掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.jds.2024.02.025

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担当区分：責任著者   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.jds.2023.10.022

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担当区分：筆頭著者,　責任著者   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.jds.2023.11.019

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記述言語：英語  

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担当区分：責任著者   記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier BV  

DOI： 10.1016/j.jds.2024.05.028

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掲載種別：研究論文（学術雑誌）   出版者・発行元：MDPI AG  

Periodontal ligament-associated protein 1 (PLAP-1), also known as Asporin, is an extracellular matrix protein expressed in the periodontal ligament and plays a crucial role in periodontal tissue homeostasis. Our previous research demonstrated that PLAP-1 may inhibit TLR2/4-mediated inflammatory responses, thereby exerting a protective function against periodontitis. However, the precise roles of PLAP-1 in the periodontal ligament (PDL) and its relationship to periodontitis have not been fully explored. In this study, we employed PLAP-1 knockout mice to investigate its roles and contributions to PDL tissue and function in a ligature-induced periodontitis model. Mandibular bone samples were collected from 10-week-old male C57BL/6 (WT) and PLAP-1 knockout (KO) mice. These samples were analyzed through micro-computed tomography (μCT) scanning, hematoxylin and eosin (HE) staining, picrosirius red staining, and fluorescence immunostaining using antibodies targeting extracellular matrix proteins. Additionally, the structure of the PDL collagen fibrils was examined using transmission electron microscopy (TEM). We also conducted tooth extraction and ligature-induced periodontitis models using both wild-type and PLAP-1 KO mice. PLAP-1 KO mice did not exhibit any changes in alveolar bone resorption up to the age of 10 weeks, but they did display an enlarged PDL space, as confirmed by μCT and histological analyses. Fluorescence immunostaining revealed increased expression of extracellular matrix proteins, including Col3, BGN, and DCN, in the PDL tissues of PLAP-1 KO mice. TEM analysis demonstrated an increase in collagen diameter within the PDL of PLAP-1 KO mice. In line with these findings, the maximum stress required for tooth extraction was significantly lower in PLAP-1 KO mice in the tooth extraction model compared to WT mice (13.89 N ± 1.34 and 16.51 N ± 1.31, respectively). In the ligature-induced periodontitis model, PLAP-1 knockout resulted in highly severe alveolar bone resorption, with a higher number of collagen fiber bundle tears and significantly more osteoclasts in the periodontium. Our results demonstrate that mice lacking PLAP-1/Asporin show alteration of periodontal ligament structures and acceleration of bone loss in periodontitis. This underscores the significant role of PLAP-1 in maintaining collagen fibrils in the PDL and suggests the potential of PLAP-1 as a therapeutic target for periodontal diseases.

DOI： 10.3390/ijms242115989

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担当区分：責任著者   掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier BV  

DOI： 10.1016/j.jds.2023.09.027

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担当区分：筆頭著者,　責任著者   掲載種別：研究論文（学術雑誌）   出版者・発行元：Springer Science and Business Media LLC  

Abstract

Dental pulp stem cells (DPSC) usually remain quiescent in the dental pulp tissue; however, once the dental pulp tissue is injured, DPSCs potently proliferate and migrate into the injury microenvironment and contribute to immuno-modulation and tissue repair. However, the key molecules that physiologically support the potent proliferation and migration of DPSCs have not been revealed. In this study, we searched publicly available transcriptome raw data sets, which contain comparable (i.e., equivalently cultured) DPSC and mesenchymal stem cell data. Three data sets were extracted from the Gene Expression Omnibus database and then processed and analyzed. MXRA5 was identified as the predominant DPSC-enriched gene associated with the extracellular matrix. MXRA5 is detected in human dental pulp tissues. Loss of MXRA5 drastically decreases the proliferation and migration of DSPCs, concomitantly with reduced expression of the genes associated with the cell cycle and microtubules. In addition to the known full-length isoform of MXRA5, a novel splice variant of MXRA5 was cloned in DPSCs. Recombinant MXRA5 coded by the novel splice variant potently induced the haptotaxis migration of DPSCs, which was inhibited by microtubule inhibitors. Collectively, MXRA5 is a key extracellular matrix protein in dental pulp tissue for maintaining the proliferation and migration of DPSCs.

