Tokushima University / Educator and Researcher Directory --- Nakanishi, Tadashi

Personal Web Page

https://researchmap.jp/tds (researchmap)

Field of Study

○	Dentistry

Subject of Study

○

Book / Paper

Book:

1.	Tadashi Nakanishi and Takashi Matsuo : 2. 感染根管における細菌感染の実態, 株式会社ヒョーロン・パブリッシャーズ, Jun. 2019.
2.	Takashi Matsuo and Tadashi Nakanishi : 第17章高齢者・有病者の歯内治療, 医歯薬出版株式会社, Sep. 2018.
3.	Takashi Matsuo and Tadashi Nakanishi : 第1章歯と歯根周囲の組織学, 永末書店, Jan. 2018.
4.	Tadashi Nakanishi : 新・歯科衛生士教育マニュアル保存修復 5 歯髄の保護法, Quintessence Publishing CO.,Ltd., 東京, Sep. 2012.
5.	Tadashi Nakanishi, Kanako Takahashi, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : Proceedings of the International Conference on Dentin/Pulp Complex 2001, --- An Immunohistologic Study on the Localization of Selected Bacteria and Chemokines in Human Deep-Carious Teeth ---, Quintessence Publishing CO.,Ltd., Tokyo, Jun. 2002.

Academic Paper (Judged Full Paper):

1.	Hitomi Kuramoto, Tadashi Nakanishi, Daisuke Takegawa, MIEDA Katsuhiro and Keiichi Hosaka : Caffeic Acid Phenethyl Ester Induces Vascular Endothelial Growth Factor Production and Inhibits CXCL10 Production in Human Dental Pulp Cells, Current Issues in Molecular Biology, Vol.44, No.11, 5691-5699, 2022. (Summary) The survival rate of root non-vital teeth is lower than that of vital teeth. Therefore, to preserve the dental pulp is very important. The vascular endothelial growth factor (VEGF) is the most potent angiogenic factor involved in the vitality of dental pulp including reparative dentin formation. Caffeic acid phenethyl ester (CAPE) is a physiologically active substance of propolis and has some bioactivities such as anti-inflammatory effects. However, there are no reports on the effects of CAPE on dental pulp inflammation. In this study, we investigated the effects of CAPE on VEGF and inflammatory cytokine production in human dental pulp cells (HDPCs) to apply CAPE to an ideal dental pulp protective agent. We found that CAPE induced VEGF production from HDPCs. Moreover, CAPE induced the phosphorylation of p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinases (ERK), and stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) in HDPCs. Furthermore, CAPE inhibited C-X-C motif chemokine ligand 10 (CXCL10) production in Pam3CSK4- and tumor necrosis factor-alpha (TNF-α)-stimulated HDPCs. In conclusion, these results suggest that CAPE might be useful as a novel biological material for vital pulp therapy by exerting the effects of VEGF production and anti-inflammatory activities. (Keyword) anti-inflammatory effect / caffeic acid phenethyl ester / dental pulp cells / pulpitis / vascular endothelial growth factor / vital pulp therapy (Tokushima University Institutional Repository) ● Metadata: 117775 (Link to Publication Site) ● Publication site (DOI): 10.3390/cimb44110385 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36421669 ● Search Scopus @ Elsevier (PMID): 36421669 ● Search Scopus @ Elsevier (DOI): 10.3390/cimb44110385 (Tokushima University Institutional Repository: 117775, DOI: 10.3390/cimb44110385, PubMed: 36421669)
2.	Hitomi Kuramoto, Kouji Hirao, Hiromichi Yumoto, Yuki Hosokawa, Tadashi Nakanishi, Daisuke Takegawa, Ayako Washio, Chiaki Kitamura and Takashi Matsuo : Caffeic acid phenethyl ester (CAPE) induces VEGF expression and production in rat odontoblastic cells, BioMed Research International, Vol.Article ID 5390720, 2019. (Summary) Caffeic acid phenethyl ester (CAPE), the main component of propolis, has various biological activities including anti-inflammatory effect and wound healing promotion. Odontoblasts located in the outermost layer of dental pulp play crucial roles such as production of growth factors and formation of hard tissue termed reparative dentin in host defense against dental caries. In this study, we investigated the effects of CAPE on the upregulation of vascular endothelial growth factor (VEGF) and calcification activities of odontoblasts, leading to development of novel therapy for dental pulp inflammation caused by dental caries. CAPE significantly induced mRNA expression and production of VEGF in rat clonal odontoblast-like KN-3 cells cultured in normal medium or osteogenic induction medium. CAPE treatment enhanced nuclear factor-kappa B (NF-B) transcription factor activation, and furthermore, the specific inhibitor of NF-B significantly reduced VEGF production. The expression of VEGF receptor- (VEGFR-) 2, not VEGFR-1, was up regulated in KN-3 cells treated with CAPE. In addition, VEGF significantly increased mineralization activity in KN-3 cells. These findings suggest that CAPE might be useful as a novel biological material for the dental pulp conservative therapy. (Tokushima University Institutional Repository) ● Metadata: 114566 (Link to Publication Site) ● Publication site (DOI): 10.1155/2019/5390720 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31930126 ● Summary page in Scopus @ Elsevier: 2-s2.0-85077441042 (Tokushima University Institutional Repository: 114566, DOI: 10.1155/2019/5390720, PubMed: 31930126, Elsevier: Scopus)
