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I Morisaki

Publications and source records attributed to I Morisaki.

At least 37 records · Page 2Linked to original sources

The importance of fimbriae in the virulence and ecology of some oral bacteria.

Cumulative evidence indicates that bacterial adherence to mucosal and tooth surfaces as well as bacterial coaggregation are essential steps for colonization of various oral bacterial species. Bacterial fimbriae have been shown to play an important role in the interaction between bacteria and host cells or among bacterial cells. The properties of fimbriae from selected species of oral bacteria are discussed in terms of virulence traits and ecological significance. Among others, Porphyromonas gingivalis fimbriae have been most extensively studied. The fimbrial structure is composed of 41-kDa fimbrillin proteins. DNA sequencing of the fimbrillin gene (fimA) from nine strains of P. gingivalis suggests intraspecies variation in the structure of fimA, while retaining common immunochemical specificities. P. gingivalis fimbriae exhibit a wide variety of biological activities including immunogenicity, binding to various host proteins, stimulation of cytokine production and promotion of bone resorption, Actinobacillus actinomycetemcomitans also possesses fimbriae; however, little is known concerning their chemical, genetical, and biological properties. Fimbriae of Prevotella intermedia are shown to induce hemagglutination reaction, while those of Prevotella loescheii are found to cause coaggregation with other bacteria, i.e., Actinomyces viscosus and sanguis streptococci. Fimbriae from gram-positive oral bacteria such as oral Actinomyces and sanguis streptococci are described. These fimbriae may participate in coaggregation, binding to saliva-coated hydroxyapatite or glycoprotein of the surface layer of oral epithelial cells. Taken together, fimbriae are key components in cell-to-surface and cell-to-cell adherence of oral bacteria and pathogenesis of some oral and systemic diseases.

Actinomyces↗

Binding of Porphyromonas gingivalis fimbriae to proline-rich glycoproteins in parotid saliva via a domain shared by major salivary components.

Porphyromonas gingivalis, a putative periodontopathogen, can bind to human saliva through its fimbriae. We previously found that salivary components from the submandibular and sublingual glands bind to P. gingivalis fimbriae and that acidic proline-rich protein (PRP) and statherin function as receptor molecules for fimbriae. In this study, we investigated the fimbria-binding components in parotid saliva. Fractionated human parotid saliva by gel-filtration chromatography was immobilized onto nitrocellulose membranes for the overlay assay following sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The salivary components on the membrane were allowed to interact with fimbriae purified from P. gingivalis ATCC 33277, and the interacted fimbriae were probed with anti-fimbria antibodies. The fimbriae were shown to bind to two forms of proline-rich glycoproteins (PRGs) as well as to acidic PRPs and statherin. Moreover, fimbriae bound to several components of smaller molecular size which appeared to be acidic PRP variants and basic PRPs. Fimbriae bound strongly to the purified PRGs adsorbed onto hydroxyapatite (HAP) beads. In contrast, PRGs in solution failed to inhibit the fimbrial binding to the immobilized PRGs on the HAP beads. These findings suggest that the appearance of binding site(s) of PRGs can be ascribed to their conformational changes. We previously identified the distinct segments within PRP and statherin molecules that are involved in fimbrial binding. The peptides analogous to the binding regions of PRP and statherin (i.e., PRP-C and STN-C) markedly inhibit the binding of fimbriae to PRP and statherin immobilized on the HAP beads, respectively. The PRP-C significantly inhibited the binding of fimbriae to PRG-coated HAP beads as well as to PRP on HAP beads. The peptide did not affect the binding of fimbriae to statherin, whereas the STN-C showed no effect on the fimbrial binding to PRPs or PRGs. In the overlay assay, the PRP-C clearly diminished the interactions between the fimbriae and the various salivary components, including PRPs, the PRGs, and the components with smaller molecular sizes but not statherin. These results strongly suggest that fimbriae bind to salivary components (except statherin) via common peptide segments. It is also suggested that fimbriae bind to saliva through the two distinct binding domains of receptory salivary components: (i) PRGs and PRPs and (ii) statherin.

