showed 42.1 %. The stellate reticulum-like cells (SRLC) of the follicular demonstrated 24.5% positively. The cells of the plexiform pattern showed 32.8% positively. PCNA-positive rate differed significantly between the patterns for SRLC. E-cadherin, P-cadherin, and VLA-3 were expressed in all parenchyma cells in the plexiform pattern. In the follicular pattern, the columnar and spindle cells expressed these adhesion molecules, but levels were decreased in SRLC. Alpha- and beta-catenins were seen in all parenchyma cells of both patterns of ameloblastomas. These findings support that SRLC of the plexiform pattern had greater adhesive ability than those of the follicular one. The degree of cell differentiation might differ between the follicular and plexiform patterns. These results suggested that the cell adhesion molecules and cell-proliferating activity mediated the morphological difference in ameloblastomas.

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Osteopetrosis is a metabolic bone disease characterized by generalized skeletal sclerosis. In mandibular condyle of the op/op mice, one of the osteopetrotic models, deformation of the condylar head and enlargement of the hypertrophic zone are known to occur. The objective of the present study was to characterize the distribution of glycosaminoglycans (GAGs) in the mandibular condyle of op/op mice as a function of age (2, 4, 8 and 16 weeks of age) using histochemical and immunohistochemical methods. At 8 weeks of age and older, a significantly enlarged hypertrophic zone in the central condylar head of op/op mice was intensely and diffusely stained for chondroitin-4-sulfate, chondroitin-6-sulfate and hyaluronic acid, while these GAGs appeared to be present essentially in the condylar head, i.e., surface to sub-perichondrium, in the control of the same age group. In both groups, cells in sub-perichondrium, blood vessels and periosteum showed immunoreactivity for keratan sulfate. In the mineralizing matrix zone in the condyle, op/op mice showed nonuniform patches of staining for these GAG components (except for keratan sulfate) while the control showed virtually no staining. The abnormal metabolism and distribution of GAGs/proteoglycans may in part contribute to the deformation of the condylar head and its poor mineralization seen in these op/op mutant mice.

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When quantifying hydroxyl radical (•OH) generated from the Fe²⁺-H₂O₂ or Cu²⁺-H₂O₂ reaction system, it is very important to know the real-time profile of •OH generation. In this study, we examined the real-time profile of DMPO-OH generated from •OH generation systems using the electron spin resonance (ESR) stop and flow technique. Temporal changes in the amount of •OH were observed, and several generation patterns were evident in the Fe²⁺-H₂O₂ and Cu²⁺-H₂O₂ reaction systems. From the Fe²⁺-H₂O₂ reaction system, three typical patterns of •OH generation were observed. The •OH was generated violently at first, and then decreased rapidly (destruction type) or slowly in a stable manner (destruction-plateau type); sometimes, •OH was not detected (negative type). On the other hand, two typical patterns of •OH generation were observed from the Cu²⁺-H₂O₂ reaction system. The amount of •OH generated reached a peak at an early stage and then decreased rapidly (decrease type) or reached a plateau (plateau type). These results suggest that the amount of •OH generated changes depending upon the concentration of the metal ion and H₂O₂ in both the Fe²⁺ and Cu²⁺-H₂O₂ reaction systems.

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Three cases of tuberculous cervical lymphadenitis are presented. All patients presented without positive chest x-ray, fluctuant mass and discharging pus because these cases were all primary and early stage. The diagnoses were very difficult, and histopathological examination was most reliable and only one method.

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Porphyromonas gingivalis has been implicated as a major pathogen in periodontal diseases. We previously succeeded in gene cloning of a 200-kDa membrane protein from P. gingivalis 381. The recombinant protein was immunoreacted by antisera from severe periodontitis patients. In this study, we attempted to identify the 200-kDa antigenic protein (200k-AP) using protein database. The recombinant 200k-AP was highly purified and digested with lysyl endopeptidase, and separated using reverse-phase high-pressure liquid column chromatography. Amino acid sequence of a chromatographic separated short peptide was examined and identified as VTVPENGK. By homology-search in protein database, the 8 amino acid sequence was exactly the same as the HagA which was known as useful immunogen to prevent colonization of P. gingivalis. This findings suggest that 200k-AP may be HagA and useful to develop the immunotherapy againstperiodontitis.

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