DOI： 10.1038/s41598-023-42684-z

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その他リンク： https://www.nature.com/articles/s41598-023-42684-z

担当区分：筆頭著者,　責任著者   記述言語：日本語   掲載種別：研究論文（学術雑誌）  

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担当区分：責任著者   掲載種別：研究論文（学術雑誌）  

DOI： 10.3390/ijms24020970

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担当区分：筆頭著者,　責任著者   記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier BV  

Periodontitis is characterized by irreversible destruction of periodontal tissue. At present, the accepted etiology of periodontitis is based on a three-factor theory including pathogenic bacteria, host factors, and acquired factors. Periodontitis development usually takes a decade or longer and is therefore called chronic periodontitis (CP). To search for genetic factors associated with CP, several genome-wide association study (GWAS) analyses were conducted; however, polymorphisms associated with CP have not been identified. Epigenetics, on the other hand, involves acquired transcriptional regulatory mechanisms due to reversibly altered chromatin accessibility. Epigenetic status is a condition specific to each tissue and cell, mostly determined by the responses of host cells to stimulations by local factors, like bacterial inflammation, and systemic factors such as nutrition status, metabolic diseases, and health conditions. Significantly, epigenetic status has been linked with the onset and progression of several acquired diseases. Thus, epigenetic factors in periodontal tissues are attractive targets for periodontitis diagnosis and treatments. In this review, we introduce accumulating evidence to reveal the epigenetic background effects related to periodontitis caused by genetic factors, systemic diseases, and local environmental factors, such as smoking, and clarify the underlying mechanisms by which epigenetic alteration influences the susceptibility of periodontitis.

DOI： 10.1016/j.jdsr.2022.06.001

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担当区分：責任著者   掲載種別：研究論文（学術雑誌）   出版者・発行元：SAGE Publications  

DOI： 10.1177/00220345221075968

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その他リンク： http://journals.sagepub.com/doi/full-xml/10.1177/00220345221075968

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Frontiers Media SA  

Cementum resorption, unlike bone resorption, is clinically known to occur only with limited pathological stimuli, such as trauma, orthodontic forces, and large apical periodontitis; however, the molecular mechanisms that control osteoclast formation on the cementum surface remain unclear. In this study, we focused on extracellular vesicles (EVs) secreted by cementoblasts and analyzed their effects on osteoclast differentiation. EVs were extracted from the conditioned medium (CM) of the mouse cementoblast cell line OCCM-30. Transmission electron microscopy (TEM) analysis confirmed the presence of EVs with a diameter of approximately 50–200 nm. The effect of the EVs on osteoclast differentiation was examined using the mouse osteoclast progenitor cell line RAW 264.7 with recombinant receptor activator of nuclear factor (NF)-κB ligand (rRANKL) stimulation. EVs enhanced the formation of tartrate-resistant acid phosphatase (TRAP) activity-positive cells upon rRANKL stimulation. EVs also enhanced the induction of osteoclast-associated gene and protein expression in this condition, as determined by real-time PCR and Western blotting, respectively. On the other hand, no enhancing effect of EVs was observed without rRANKL stimulation. A Western blot analysis revealed no expression of receptor activator of NF-κB ligand (RANKL) in EVs themselves. The effect on rRANKL-induced osteoclast differentiation was examined using the CM of cementoblasts in terms of TRAP activity-positive cell formation and osteoclast-associated gene expression. The conditioned medium partly inhibited rRANKL-induced osteoclast differentiation and almost completely suppressed its enhancing effect by EVs. These results indicate that cementoblasts secreted EVs, which enhanced RANKL-induced osteoclast differentiation, and simultaneously produced soluble factors that neutralized this enhancing effect of EVs, implicating this balance in the regulation of cementum absorption. A more detailed understanding of this crosstalk between cementoblasts and osteoclasts will contribute to the development of new therapies for pathological root resorption.