Adult↗

Senescence-related change in autologous mixed-lymphocyte reaction in senescence-accelerated mice.

Using the senescence-accelerated mouse (SAM) strains, we examined the senescence-related changes of autologous mixed-lymphocyte reaction (AMLR) as well as the phenotypic alteration of the T cell subsets. Splenic T cells from senescence-prone (SAM-P) and resistant (SAM-R) strains of mice were incubated with autologous non-T cells, and AMLR was measured on day 1-5. The kinetics of AMLR responses revealed a marked alteration in senescent SAM-P but not in non-senescent SAM-R mice, in which the peak response occurred at day 1, the response decreasing thereafter up to day 5. Similar senescence-related change was observed in aged (24-month-old) SAM-R and BALB/c mice. Furthermore, the T cells from the aged SAM-R mice cultured with non-senescent syngeneic non-T cells showed a very similar pattern to that cultured with autologous non-T cells. Flow cytometric analysis of T cell phenotype indicated that the percentage of CD4+ CD45RBhi T cells correlated with the peak AMLR responses in both SAM-P and SAM-R mice, and that the percentage of the T cell subset with extrathymic properties was significantly higher in SAM-P mice. These findings suggest that the alteration in kinetics of AMLR is related to senescence but not to the strain of mice, and may reflect a senescence-related dysfunction of the autoregulatory immune mechanisms of T cells.

Aging↗

Effects of K+ channel blockers and K+ ionophore on isoprenaline-induced secretion of amylase from rat parotid acini.

The involvement of K+ channels in regulating secretion of amylase from isolated rat parotid acini was studied in conjunction with beta-adrenoceptor function. It was observed that increasing the concentration of extracellular K- or adding K+ channel blockers enhanced the secretion of amylase. Among several K+ channel blockers, tetraethylammonium, apamin and charybdotoxin were effective to enhance secretion by 48, 69 and 84%, respectively. Glibenclamide was without effect. A low concentration of isoprenaline (10(-7) M) enhanced secretion by 154% and its simultaneous application with tetraethylammonium gave a synergistic effect, producing 371% stimulation. Combination of tetraethylammonium and a low concentration of carbachol (10(-6) M) did not give the synergistic effect. Isoprenaline at the concentration of 10(-6) M enhanced secretion by 313% and this was reduced to 116% by 10(-5) M valinomycin, a K+ ionophore. Valinomycin was without effect on carbachol (10(-5) M)-induced secretion. Somatostatin (10(-5) M) and morphine (10(-4) M) also reduced isoprenaline-induced secretion of amylase. These results suggested the regulation of Ca(2+)-activated K+ channels by isoprenaline in amylase secretory processes in parotid acini.

Adrenergic beta-Agonists↗

Alveolar bone loss in rats infected with a strain of Prevotella intermedia and Fusobacterium nucleatum isolated from a child with prepubertal periodontitis.

Prevotella intermedia and fusobacterium nucleatum are associated with various forms of periodontal disease. The purpose of the present study was to infect the clinical isolates of these periodontopathic bacteria and to induce a significant loss of alveolar bone in specific pathogen-free (SPF) rats in the absence of ligatures. P. intermedia YKD8 and F. nucleatum YKZ5 were isolated from a prepubertal periodontitis patient, while P. gingivalis MWB13 was from a patient with juvenile periodontitis. At first, SPF Sprague-Dawley rats (70 days of age, male) were infected with A. viscosus Ny1R and subsequently superinfected with P. gingivalis MWB13, P. intermedia YKD8, or F. nucleatum YKZ5, respectively. The control group was infected with A. viscosus Ny1R alone. All rats were killed and periodontal bone levels were assessed morphometrically 135 days after the first infection with A. viscosus. P. intermedia YKD8 was recovered frequently from rats, with serum antibody levels remaining highly elevated throughout the experiment. Significant loss of alveolar bone was found in rats infected with P. intermedia YKD8, the virulence of which was equivalent to that of P. gingivalis MWB13. F. nucleatum YKZ5 also induced alveolar bone loss, but not significantly when compared with rats infected with A. viscosus Ny1R alone.