3.	Kouji Hirao, Hiromichi Yumoto, Yuki Hosokawa, Hitomi Kuramoto, 鷲尾絢子, Tadashi Nakanishi, Daisuke Takegawa, 北村知昭 and Takashi Matsuo : Anti-inflammatory Effects of Catechin on Rat Odontoblastic Cells (KN-3), The Japanese Journal of Conservative Dentistry, Vol.60, No.5, 235-244, 2017. (Link to Publication Site) ● Publication site (DOI): 10.11471/shikahozon.60.235 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680498132224 ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.60.235 (DOI: 10.11471/shikahozon.60.235, CiNii: 1390282680498132224)
4.	Yuki Hosokawa, Kouji Hirao, Hiromichi Yumoto, Ayako Washio, Tadashi Nakanishi, Daisuke Takegawa, Chiaki Kitamura and Takashi Matsuo : Functional roles of NOD1 in odontoblasts on dental pulp innate immunity, BioMed Research International, Vol.2016, 9325436, 2016. (Summary) Caries-related pathogens are first recognized by odontoblasts and induce inflammatory events that develop to pulpitis. Generally, initial sensing of microbial pathogens is mediated by pattern recognition receptors, such as Toll-like receptor and nucleotide-binding oligomerization domain (NOD); however, little is known about NODs in odontoblasts. In this study, the levels of NODs expressed in rat odontoblastic cell line, KN-3, were assessed by flow cytometry and the levels of chemokines in NOD-specific ligand-stimulated KN-3 cells were analyzed by real-time PCR and ELISA. The signal transduction pathway activated with NOD-specific ligand was assessed by blocking assay with specific inhibitors and reporter assay. In KN-3 cells, the expression level of NOD1 was stronger than that of NOD2 and the production of chemokines, such as CINC-1, CINC-2, CCL20, and MCP-1, was upregulated by stimulation with NOD1-specific ligand, but not with NOD2-specific ligand. CINC-2 and CCL20 production by stimulation with NOD1-specific ligand was reduced by p38 MAPK and AP-1 signaling inhibitors. Furthermore, the reporter assay demonstrated AP-1 activation in NOD1-specific ligand-stimulated KN-3 cells. These findings indicated that NOD1 expressed in odontoblasts functions to upregulate the chemokines expression via p38-AP-1 signaling pathway and suggested that NOD1 may play important roles in the initiation and progression of pulpitis. (Keyword) Animals / Cell Line / cytokinesis / Dental Pulp / innate immunity / Inflammation Mediators / Nod1 Signaling Adaptor Protein / Odontoblasts / Rats (Tokushima University Institutional Repository) ● Metadata: 112386 (Link to Publication Site) ● Publication site (DOI): 10.1155/2016/9325436 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 27747243 ● Summary page in Scopus @ Elsevier: 2-s2.0-84991669747 (Tokushima University Institutional Repository: 112386, DOI: 10.1155/2016/9325436, PubMed: 27747243, Elsevier: Scopus)
5.	Tadashi Nakanishi, Kayo Mukai, Yoshitaka Hosokawa, Daisuke Takegawa and Takashi Matsuo : Catechins inhibit vascular endothelial growth factor production and cyclooxygenase-2 expression in human dental pulp cells, International Endodontic Journal, Vol.48, No.3, 277-282, 2015. (Summary) To investigate the effect of catechins on vascular endothelial growth factor (VEGF) production and cyclooxygenase-2 (COX-2) expression in human dental pulp cells (HDPC) stimulated with bacteria-derived factors or pro-inflammatory cytokines. Morphologically fibroblastic cells established from explant cultures of healthy human dental pulp tissues were used as HDPC. HDPC pre-treated with catechins, epigallocatechin-3-gallate (EGCG) or epicatechin gallate (ECG), were exposed to lipopolysaccharide (LPS), peptidoglycan (PG), interlukin-1β (IL-1β) or tumour necrosis factor-α (TNF-α). VEGF production was examined by enzyme-linked immunosorbent assay, and COX-2 expression was assessed by immunoblot. EGCG and ECG significantly reduced LPS- or PG-mediated VEGF production in the HDPC in a dose-dependent manner. EGCG also prevented IL-1β-mediated VEGF production. Although TNF-α did not enhance VEGF production in the dental pulp cells, treatment of 20 μg mL(-1) of EGCG decreased the level of VEGF. In addition, the catechins attenuated COX-2 expression induced by LPS and IL-1β. The up-regulated VEGF and COX-2 expressions in the HDPC stimulated with these bacteria-derived factors or IL-1β were diminished by the treatment of EGCG and ECG. These findings suggest that the catechins may be beneficial as an anti-inflammatory tool of the treatment for pulpal inflammation. (Keyword) catechin / cyclooxygenase-2 / dental pulp / vascular endothelial growth factor (Link to Publication Site) ● Publication site (DOI): 10.1111/iej.12312 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24847951 ● Search Scopus @ Elsevier (PMID): 24847951 ● Search Scopus @ Elsevier (DOI): 10.1111/iej.12312 (DOI: 10.1111/iej.12312, PubMed: 24847951)