DOI： 10.3389/fphys.2022.825596

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掲載種別：研究論文（学術雑誌）   出版者・発行元：Public Library of Science (PLoS)  

Amelogenins, major extra cellular matrix proteins of developing tooth enamel, are predominantly expressed by ameloblasts and play significant roles in the formation of enamel. Recently, amelogenin has been detected in various epithelial and mesenchymal tissues, implicating that it might have distinct functions in various tissues. We have previously reported that leucine rich amelogenin peptide (LRAP), one of the alternate splice forms of amelogenin, regulates receptor activator of NF-kappa B ligand (RANKL) expression in cementoblast/periodontal ligament cells, suggesting that the amelogenins, especially LRAP, might function as a signaling molecule in bone metabolism. The objective of this study was to identify and define LRAP functions in bone turnover. We engineered transgenic (TgLRAP) mice using a murine 2.3kb α1(I)-collagen promoter to drive expression of a transgene consisting of LRAP, an internal ribosome entry site (IRES) and enhanced green fluorescent protein (EGFP) to study functions of LRAP in bone formation and resorption. Calvarial cell cultures from the TgLRAP mice showed increased alkaline phosphatase (ALP) activity and increased formation of mineralized nodules compared to the cells derived from wild-type (WT) mice. The TgLRAP calvarial cells also showed an inhibitory effect on osteoclastogenesis <italic>in vitro</italic>. Gene expression comparison by quantitative polymerase chain reaction (Q-PCR) in calvarial cells indicated that bone formation makers such as <italic>Runx2</italic>, <italic>Alp</italic>, and <italic>osteocalcin</italic> were increased in TgLRAP compared to the WT cells. Meanwhile, <italic>Rankl</italic> expression was decreased in the TgLRAP cells <italic>in vitro</italic>. The ovariectomized (OVX) TgLRAP mice resisted bone loss induced by ovariectomy resulting in higher bone mineral density in comparison to OVX WT mice. The quantitative analysis of calcein intakes indicated that the ovariectomy resulted in increased bone formation in both WT and TgLRAP mice; OVX TgLRAP appeared to show the most remarkably increased bone formation. The parameters for bone resorption in tissue sections showed increased number of osteoclasts in OVX WT, but not in OVX TgLRAP over that of sham operated WT or TgLRAP mice, supporting the observed bone phenotypes in OVX mice. This is the first report identifying that LRAP, one of the amelogenin splice variants, affects bone turnover <italic>in vivo</italic>.

DOI： 10.1371/journal.pone.0259966

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担当区分：責任著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

The periodontal ligament is a soft connective tissue embedded between the alveolar bone and cementum, the surface hard tissue of teeth. Periodontal ligament fibroblasts (PDLF) actively express osteo/cementogenic genes, which contribute to periodontal tissue homeostasis. However, the key factors maintaining the osteo/cementogenic abilities of PDLF remain unclear. We herein demonstrated that PPARγ was expressed by in vivo periodontal ligament tissue and its distribution pattern correlated with alkaline phosphate enzyme activity. The knockdown of PPARγ markedly reduced the osteo/cementogenic abilities of PDLF in vitro, whereas PPARγ agonists exerted the opposite effects. PPARγ was required to maintain the acetylation status of H3K9 and H3K27, active chromatin markers, and the supplementation of acetyl-CoA, a donor of histone acetylation, restored PPARγ knockdown-induced decreases in the osteo/cementogenic abilities of PDLF. An RNA-seq/ChIP-seq combined analysis identified four osteogenic transcripts, RUNX2, SULF2, RCAN2, and RGMA, in the PPARγ-dependent active chromatin region marked by H3K27ac. Furthermore, RUNX2-binding sites were selectively enriched in the PPARγ-dependent active chromatin region. Collectively, these results identified PPARγ as the key transcriptional factor maintaining the osteo/cementogenic abilities of PDLF and revealed that global H3K27ac modifications play a role in the comprehensive osteo/cementogenic transcriptional alterations mediated by PPARγ.