Aggregatibacter actinomycetemcomitans↗

Positive correlation between blood cyclosporin A level and severity of gingival overgrowth in rats.

Cyclosporin a is a drug used to control rejection of organ transplantation and autoimmune diseases; however, it has also been implicated in gingival overgrowth. The present study investigates the relationship between severity of gingival overgrowth and blood cyclosporin A (CsA) levels in Fischer rats treated orally with CsA. Thirty-six 15-day-old male rats were divided into six experimental groups and given powdered rat chow containing 0, 50, 100, 200, 300, and 400 micrograms CsA/g diet ad libitum for 40 days. At the end of the 40-day treatment period, whole blood samples were collected from each rat for assessment of CsA levels. The rats were then sacrificed and the gingival sulcus depth (pseudopocket) around mandibular molars measured to estimate gingival overgrowth. The blood levels of CsA in rats increased with increasing amounts of CsA provided in their food. A 100% incidence in gingival overgrowth was induced in all the rats treated orally with CsA. The overgrowth was more severe in buccal than in lingual gingiva. A significantly positive correlation was found between gingival sulcus depth and the blood CsA level (rs = 0.914, P < 0.0001; Spearman's correlation coefficient by rank). On histological examination, the overgrown gingiva consisted of a thickened epithelial layer and an accumulation of subepithelial fibrous connective tissue components without marked distortion of their proportion.

Analysis of Variance↗

Calbindin D28k-like immunoreactivity in the gustatory epithelium in the rat.

The distribution of calbindin D28k (CB)-like immunoreactivity (-LI) in the gustatory epithelium was examined in the adult rat. In the circumvallate and foliate papillae, CB-like immunoreactive (-IR) nerve fibers were observed in the subgemmal region, and some of these penetrated the taste buds. Two or three spindle-shaped gustatory cells displayed CB-LI in each taste bud of these lingual papillae; the immunoreactivity was restricted to the cytoplasm. In the fungiform papilla, CB-IR nerve fibers were detected in the subgemmal region, but no CB-IR cells were observed in the taste buds of the fungiform papillae. In the taste buds of the incisive papillae, many CB-IR intragemmal nerve fibers were observed, but no apparent CB-IR cells were detected. In the soft palate, CB-IR nerve fibers associated with the taste buds were also observed, but no CB-IR cells were detected in the taste buds. The present findings indicate that CB-IR gustatory cells were only localized in the taste buds in the posterior lingual papillae (circumvallate and foliate papillae), but not in the taste buds in other gustatory epithelium.

Animals↗

Pathogenesis of drug-induced gingival overgrowth. A review of studies in the rat model.

Drug-induced gingival overgrowth is a side effect associated principally with 3 types of drugs: anticonvulsant (phenytoin), immunosuppressant (cyclosporine A), and various calcium channel blockers (nifedipine, verapamil, diltiazem). In this review, we describe the features of phenytoin-, cyclosporine A- and nifedipine-induced gingival overgrowth in rats and discuss factors influencing the onset and severity of these disorders. There are several features common to the gingival overgrowth induced by these drugs: 1) gingival overgrowth is more conspicuous in the buccal than in the lingual gingiva and less severe in the maxilla than in the mandible; 2) once the blood concentration of the drug reaches a certain level as a result of increasing the dose, the incidence of gingival overgrowth is 100% and its severity is dependent on the blood level, the most severe overgrowth being induced by cyclosporine A; 3) the duration of drug administration for maximal gingival overgrowth to develop is about 40 days; 4) the gingival overgrowth regresses spontaneously after discontinuing the drug; 5) accumulation of dental plaque is not essential for the onset of overgrowth, but plays a role in its severity; and 6) more severe overgrowth is induced in young than in old rats. Furthermore, male rats are more susceptible than females to nifedipine-induced gingival overgrowth. These results suggest that drug-induced gingival overgrowth in rats is dependent on the oral drug dose, blood drug level, age, and sex and that preexisting gingival inflammation is a factor relevant to its severity. Since these factors have also been suggested to be important determinants for human drug-induced gingival overgrowth, the rat model may prove valuable in the future for elucidating the molecular pathogenesis of the disorder.