6.	Daisuke Takegawa, Tadashi Nakanishi, Kouji Hirao, Hiromichi Yumoto, Kanako Takahashi and Takashi Matsuo : Modulatory roles of interferon-γ through indoleamine 2, 3-dioxygenase induction in innate immune response of dental pulp cells., Journal of Endodontics, Vol.40, No.9, 1382-1387, 2014. (Summary) Marked infiltration of inflammatory cells such as activated T cells producing interferon-γ (IFN-γ) is observed in severe pulpitis. However, the roles of IFN-γ in the innate immune response of dental pulp have not been reported. Indoleamine 2, 3-dioxygenase (IDO) is a regulator of immune responses, and the IDO expression is induced by IFN-γ in many cells whose expression in dental pulp is unknown. The purpose of this study was to determine the role of IFN-γ in the immune response through microbial pattern recognition receptors (PRRs) such as Toll-like receptors or nucleotide-binding oligomerization domain-like receptors on the production of proinflammatory cytokines such as CXCL10 and interleukin (IL)-6 and the expression of IDO in cultured human dental pulp cells (HDPCs). HDPCs were established from explant cultures of healthy pulp tissues. CXCL10 and IL-6 production was determined using enzyme-linked immunosorbent assay. Confirmation of IDO localization in dental pulp tissues was examined using immunohistochemistry. IDO expression in HDPCs was analyzed by immunoblot. IFN-γ significantly up-regulated CXCL10 and IL-6 production in the HDPCs stimulated with ligands for PRRs in a concentration-dependent manner. The expression of IDO was detected in inflamed pulp tissue. In addition, IFN-γ in combination with the PRR ligands enhanced IDO expression in HDPCs compared with IFN-γ alone. Moreover, CXCL10 production in IFN-γ-stimulated HDPCs was inhibited by an IDO inhibitor. This study showed the synergistic effects by IFN-γ on cytokine production and IDO expression in HDPCs, suggesting that IFN-γ may modulate the innate immune response of dental pulp. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.joen.2014.03.018 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25146019 ● Summary page in Scopus @ Elsevier: 2-s2.0-85027943562 (DOI: 10.1016/j.joen.2014.03.018, PubMed: 25146019, Elsevier: Scopus)
7.	Tadashi Nakanishi, Daisuke Takegawa, Kouji Hirao, Kanako Takahashi, Hiromichi Yumoto and Takashi Matsuo : Roles of dental pulp fibroblasts in the recognition of bacterium-related factors and subsequent development of pulpitis, Japanese Dental Science Review, Vol.47, No.2, 161-166, 2011. (Keyword) Toll-like receptor (TLR) / Nucleotide-binding oligomerization domain (NOD) / Dental pulp fibroblast / Cytokine / Pulpitis (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jdsr.2011.02.001 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1360565165959499264 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jdsr.2011.02.001 (DOI: 10.1016/j.jdsr.2011.02.001, CiNii: 1360565165959499264)
8.	Yoshitaka Hosokawa, Ikuko Hosokawa, Satoru Shindo, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Black tea polyphenol inhibits CXCL10 production in oncostatin M-stimulated human gingival fibroblasts., International Immunopharmacology, Vol.11, No.6, 670-674, 2011. (Summary) CXC chemokine ligand 10 (CXCL10) plays an important role in the infiltration of Th1 cells and thus in the exacerbation of periodontal disease. Theaflavin-3,3'-digallate (TFDG), polyphenol in black tea, has some beneficial effects but the effect of TFDG on CXCL10 production from human gingival fibroblasts (HGFs) is uncertain. In this study, we investigated the mechanisms by which TFDG may inhibit oncostatin M (OSM)-induced CXCL10 production in human gingival fibroblasts. TFDG prevented OSM-mediated CXCL10 production by HGFs in a dose dependent manner. TFDG significantly inhibited OSM-induced phosphorylation of c-Jun N terminal kinase (JNK), protein kinase B (Akt) (Ser473) that are related to CXCL10 production from OSM-stimulated HGFs. In addition, TFDG suppressed OSM receptor (OSMR) β expression on HGFs. These data provide a novel mechanism where the black tea flavonoid, theaflavin, could provide direct benefits in periodontal disease. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.intimp.2011.01.009 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21255696 ● Search Scopus @ Elsevier (PMID): 21255696 ● Search Scopus @ Elsevier (DOI): 10.1016/j.intimp.2011.01.009 (DOI: 10.1016/j.intimp.2011.01.009, PubMed: 21255696)