DOI： 10.3390/ijms22168646

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掲載種別：研究論文（学術雑誌）   出版者・発行元：Frontiers Media {SA}  

<jats:p>Loeys–Dietz syndrome (LDS) is a syndromic connective tissue disorder caused by a heterozygous missense mutation in genes that encode transforming growth factor (TGF)-β receptor (<jats:italic>TGFBR</jats:italic>) <jats:italic>1</jats:italic> and <jats:italic>2</jats:italic>. We encountered a patient with LDS, who had severe periodontal tissue destruction indicative of aggressive periodontitis. The patient had a missense mutation in the glycine and serine-rich domain of <jats:italic>TGFBR1</jats:italic> exon 3. This G-to-T mutation at base 563 converted glycine to valine. We established an LDS model knock-in mouse that recapitulated the LDS phenotype. Homozygosity of the mutation caused embryonic lethality and heterozygous knock-in mice showed distorted and ruptured elastic fibers in the aorta at 24 weeks of age and died earlier than wildtype (WT) mice. We stimulated mouse embryonic fibroblasts (MEFs) from the knock-in mouse with TGF-β and examined their responses. The knock-in MEFs showed downregulated <jats:italic>Serpine 1</jats:italic> mRNA expression and phosphorylation of Smad2 to TGF-β compared with WT MEFs. To clarify the influence of TGF-β signaling abnormalities on the pathogenesis or progression of periodontitis, we performed pathomolecular analysis of the knock-in mouse. There were no structural differences in periodontal tissues between WT and LDS model mice at 6 or 24 weeks of age. Micro-computed tomography revealed no significant difference in alveolar bone resorption between WT and knock-in mice at 6 or 24 weeks of age. However, TGF-β-related gene expression was increased significantly in periodontal tissues of the knock-in mouse compared with WT mice. Next, we assessed a mouse periodontitis model in which periodontal bone loss was induced by oral inoculation with the bacterial strain <jats:italic>Porphyromonas gingivalis</jats:italic> W83. After inoculation, we collected alveolar bone and carried out morphometric analysis. <jats:italic>P. gingivalis</jats:italic>-induced alveolar bone loss was significantly greater in LDS model mice than in WT mice. Peritoneal macrophages isolated from <jats:italic>Tgfbr1<jats:sup><jats:italic>G</jats:italic>188V/+</jats:sup></jats:italic> mice showed upregulation of inflammatory cytokine mRNA expression induced by <jats:italic>P. gingivalis</jats:italic> lipopolysaccharide compared with WT macrophages. In this study, we established an LDS mouse model and demonstrated that LDS model mice had elevated susceptibility to <jats:italic>P. gingivalis</jats:italic>-induced periodontitis, probably through TGF-β signal dysfunction. This suggests that TGF-β signaling abnormalities accelerate the pathogenesis or progression of periodontitis.</jats:p>

DOI： 10.3389/fphys.2021.715687

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担当区分：筆頭著者,　責任著者   記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Springer Science and Business Media {LLC}  

Accumulating evidence suggests that specific non-coding RNAs exist in many types of malignant tissues, and are involved in cancer invasion and metastasis. However, little is known about the precise roles of non-coding RNAs in squamous cell carcinoma (SQCC) invasion and migration. Recently, the dentin matrix protein-1 (DMP-1) gene locus was identified as a transcriptionally active site in squamous cell carcinoma (SQCC) tissue and cells. However, it is unclear whether RNA associated with cell migration exist at the DMP-1 gene locus in SQCC cells. We identified a novel promoter-associated non-coding RNA in the antisense strand of DMP-1 gene locus, promoter-associated non-coding RNA (panRNA)-DMP-1, by the RACE method in SQCC cells and tissues, and characterized the functions of panRNA-DMP-1 in EGF-driven SQCC cell migration. The inhibition of endogenous panRNA-DMP-1 expression by specific siRNAs and exogenous over-expression of panRNA-DMP-1 resulted in increased and suppressed cellular migration toward EGF in SQCC cells, respectively, and nuclear expression of panRNA-DMP-1 was induced by EGF stimulation. Mechanistically, suppression of panRNA-DMP-1 expression increased EGFR nuclear localization upon EGF treatment and nuclear panRNA-DMP-1 physically interacted with EGFR, which was confirmed by RNA immunoprecipitation assay using a bacteriophage-delivered PP7 RNA labeling system. Furthermore, co-immunoprecipitation assay revealed that suppression of panRNA-DMP-1 stabilized EGFR interaction with STAT3, a known co-transcription factors of EGFR, to induce migratory properties in many cancer cells. Based on these findings, panRNA-DMP-1 is an EGFR-associating RNA that inhibits the EGF-induced migratory properties of SQCC possibly by regulating EGFR nuclear localization and EGFR binding to STAT3.