Age Factors↗

Clinical, microbiological and host defense parameters associated with a case of localized prepubertal periodontitis.

A 4-year-old Japanese boy was referred to Osaka University Dental Hospital because of severe mobility and pain of the right lower primary canine. The canine had severe bone loss and a pocket depth exceeding 5-6 mm. The left lower canine showed slight mobility and moderate alveolar bone loss. The other primary teeth showed no pathogenic findings. The subgingival microflora from the right lower canine was dominated by gram-negative rods, especially capnocytophaga and fusobacterium, while actinomyces sp. were the most common gram-positive bacteria. While neutrophil functions of the patient were within the normal ranges of healthy subjects, some lymphocyte functions such as IL-2 production and IgG and IgM syntheses were lower in the patient. 7 months after the extraction of the right lower primary canine, the patient complained of pain around the right lower primary lateral incisor. In 3-4 weeks, the alveolar bone was lost rapidly and mobility of the lower anterior teeth increased significantly. The primary lateral incisor was extracted and the other primary teeth were treated by sealing and systemic and local administration of antibiotics. After treatment, the lower anterior teeth became less mobile and the gram-positive cocci predominated.

Actinomyces↗

Factors influencing nifedipine-induced gingival overgrowth in rats.

Factors such as age, the dose of nifedipine administered in the diet, serum drug level, duration of drug administration, and sex which may influence nifedipine-induced gingival overgrowth were examined in a rat model using 20-, 50-, and 90-days-old male and female rats. Oral administration of nifedipine (50 to 250 mg/kg diet) increased the serum level of the drug in a dose-dependent manner in both males and females. However, a higher serum level was required in females than males to attain the same degree of gingival overgrowth. The minimum dietary concentrations of the drug required to elicit gingival overgrowth in males and females were 150 and 100 mg/kg, respectively, which gave respective minimum serum levels of 800 and 1100 ng/ml. The degree of overgrowth depended on the serum concentration of the drug after it had reached the required minimum in male and female animals. Administration of nifedipine (250 mg/kg diet) for 20 days was enough to induce maximal overgrowth, but this induction occurred only in rats that started to receive the drug when they were 20 days old, not in those that started at 50 and 90 days of age for the same administration period of 55 days, and the overgrowth regressed and the gingiva were normal 40 days after ceasing drug administration. These results suggest that gingival overgrowth occurred in accordance with the drug concentration in the diet, as well as that in the serum, and was more likely to occur in males and younger individuals.

Age Factors↗

Clinical application of dental prosthesis with magnetic attachment to a patient with cerebral palsy.

Removable dental prosthesis with magnetic attachment was applied to a fifty-two-year old female with cerebral palsy. New magnetic attachments made of rare earth metal, a pair of Sm-Co magnets housed in a magnetic stainless steel keeper, were used as a safe and simple retention apparatus instead of the conventional cast metal or wire clasps for partial denture. The patient even with her severe physical disability could manipulate this denture without much difficulty.

Cerebral Palsy↗

Nifedipine-induced gingival overgrowth in the presence or absence of gingival inflammation in rats.

One adverse effect of nifedipine, a long-acting vasodilator, is gingival overgrowth. Preexisting gingival inflammation and/or dental plaque has been suggested to be responsible for the progression of this side effect, but the precise mechanism is uncertain because of a lack of suitable animal models. A study was therefore done to establish an experimental model of gingival overgrowth in rats and to investigate the possible involvement of gingival inflammation and/or dental plaque in its development. Specific pathogen-free Fischer rats (male, 14 days old) were used. Gingival inflammation and dental plaque accumulation were induced by infection with Streptococcus mutans MT8148R. The nifedipine-treated rats (experimental group) were fed a caries-inducing diet containing nifedipine either with or without infection, while the nifedipine-untreated rats (control group) were fed the same diet, similarly with or without the infection. Marked gingival overgrowth was induced in the mandibular molar region of nifedipine-treated rats regardless of S. mutans infection, although the infection resulted in a further increase in the degree of gingival overgrowth. Histological examination of the gingival overgrowth revealed the presence of redundant subepithelial connective tissue in the treated rats, and inflammatory cell infiltration was apparent only in the tissue of the S. mutans-infected rats regardless of the nifedipine administration. These findings suggest that nifedipine induces gingival overgrowth in rats either in the presence or absence of gingival inflammation and/or dental plaque, although these factors can augment the effect of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Dental findings of the elderly with or without senile dementia at a special nursing home.