9.	Gilson C. N. Franco, Mikihito Kajiya, Tadashi Nakanishi, Kouji Ohta, Pedro L. Rosalen, Francisco C. Groppo, Cory W. O. Ernst, Janie L. Boyesen, John D. Bartlett, Philip Stashenko, Martin A. Taubman and Toshihisa Kawai : Inhibition of matrix metalloproteinase-9 activity by doxycycline ameliorates RANK ligand-induced osteoclast differentiation in vitro and in vivo., Experimental Cell Research, Vol.317, No.10, 1454-1464, 2011. (Summary) Tetracycline antibiotics, including doxycycli (DOX), have been used to treat bone resorptive diseases, partially because of their activity to suppress osteoclastogenesis induced by receptor activator of nuclear factor kappa B ligand (RANKL). However, their precise inhibitory mechanism remains unclear. Therefore, the present study examined the effect of Dox on osteoclastogenesis signaling induced by RANKL, both in vitro and in vivo. Although Dox inhibited RANKL-induced osteoclastogenesis and down-modulated the mRNA expression of functional osteoclast markers, including tartrate-resistant acid phosphatase (TRAP) and cathepsin K, Dox neither affected RANKL-induced MAPKs phosphorylation nor NFATc1 gene expression in RAW264.7 murine monocytic cells. Gelatin zymography and Western blot analyses showed that Dox down-regulated the enzyme activity of RANKL-induced MMP-9, but without affecting its protein expression. Furthermore, MMP-9 enzyme inhibitor also attenuated both RANKL-induced osteoclastogenesis and up-regulation of TRAP and cathepsin K mRNA expression, indicating that MMP-9 enzyme action is engaged in the promotion of RANKL-induced osteoclastogenesis. Finally, Dox treatment abrogated RANKL-induced osteoclastogenesis and TRAP activity in mouse calvaria along with the suppression of MMP9 enzyme activity, again without affecting the expression of MMP9 protein. These findings suggested that Dox inhibits RANKL-induced osteoclastogenesis by its inhibitory effect on MMP-9 enzyme activity independent of the MAPK-NFATc1 signaling cascade. (Keyword) Acid Phosphatase / Animals / Anti-Bacterial Agents / Blotting, Western / Bone Resorption / Bone and Bones / Cathepsin K / Cell Differentiation / Cells, Cultured / Doxycycline / Isoenzymes / Male / Matrix Metalloproteinase 9 / Mice / Mice, Inbred BALB C / NFATC Transcription Factors / Osteoclasts / Phosphorylation / RANK Ligand / RNA, Messenger / Reverse Transcriptase Polymerase Chain Reaction / Skull (Link to Publication Site) ● Publication site (DOI): 10.1016/j.yexcr.2011.03.014 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21420951 ● Search Scopus @ Elsevier (PMID): 21420951 ● Search Scopus @ Elsevier (DOI): 10.1016/j.yexcr.2011.03.014 (DOI: 10.1016/j.yexcr.2011.03.014, PubMed: 21420951)
10.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Tea polyphenols inhibit IL-6 production in tumor necrosis factor superfamily 14-stimulated human gingival fibroblasts., Molecular Nutrition & Food Research, Vol.54 Suppl 2, S151-8, 2010. (Summary) IL-6 is well recognized to be a potent bone resorptive agent and thus in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins in green tea, and theaflavin-3,3'-digallate (TFDG), polyphenol in black tea, have multiple beneficial effects, but the effects of catechins and theaflavins on IL-6 production in human gingival fibroblasts (HGFs) are not known. In this study, we investigated the mechanisms by which EGCG, ECG, and TFDG inhibit tumor necrosis factor superfamily 14 (TNFSF14)-induced IL-6 production in HGFs. We detected TNFSF14 mRNA expression in human diseased periodontal tissues. TNFSF14 increased IL-6 production in HGFs in a concentration-dependent manner. EGCG, ECG, and TFDG prevented TNFSF14-mediated IL-6 production in HGFs. EGCG, ECG, and TFDG prevented TNFSF14-induced extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and nuclear factor-kappaB activation in HGFs. Inhibitors of ERK, JNK, and nuclear factor-kappaB decreased TNFSF14-induced IL-6 production. In addition, EGCG, ECG, and TFDG attenuated TNFSF14 receptor expression on HGFs. These data provide a novel mechanism through which the green tea and black tea polyphenols could be used to provide direct benefits in periodontal disease. (Link to Publication Site) ● Publication site (DOI): 10.1002/mnfr.200900549 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20461739 ● Search Scopus @ Elsevier (PMID): 20461739 ● Search Scopus @ Elsevier (DOI): 10.1002/mnfr.200900549 (DOI: 10.1002/mnfr.200900549, PubMed: 20461739)