DOI： 10.1007/s11010-020-04046-5

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その他リンク： http://link.springer.com/article/10.1007/s11010-020-04046-5/fulltext.html

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Springer Science and Business Media LLC  

<title>Abstract</title>Apical periodontitis (AP) is an acute or chronic inflammatory disease caused by complex interactions between infected root canal and host immune system. It results in the induction of inflammatory mediators such as chemokines and cytokines leading to periapical tissue destruction. To understand the molecular pathogenesis of AP, we have investigated inflammatory-related genes that regulate AP development. We found here that macrophage-derived CXCL9, which acts through CXCR3, is recruited by progressed AP. The inhibition of CXCL9 by a CXCR3 antagonist reduced the lesion size in a mouse AP model with decreasing IL-1β, IL-6 and TNFα expression. The treatment of peritoneal macrophages with CXCL9 and LPS induced the transmigration and upregulation of osteoclastogenic cytokines such as IL-1β, IL-6 and matrix metalloprotease 2, a marker of activated macrophages. This suggests that the CXCL9-CXCR3 axis plays a crucial role in the development of AP, mediated by the migration and activation of macrophages for periapical tissue destruction. Our data thus show that CXCL9 regulates the functions of macrophages which contribute to AP pathogenesis, and that blocking CXCL9 suppresses AP progression. Knowledge of the principal factors involved in the progression of AP, and the identification of related inflammatory markers, may help to establish new therapeutic strategies.

DOI： 10.1038/s41598-021-82167-7

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その他リンク： http://www.nature.com/articles/s41598-021-82167-7

担当区分：責任著者   記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：MDPI AG  

The spread of root canal infection to surrounding periodontal tissue through accessory root canals reduces the success rate of endodontic treatment. In this case, cone-beam computed tomography revealed a lesion (4 mm from the apex) resulting from an accessory root canal of the maxillary left central incisor. First, non-surgical endodontic treatment was conducted but the sinus tract remained. Surgical preparation of the root cavity was then conducted to remove potentially infected dentin surrounding the accessory root canal. The cavity was filled and the foramen was sealed with resin containing bioactive surface pre-reacted glass (S-PRG) filler. The photopolymerized resin was then contoured and polished. In combination with subsequent supportive non-surgical endodontic treatment, a good clinical outcome with the disappearance of the sinus tract and clinical symptoms such as discomfort and pressure pain and the regeneration of the alveolar bone hanging over the cavity was obtained. In this case, the good clinical outcome may have been due to the dentin-adhesive property and durability of the pre-adhesive system and composite resin. The better biocompatibility of S-PRG fillers presumably facilitated periodontal tissue healing.