Survey of dental health condition was performed at a special nursing home for the elderly with senile dementia (28 subjects, 83.3 +/- 6.8 year-old; SD group) or without senile dementia (68 subjects, 84.6 +/- 7.2 year-old; NSD group). There was no difference in number of teeth survived between SD and NSD groups. However, the elderly in SD group had more unfunctionable and/or unrestorable teeth (C4) and less sound and filled teeth (SFT) than those in NSD group. Number of teeth of the elderly in 85- to 89-year-old group was smaller than those of not only younger but older age groups, irrespective of senile dementia. Lower canines showed the highest survival rate among all kinds of teeth in SD as well as in NSD group.

Aged↗

Latex agglutination test for detection of mutans streptococci in relation to dental caries in children.

A simple and rapid system based on a latex agglutination (LA) reaction was devised for the detection of mutans streptococci in dental plaque. Latex particles were sensitized with antibodies against whole cells of Streptococcus mutans strains MT8148 (serotype c), MT703R (e) and OMZ175 (f) and Strep. sobrinus strains B13 (d) and 6715 (g). These sensitized particles were agglutinated within a few minutes after addition of 1.0-10 ng serotype-specific antigen from the homologous organisms or the nitrous acid extract of whole cells at 10(5)-10(6) c.f.u. The LA test specifically differentiated not only mutans streptococci from the other oral streptococci but also Strep. sobrinus from Strep. mutans. The LA test was also applicable to extracts of plaque from 206 human subjects who harboured mutans streptococci. In clinical trials, the outcome of the LA test correlated significantly with the number of mutans streptococci found in plaque (p less than 0.0001), which was quantified by the selective cultivation of mutans streptococci. Furthermore, the LA test discriminated between Strep. mutans and Strep. sobrinus from human dental plaque. The sensitivity and the specificity of the LA test for detection of mutans streptococci were 78.9 and 100%. The degree of reactivity in the LA test correlated significantly with the number of decayed tooth surfaces (p less than 0.0001) and decayed and filled tooth surfaces (p less than 0.0001). These results suggest that the LA test could be useful clinically for the detection of mutans streptococci in dental plaque as well as serving as a caries-activity test.

Antibodies, Bacterial↗

Purification and properties of extracellular mutacin, a bacteriocin from Streptococcus sobrinus.

Mutacin MT6223, a cell-free bacteriocin produced by Streptococcus sobrinus MT6223, was purified by ammonium sulphate precipitation, chromatofocusing with PBE 94 and column chromatography on SP Sephadex C-25. The specific activity of the purified mutacin was increased 1950-fold with a recovery of 9.7%. The molecular mass of the purified mutacin preparation was estimated to be 6.5 kDa. The mutacin activity was stable from pH 2-7, and was resistant to treatment at 100 degrees C for 20 min. It was inactivated by papain or ficin digestion, and was partially inhibited by alpha-chymotrypsin. The mutacin was found to be active against strains of serotypes c, e and f of Streptococcus mutans and the addition of purified mutacin MT6223 to growing cells of S. mutans MT8148 resulted in a rapid inhibition of incorporation of [3H]thymidine, [3H]uracil or L-[3H]glutamic acid into DNA, RNA or protein, respectively. Specific pathogen-free Fischer rats fed diet 2000 and infected with S. mutans MT8148R showed significantly fewer caries and lower plaque scores when mutacin was administered through drinking water. The present study demonstrates that mutacin MT6223 inhibited the growth of mutans streptococci. Thus, mutacin MT6223 may be a candidate for use in dental caries prevention.