11.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Catechins inhibit CXCL10 production from oncostatin M-stimulated human gingival fibroblasts, The Journal of Nutritional Biochemistry, Vol.21, No.7, 659-664, 2010. (Summary) CXC chemokine ligand 10 (CXCL10) plays a pivotal role in the recruitment of Th1 cells and, thus, in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins derived from green tea, have multiple beneficial effects, but the effects of catechins on CXCL10 production from human gingival fibroblasts (HGFs) is not known. In this study, we investigated the mechanisms by which EGCG and ECG inhibit oncostatin M (OSM)-induced CXCL10 production in HGFs. HGFs constitutively expressed glycoprotein 130 and OSM receptor beta (OSMR beta), which are OSM receptors. OSM increased CXCL10 production in a concentration-dependent manner. EGCG and ECG prevented OSM-mediated CXCL10 production by HGFs. Inhibitors of p38 mitogen-activated protein kinase, c-Jun N-terminal kinase (JNK), phosphatidylinositol-3-OH kinase and signal transducer and activator of transcription (STAT)3 decreased OSM-induced CXCL10 production. EGCG significantly prevented OSM-induced phosphorylation of JNK, Akt (Ser473) and STAT3 (Tyr705 and Ser727). ECG prevented phosphorylation of JNK and Akt (Ser473). In addition, EGCG and ECG attenuated OSMR beta expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids, catechins, can provide direct benefits in periodontal disease. (Keyword) Anti-Inflammatory Agents, Non-Steroidal / Antioxidants / Catechin / Cells, Cultured / Chemokine CXCL10 / Cytokine Receptor gp130 / Enzyme Inhibitors / Fibroblasts / Gene Expression Regulation / Gingiva / Humans / Oncostatin M / Oncostatin M Receptor beta Subunit / Osmolar Concentration / Periodontal Diseases / Phosphorylation / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jnutbio.2009.04.005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19616927 ● Search Scopus @ Elsevier (PMID): 19616927 ● Search Scopus @ Elsevier (DOI): 10.1016/j.jnutbio.2009.04.005 (DOI: 10.1016/j.jnutbio.2009.04.005, PubMed: 19616927)
12.	Kouji Hirao, Hiromichi Yumoto, Tadashi Nakanishi, Kayo Mukai, Kanako Takahashi, Daisuke Takegawa and Takashi Matsuo : Tea catechins reduce inflammatory reactions via mitogen-activated protein kinase pathways in toll-like receptor 2 ligand-stimulated dental pulp cells., Life Sciences, Vol.86, No.17-18, 654-660, 2010. (Summary) These findings suggest that catechins might be useful therapeutically as an anti-inflammatory modulator of dental pulpal inflammation. (Keyword) Anti-Inflammatory Agents / catechin / Cells, Cultured / Dental Pulp / Enzyme-Linked Immunosorbent Assay / Fibroblasts / Humans / Inflammation / Inflammation Mediators / Ligands / Mitogen-Activated Protein Kinases / Phosphorylation / Receptors, Pattern Recognition / Reverse Transcriptase Polymerase Chain Reaction / Signal Transduction / Streptococcus / Tea / Toll-Like Receptor 2 / Up-Regulation (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lfs.2010.02.017 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20176036 ● Search Scopus @ Elsevier (PMID): 20176036 ● Search Scopus @ Elsevier (DOI): 10.1016/j.lfs.2010.02.017 (DOI: 10.1016/j.lfs.2010.02.017, PubMed: 20176036)
13.	Tadashi Nakanishi, Kayo Mukai, Hiromichi Yumoto, Kouji Hirao, Yoshitaka Hosokawa and Takashi Matsuo : Anti-inflammatory effect of catechin on cultured dental pulp cells affected by bacteria-derived factors, European Journal of Oral Sciences, Vol.118, No.2, 145-150, 2010. (Summary) Catechins (bioactive polyphenols in green tea) are known to exhibit potent anti-inflammatory properties. However, the anti-inflammatory effects of catechins on inflamed dental pulp tissue are not known. In this study, we investigated the effect of epigallocatechin-3-gallate (EGCG) and epicatechin gallate (ECG), the major components of green tea catechins, on the expression of pro-inflammatory cytokines and adhesion molecules in human dental pulp cells stimulated with bacteria-derived factors such as lipopolysaccharide (LPS) and peptidoglycan (PG). The expression of interleukin (IL)-6 and of IL-8 was examined using the reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assays. The expression of intercellular adhesion molecule-1 (ICAM-1) and of vascular cell adhesion molecule-1 (VCAM-1) on dental pulp cells was analyzed using flow cytometry. The presence of EGCG and ECG significantly reduced, in a concentration-dependent manner, the expression of IL-6 and IL-8 in dental pulp cells exposed to LPS or PG. Increased expression of ICAM-1 and VCAM-1 on the dental pulp cells in response to bacterial components was also decreased by treatment with EGCG and ECG. These findings suggest that green tea catechins may prevent the exacerbation of pulpitis. (Keyword) Anti-Inflammatory Agents / Antioxidants / Catechin / Cells, Cultured / Dental Pulp / Escherichia coli / Flow Cytometry / Humans / Intercellular Adhesion Molecule-1 / Interleukin-6 / Interleukin-8 / Lipopolysaccharides / Peptidoglycan / Reverse Transcriptase Polymerase Chain Reaction / Staphylococcus aureus / Time Factors / Vascular Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1600-0722.2010.00714.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 20487003 ● Search Scopus @ Elsevier (PMID): 20487003 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1600-0722.2010.00714.x (DOI: 10.1111/j.1600-0722.2010.00714.x, PubMed: 20487003)