DOI： 10.3390/dj8040131

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担当区分：責任著者   記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Springer Science and Business Media {LLC}  

Pro-inflammatory cytokines prevent bone regeneration in vivo and activation of nuclear factor-κB (NF-κB) signaling has been proposed to lead to suppression of bone morphogenetic protein (BMP)-induced osteogenesis via direct binding of p65 to Smad4 in vitro. Application of a small nuclear acidic protein (MTI-II) and its delivered peptide, MPAID (MTI-II peptide anti-inflammatory drug) has been described to elicit therapeutic potential via strong anti-inflammatory action following the physical association of MTI-II and MPAID with p65. However, it is unclear whether MTI-II attenuates tumor necrosis factor (TNF)-α inhibition of BMP-induced osteogenesis. Herein, we found that TNF-α-mediated suppression of responses associated with BMP4-induced osteogenesis, including expression of the osteocalcin encoding gene Ocn, Smad binding element (SBE)-dependent luciferase activity, alkaline phosphatase activity, and alizarin red S staining were largely restored by MTI-II and MPAID in MC3T3-E1 cells. Mechanistically, MTI-II and MPAID did not inhibit nuclear translocation of p65 or disassociate Smad4 from p65. Further, results from chromatin immunoprecipitation (ChIP) analyses revealed that Smad4 enrichment in cells over-expressing MTI-II and treated with TNF-α was equivalent to that in cells without TNF-α treatment. Alternatively, Smad4 enrichment was considerably decreased following TNF-α treatment in control cells. Moreover, p65 enrichment in the Id-1 promoter SBE was detected only when cells over-expressing MTI-II were stimulated with TNF-α. Overall, our study concludes that MTI-II restored TNF-α-inhibited suppression of BMP-Smad-induced osteogenic differentiation by enhancing accessibility of the Smad4-p65 complex to the SBE rather than by liberating Smad4 from p65.

DOI： 10.1007/s11010-020-03734-6

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担当区分：責任著者   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.archoralbio.2019.104634

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1038/s41598-019-40046-2

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担当区分：責任著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1111/iej.13130

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.3389/fimmu.2019.01310

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担当区分：責任著者   記述言語：日本語   掲載種別：研究論文（学術雑誌）   出版者・発行元：(NPO)日本歯周病学会  

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担当区分：筆頭著者,　責任著者   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.bbrc.2017.12.136

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.numecd.2016.11.008

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担当区分：筆頭著者,　責任著者   記述言語：英語   出版者・発行元：Japanese Association for Oral Biology  

DOI： 10.1016/j.job.2016.08.002

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Elsevier BV  

DOI： 10.1016/j.bbrep.2016.04.004

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担当区分：責任著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.archoralbio.2015.05.013

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1002/jbmr.2444

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担当区分：筆頭著者,　責任著者   掲載種別：研究論文（学術雑誌）  

DOI： 10.1371/journal.pone.0112490

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掲載種別：研究論文（学術雑誌）  

DOI： 10.1093/ndt/gft449

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担当区分：筆頭著者,　責任著者   記述言語：日本語   掲載種別：研究論文（学術雑誌）   出版者・発行元：The Japanese Society of Conservative Dentistry  

目的 : Matrix trioxide aggregate (MTA) は高い被蓋硬組織形成能を有することから, 穿孔部の閉鎖や直接覆髄材として用いられている. 破折や術中の露髄を歯髄組織の物理的損傷と捉えれば, 損傷組織への周囲残存組織からの歯髄細胞の遊走, 遊走細胞の基質への接着, 増殖や分化などの細胞機能の発現からなる一連の経過が歯髄保存的処置の成否に重要である. そのような背景から, 直接覆髄材が歯髄細胞に対して接着・増殖誘導能をもつかは, 露髄後組織修復の予後を左右すると考えられる. 臨床では, 歯髄に近接する深い窩洞や軽度露髄に対してはコンポジットレジン (CR) 充塡も選択される. そこで, 本研究ではMTAの歯髄細胞に対する接着や接着後の増殖, アポトーシス誘導能を, CRおよび間接覆髄剤であるグラスアイオノマーセメント (GIC) を対照群として検討した. <br> 材料および方法 : 96ウェルプレートをMTA, CR, GICまたはfibronectinでコートし, 血清非存在下でヒト歯髄細胞をコートずみウェルに播種し, 1.5時間後の接着細胞数を定量した. MTA, CR, GIC上での細胞増殖能の検討は, 播種1.5時間後に血清培地に交換し72時間後まで検討した. アポトーシス誘導能はカスパーゼ3/7活性を指標に検討した. <br> 結果 : MTAは血清非存在下でヒト歯髄細胞の接着を誘導したが, CRおよびGICは誘導しなかった. 一方, ヒト歯髄細胞のMTAへの細胞接着数をfibronectinと比較すると, MTAのヒト歯髄細胞接着誘導能は有意に低かった. MTAへのヒト歯髄細胞の接着は播種72時間後においても認められたが, その細胞数は播種後と比較して減少していた. CRやGICに播種したヒト歯髄細胞ではカスパーゼ3/7活性の著しい上昇が認められたが, MTA上に播種したヒト歯髄細胞では活性の上昇はみられなかった. <br> 結論 : MTAはCRやGICと比較して有意に高いヒト歯髄細胞の接着誘導能を示した. これはCRやGICと異なり, MTA上ではヒト歯髄細胞のアポトーシスが誘導されないためと示唆される. 一方, MTAの増殖誘導能は低く, 接着誘導能はfibronectinと比較すると非常に弱かったことから, 今後, 遊走・接着能をもつ有機質接着因子とMTAの混合利用により, さらに良好な創面被覆, 歯髄組織再生が行える可能性がある.