Animals↗

Induction of interleukin-1 and -6 in human gingival fibroblast cultures stimulated with Bacteroides lipopolysaccharides.

Normal human gingival fibroblasts stimulated in vitro by lipopolysaccharides (LPS) from oral Bacteroides species produced cell-free and cell-associated thymocyte-activating factors (TAF). Neutralization assays using antisera to human interleukin-1 alpha (HuIL-1 alpha), HuIL-1 beta, and HuIL-6 revealed that cell-free TAF was attributable mainly to IL-1 beta and that IL-6 augmented the TAF activity of IL-1 beta in the culture supernatant. Another factor(s), however, may also be involved in cell-free TAF. By contrast, the active entity of cell-associated TAF was ascribed to IL-1 alpha alone. Furthermore, IL-6 was detected mainly in the supernatant of fibroblast cultures stimulated with Bacteroides LPS. Fibroblasts pretreated with natural human beta or gamma interferon, but not those pretreated with alpha interferon, synthesized higher levels of cell-associated IL-1 alpha in response to stimulation by Bacteroides LPS; however, no interferons exhibited direct IL-1-inducing activity or synergistic IL-1-inducing activity with LPS. Endogenously induced beta interferon was suggested to be necessary for fibroblasts to produce cell-associated IL-1 alpha in response to Bacteroides LPS.

Antigens, Differentiation, T-Lymphocyte↗

[Cyclosporin-A induced gingival overgrowth--strain differences in the rats].

Cyclosporin-A (CsA) which is an effective immunosuppressive agent to control the rejection of organ transplants causes gingival overgrowth as one of accompanying side effects. However, the mechanism of this particular gingival overgrowth still remains unclear. This seems to be largely due to the difficulty of reproducing gingival overgrowth in experimental animals, especially in rodents. The purpose of the present study was to establish a rat model for CsA-induced gingival overgrowth. Specific pathogen-free Fischer and Sprague-Dawley rats (20 days old) were used and fed a caries inducing diet containing CsA. The degree of gingival overgrowth was measured, and histological examination of the gingival sections was performed. The results obtained were as follows; 1. Marked gingival overgrowth was noted around mandibular molars of all rats fed died 2000 containing 56% sucrose supplemented with CsA (a diet of 120-200 mg/kg). This overgrowth was more conspicuous in buccal than in lingual gingiva. However, there were no differences between the two strains of rat in the macroscopic findings as well as in the severity of CsA-induced gingival overgrowth. 2. Rats receiving CsA treatment for 40 days (at 63 days of age) showed the maximum level of gingival overgrowth in both strains of rats. When the gingival sulcus depths at 48 days of age were compared, the S.D. rats seemed to be a higher responder to CsA than the Fischer rats. 3. CsA treated rats showed significantly higher plaque scores than untreated rats. However, CsA-induced gingival overgrowth was little affected by this enhancement of plaque accumulation in the rats infected with S. sobrinus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Phenytoin-induced gingival overgrowth in rats infected with Streptococcus sobrinus 6715.

Inbred Fischer rats were fed a high sucrose diet (No. 2000) containing phenytoin (5,5-diphenyl-hydantoin) for 52 days, which produced serum and salivary PHT levels of 13-14 and 2.6-2.7 micrograms/ml, respectively. Gingival overgrowth was induced in the molar region of all PHT-treated rats but was more severe in Streptococcus sobrinus 6715-infected rats than in non-infected rats, which had lower plaque scores. No significant overgrowth was found in rats infected with Strep. sobrinus and fed the same diet without PHT. Thus dental plaque accumulation enhanced, but was not essential for the development of the PHT-induced gingival overgrowth. Histological examination showed that the density of fibroblasts and connective tissue fibres was similar in all groups. This experimental model could serve as a useful means of understanding the pathogenesis of PHT-induced gingival overgrowth.

Animals↗