14.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Catechins Inhibit CCL20 Production in IL-17A-stimulated Human Gingival Fibroblasts, Cellular Physiology and Biochemistry, Vol.24, No.5-6, 391-396, 2009. (Summary) CC chemokine ligand 20 (CCL20) plays a pivotal role in the recruitment of Th17 cells and thus in the development of periodontal disease. Epigallocatechin gallate (EGCG) and epicatechin gallate (ECG), the major catechins in green tea, have multiple beneficial effects, but the effects of catechins on CCL20 production in human gingival fibroblasts (HGFs) are not known. In this study, we investigated the mechanisms by which EGCG and ECG inhibit interleukin (IL)-17A-induced CCL20 production in human gingival fibroblasts. IL-17A increased CCL20 production in HGFs in a concentration-dependent manner. EGCG and ECG prevented IL-17A-mediated CCL20 production in HGFs. Inhibitors of p38 mitogen-activated protein kinase (MAPK) or extracellular signal-regulated kinase (ERK) decreased IL-17A-induced CCL20 production. EGCG and ECG prevented IL-17A-induced phosphorylation of p38 MAPK and ERK in HGFs. In addition, EGCG and ECG attenuated IL-17 receptor expression on HGFs. These data provide a novel mechanism through which the green tea flavonoids catechins could be used to provide direct benefits in periodontal disease. (Keyword) Antioxidants / Catechin / Cells, Cultured / Chemokine CCL20 / Extracellular Signal-Regulated MAP Kinases / Fibroblasts / Gingiva / Humans / Interleukin-17 / Phosphorylation / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1159/000257431 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19910679 ● Search Scopus @ Elsevier (PMID): 19910679 ● Search Scopus @ Elsevier (DOI): 10.1159/000257431 (DOI: 10.1159/000257431, PubMed: 19910679)
15.	Kouji Hirao, Hiromichi Yumoto, Kanako Takahashi, Kayo Mukai, Tadashi Nakanishi and Takashi Matsuo : Roles of TLR2, TLR4, NOD2, and NOD1 in pulp fibroblasts., Journal of Dental Research, Vol.88, No.8, 762-767, 2009. (Summary) Pulp fibroblasts express various pro-inflammatory mediators leading to marked infiltration of inflammatory cells in the progression of pulpitis. We hypothesized that pulp fibroblasts play roles in the recognition of invaded caries-related bacteria and the subsequent innate immune responses. We found clear expressions of TLR2, NOD1, and NOD2 and a faint expression of TLR4 in human dental pulp fibroblasts (HDPF) by RT-PCR and flow cytometry. We also observed that various pro-inflammatory mediators, including cytokines, chemokines, adhesion molecules, prostaglandin E(2) and its key enzyme COX-2, not iNOS or caspase-1, were markedly up-regulated by stimulation with these TLR and NOD agonists. More over, the NOD2 agonist acted synergistically with the TLR2, not the TLR4, agonist to stimulate the production of pro-inflammatory mediators in HDPF. These findings indicate that TLR2, TLR4, NOD2, and NOD1 in HDPF are functional receptors, and NOD2 is a modulator of signals transmitted through TLR2 in pulpal immune responses, leading to progressive pulpitis. (Keyword) Acetylmuramyl-Alanyl-Isoglutamine / Apoptosis / Cells, Cultured / Chemokine CCL2 / Chemokine CXCL10 / Cyclooxygenase 2 / Dental Pulp / Diaminopimelic Acid / Dinoprostone / Escherichia coli / Fibroblasts / Humans / Inflammation Mediators / Interleukin-6 / Interleukin-8 / Lipopeptides / Lipopolysaccharides / Nod1 Signaling Adaptor Protein / Nod2 Signaling Adaptor Protein / Pulpitis / Signal Transduction / Streptococcus mutans / Toll-Like Receptor 2 / Toll-Like Receptor 4 / Vascular Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1177/0022034509341779 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19734466 ● Search Scopus @ Elsevier (PMID): 19734466 ● Search Scopus @ Elsevier (DOI): 10.1177/0022034509341779 (DOI: 10.1177/0022034509341779, PubMed: 19734466)
16.	Kanako Takahashi, Tadashi Nakanishi, Hiromichi Yumoto, Tomohiko Adachi and Takashi Matsuo : CCL20 production is induced in human dental pulp upon stimulation by Streptococcus mutans and pro-inflammatory cytokines, Oral Microbiology and Immunology, Vol.23, No.4, 320-327, 2008. (Summary) Pulpitis is characterized by the marked infiltration of inflammatory cells in response to an invasion of caries-related bacteria. It is well known that chemokines regulate the trafficking of lymphocytes, and CC chemokine ligand 20 (CCL20) has been recently shown to play a crucial role in the recruitment of memory T cells and immature dendritic cells into inflammatory lesions. We previously reported that CCL20 was mainly expressed in microvascular endothelial cells and macrophages that accumulated in inflamed pulp tissues and that its specific receptor, CCR6, was expressed on infiltrated lymphocytes. However, the