DOI： 10.11471/shikahozon.57.547

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その他リンク： http://search.jamas.or.jp/link/ui/2015182150

担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.2174/978160805465711202010221

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担当区分：筆頭著者,　責任著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.archoralbio.2012.03.005

Web of Science

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1186/1617-9625-10-3

Web of Science

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

<jats:p>Tooth and bone specimen require extensive demineralization for careful analysis of cell morphology, as well as gene and protein expression levels. The LacZ gene, which encodes the ß-galactosidase enzyme, is often used as a reporter gene to study gene-structure function, tissue-specific expression by a promoter, cell lineage and fate. This reporter gene is particularly useful for analyzing the spatial and temporal gene expression pattern, by expressing the LacZ gene under the control of a promoter of interest. To analyze LacZ activity, and the expression of other genes and their protein products in teeth and bones, it is necessary to carry out a complete demineralization of the specimen before cutting sections. However, strong acids, such as formic acid used for tooth demineralization, destroy the activities of enzymes including those of ß-galactosidase. Therefore, most protocols currently use mild acids such as 0.1 M ethylene diamine tetra-acetic acid (EDTA) for demineralization of tooth and bone specimen, which require a longer period of treatment for complete demineralization. A method by which hard tissue specimens such as teeth and bones can be rapidly, but gently, decalcified is necessary to save time and effort. Here, we report a suitable method for rapid demineralization of mouse teeth in 0.1M EDTA at 42˚C without any loss of ß-galactosidase activity.</jats:p>

DOI： 10.2174/1874210601004010223

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.bbrc.2010.06.112

Web of Science

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記述言語：日本語   掲載種別：研究論文（学術雑誌）  

DOI： 10.11471/shikahozon.53.73

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担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.matbio.2009.03.006

Web of Science

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.matbio.2009.01.005

Web of Science

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1177/0022034509334749

Web of Science

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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記述言語：英語  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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記述言語：英語  

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J-GLOBAL

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J-GLOBAL

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記述言語：日本語   出版者・発行元：(NPO)日本歯科保存学会  

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記述言語：日本語   出版者・発行元：(NPO)日本歯科保存学会  

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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記述言語：日本語   出版者・発行元：(NPO)日本歯科保存学会  

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記述言語：日本語   出版者・発行元：(NPO)日本歯科保存学会  

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J-GLOBAL

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J-GLOBAL

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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J-GLOBAL

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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記述言語：日本語   掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）   出版者・発行元：The Japanese Society of Conservative Dentistry  