mechanism of CCL20 expression remains unclear. In this study, we investigated the expression of CCL20 in monocytes/macrophages, endothelial cells, and pulpal fibroblasts after stimulation with Streptococcus mutans, a representative of caries-related bacteria, or proinflammatory cytokines. CCL20 messenger RNA was detected by reverse transcription-polymerase chain reaction in inflamed pulp, but not in clinically normal pulp. By enzyme-linked immunosorbent assay, S. mutans induced a human monocytic cell line, differentiated macrophage-like THP-1 cells, and human umbilical vein endothelial cells (HUVEC) to produce an increased amount of CCL20. Lipoteichoic acid from S. mutans also elicited CCL20 production by HUVEC. Moreover, CCL20 production from pulpal fibroblasts was increased by stimulation with inetrleukin-1beta and tumor necrosis factor-alpha. Our results indicate that CCL20 expression is induced by stimulation with caries-related bacteria that have invaded deeply into the dentinal tubules as well as by proinflammatory cytokines in the inflamed pulpal lesions. It may be involved in the progression of pulpitis via accumulation of inflammatory cells. (Keyword) Adult / Aged / Cell Differentiation / Cell Line / Cells, Cultured / Chemokine CCL20 / Cytokines / Dental Pulp / Endothelial Cells / Endothelium, Vascular / Female / Fibroblasts / Humans / Inflammation Mediators / Intercellular Adhesion Molecule-1 / Interleukin-1beta / Interleukin-8 / Lipopolysaccharides / Macrophages / Male / Middle Aged / Monocytes / Pulpitis / Streptococcus mutans / Teichoic Acids / Tumor Necrosis Factor-alpha / Vascular Cell Adhesion Molecule-1 (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1399-302X.2008.00431.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18582332 ● Search Scopus @ Elsevier (PMID): 18582332 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1399-302X.2008.00431.x (DOI: 10.1111/j.1399-302X.2008.00431.x, PubMed: 18582332)
17.	Tomohiko Adachi, Tadashi Nakanishi, Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Kayo Mukai, Hideaki Nakae and Takashi Matsuo : Caries-related bacteria and cytokines induce CXCL10 in dental pulp., Journal of Dental Research, Vol.86, No.12, 1217-1222, 2007. (Summary) Marked infiltration of inflammatory cells, such as activated T-cells, is observed in the progression of pulpitis; however, little is known about the mechanism of their recruitment into pulpal lesions. It has been recently demonstrated that CXC chemokine ligand 10 (CXCL10) chemoattracts CXC chemokine receptor 3 (CXCR3)-positive activated T-cells. We therefore examined whether CXCL10 is involved in the pathogenesis of pulpitis. CXCL10 mRNA expression levels in clinically inflamed dental pulp were higher than those in healthy dental pulp. Immunostaining results revealed that CXCL10 was detected in macrophages, endothelial cells, and fibroblasts in inflamed dental pulp, and that CXCR3 expression was observed mainly on T-cells. Moreover, cultured dental pulp fibroblasts produced CXCL10 after stimulation with live caries-related bacteria, peptidoglycans, and pro-inflammatory cytokines. In contrast, heat-killed bacteria did not induce CXCL10 secretion. These findings suggest that CXCL10-CXCR3 may play an important role in the pulpal immune response to caries-related bacterial invasion. Abbreviations: CXCL10, CXC chemokine ligand 10; CXCR3, CXC chemokine receptor 3; IFN, interferon; FBS, fetal bovine serum; LTA, lipoteichoic acid; PGN, peptidoglycan; IL, interleukin; TNF, tumor necrosis factor; PBS, phosphate-buffered saline; ELISA, enzyme-linked immunosorbent assay; CCL, C-C chemokine ligand; TLR, Toll-like receptor; NOD, nucleotide oligomerization domain; HDPF, human dental pulp fibroblasts. (Keyword) Adult / Bacteroides / Chemokine CXCL10 / Dental Caries / Dental Pulp / Fibroblasts / Humans / Immunohistochemistry / Lymphocyte Subsets / Middle Aged / RNA, Messenger / Receptors, CXCR3 (Link to Publication Site) ● Publication site (DOI): 10.1177/154405910708601215 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18037659 ● Search Scopus @ Elsevier (PMID): 18037659 ● Search Scopus @ Elsevier (DOI): 10.1177/154405910708601215 (DOI: 10.1177/154405910708601215, PubMed: 18037659)