目的 : Matrix trioxide aggregate (MTA) は高い被蓋硬組織形成能を有することから, 穿孔部の閉鎖や直接覆髄材として用いられている. 破折や術中の露髄を歯髄組織の物理的損傷と捉えれば, 損傷組織への周囲残存組織からの歯髄細胞の遊走, 遊走細胞の基質への接着, 増殖や分化などの細胞機能の発現からなる一連の経過が歯髄保存的処置の成否に重要である. そのような背景から, 直接覆髄材が歯髄細胞に対して接着・増殖誘導能をもつかは, 露髄後組織修復の予後を左右すると考えられる. 臨床では, 歯髄に近接する深い窩洞や軽度露髄に対してはコンポジットレジン (CR) 充塡も選択される. そこで, 本研究ではMTAの歯髄細胞に対する接着や接着後の増殖, アポトーシス誘導能を, CRおよび間接覆髄剤であるグラスアイオノマーセメント (GIC) を対照群として検討した. <br> 材料および方法 : 96ウェルプレートをMTA, CR, GICまたはfibronectinでコートし, 血清非存在下でヒト歯髄細胞をコートずみウェルに播種し, 1.5時間後の接着細胞数を定量した. MTA, CR, GIC上での細胞増殖能の検討は, 播種1.5時間後に血清培地に交換し72時間後まで検討した. アポトーシス誘導能はカスパーゼ3/7活性を指標に検討した. <br> 結果 : MTAは血清非存在下でヒト歯髄細胞の接着を誘導したが, CRおよびGICは誘導しなかった. 一方, ヒト歯髄細胞のMTAへの細胞接着数をfibronectinと比較すると, MTAのヒト歯髄細胞接着誘導能は有意に低かった. MTAへのヒト歯髄細胞の接着は播種72時間後においても認められたが, その細胞数は播種後と比較して減少していた. CRやGICに播種したヒト歯髄細胞ではカスパーゼ3/7活性の著しい上昇が認められたが, MTA上に播種したヒト歯髄細胞では活性の上昇はみられなかった. <br> 結論 : MTAはCRやGICと比較して有意に高いヒト歯髄細胞の接着誘導能を示した. これはCRやGICと異なり, MTA上ではヒト歯髄細胞のアポトーシスが誘導されないためと示唆される. 一方, MTAの増殖誘導能は低く, 接着誘導能はfibronectinと比較すると非常に弱かったことから, 今後, 遊走・接着能をもつ有機質接着因子とMTAの混合利用により, さらに良好な創面被覆, 歯髄組織再生が行える可能性がある.

DOI： 10.11471/shikahozon.57.547

CiNii Article

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その他リンク： http://search.jamas.or.jp/link/ui/2015182150

掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

J-GLOBAL

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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記述言語：日本語   掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）   出版者・発行元：(NPO)日本歯周病学会  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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記述言語：日本語   掲載種別：研究発表ペーパー・要旨（国際会議）   出版者・発行元：特定非営利活動法人 日本歯周病学会  

DOI： 10.14833/amjsp.2011s.0.23.0

CiNii Article

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掲載種別：研究発表ペーパー・要旨（国際会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（国際会議）  

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掲載種別：研究発表ペーパー・要旨（全国大会，その他学術会議）  

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掲載種別：研究発表ペーパー・要旨（国際会議）  

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記述言語：日本語  

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掲載種別：研究発表ペーパー・要旨（国際会議）  

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記述言語：日本語   出版者・発行元：日本炎症・再生医学会  

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記述言語：日本語  

DOI： 10.14833/amjsp.2006s.0.71.0

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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記述言語：日本語   出版者・発行元：日本炎症・再生医学会  

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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掲載種別：研究発表ペーパー・要旨（国際会議）  

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掲載種別：研究発表ペーパー・要旨（国際会議）  

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

CiNii Article

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

CiNii Article

CiNii Books

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

CiNii Article

CiNii Books

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

CiNii Article

CiNii Books

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記述言語：日本語   出版者・発行元：(NPO)日本歯周病学会  

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記述言語：日本語   出版者・発行元：大阪大学歯学会  

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記述言語：英語   会議種別：口頭発表（招待・特別）  

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記述言語：英語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：日本語   会議種別：口頭発表（招待・特別）  

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記述言語：英語   会議種別：口頭発表（招待・特別）  

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