18.	Cory W. Ernst, Jang Eun Lee, Tadashi Nakanishi, Nadeem Y. Karimbux, Taia M. Rezende, Philip Stashenko, Makoto Seki, Martin A Taubman and Toshihisa Kawai : Diminished forkhead box P3/CD25 double-positive T regulatory cells are associated with the increased nuclear factor-kB ligand (RANKL(+)) T cells in bone resorption lesion of periodontal disease, Clinical and Experimental Immunology, Vol.148, No.2, 271-280, 2007. (Summary) Periodontal disease involves multi-bacterial infections accompanied by inflammatory bone resorption lesions. The abundant T and B lymphocyte infiltrates are the major sources of the osteoclast differentiation factor, receptor activator for nuclear factor-kappaB ligand (RANKL) which, in turn, contributes to the development of bone resorption in periodontal disease. In the present study, we found that the concentrations of RANKL and regulatory T cell (T(reg))-associated cytokine, interleukin (IL)-10, in the periodontal tissue homogenates were correlated negatively, whereas RANKL and proinflammatory cytokine, IL-1beta, showed positive correlation. Also, according to the fluorescent-immunohistochemistry, the frequency of forkhead box P3 (FoxP3)/CD25 double-positive cells was diminished strikingly in the bone resorption lesion of periodontal disease compared to healthy gingival tissue, while CD25 or FoxP3 single positive cells were still observed in lesions where abundant RANKL+ lymphocytes were present. Very importantly, few or no expressions of FoxP3 by the RANKL+ lymphocytes were observed in the diseased periodontal tissues. Finally, IL-10 suppressed both soluble RANKL (sRANKL) and membrane RANKL (mRANKL) expression by peripheral blood mononuclear cells (PBMC) activated in vitro in a bacterial antigen-specific manner. Taken together, these results suggested that FoxP3/CD25 double-positive T(reg) cells may play a role in the down-regulation of RANKL expression by activated lymphocytes in periodontal diseased tissues. This leads to the conclusion that the phenomenon of diminished CD25+FoxP3+ T(reg) cells appears to be associated with the increased RANKL+ T cells in the bone resorption lesion of periodontal disease. (Keyword) FoxP3 / periodontal/oral immunology / RANKL / T cells / Treg cells (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2249.2006.03318.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 17355249 ● Search Scopus @ Elsevier (PMID): 17355249 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2006.03318.x (DOI: 10.1111/j.1365-2249.2006.03318.x, PubMed: 17355249)
19.	Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Hideaki Nakae and Takashi Matsuo : Expression of fractalkine (CX3CL1) and its receptor, CX3CR1, in periodontal diseased tissue, Clinical and Experimental Immunology, Vol.139, No.3, 506-512, 2005. (Summary) The regulatory role of chemokines and chemokine receptors on specific leucocyte recruitment into periodontal diseased tissue is poorly characterized. We observed that leucocytes infiltrating inflamed gingival tissue expressed marked levels of CX3CR1. In periodontal diseased tissue, the expression of fractalkine and CX3CR1 mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR) and further, fractalkine was distributed mainly on endothelial cells, as shown by immunohistochemistry. Moreover, we can detect CX3CR1-expressing cells infiltrated in periodontal diseased tissue by immunohistochemical staining. Furthermore, fractalkine production by human umbilical vein endothelial cells (HUVEC) was up-regulated by pathogen-associated molecular patterns (PAMPs), including Porphyromonas gingivalis lipopolysaccharide (LPS). Thus, these findings suggested that CX3CR1 and the corresponding chemokine, fractalkine may have an important regulatory role on specific leucocyte migration into inflamed periodontal tissue. (Keyword) CX3CR1 / fractalkine / periodontal disease (Link to Publication Site) ● Publication site (DOI): 10.1111/j.1365-2249.2005.02675.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15730397 ● Search Scopus @ Elsevier (PMID): 15730397 ● Search Scopus @ Elsevier (DOI): 10.1111/j.1365-2249.2005.02675.x (DOI: 10.1111/j.1365-2249.2005.02675.x, PubMed: 15730397)
20.	Tadashi Nakanishi, Kanako Takahashi, Yoshitaka Hosokawa, Tomohiko Adachi, Hideaki Nakae and Takashi Matsuo : Expression of macrophage inflammatory protein 3alpha in human inflamed dental pulp tissue, Journal of Endodontics, Vol.31, No.2, 84-87, 2005. (Summary) Severe pulpitis resulting from dental caries is characterized by marked inflammatory infiltrate such as lymphocytes. Little is known about the recruitment of these cells into the dental pulp lesions of carious teeth. Macrophage inflammatory protein-3alpha (MIP-3alpha), a CC chemokine attracts CC chemokine receptor 6 (CCR6)-expressing T cells. We examined the distribution of MIP-3alpha-positive and/or CCR6-positive cells in human inflamed and normal dental pulp by immunohistochemistry. MIP-3alpha was observed in all inflamed pulp sections, and was mostly distributed in macrophages that had accumulated in the area adjacent to carious lesions. Furthermore, CCR6 expression was also observed in the infiltrating lymphocytes. In contrast, MIP-3alpha and CCR6 were rarely detected in normal pulp. These findings suggest that MIP-3alpha plays a role in the advancement of pulpal inflammation via the recruitment of CCR6-expressing lymphocytes. (Keyword) Adult / Case-Control Studies / Chemokine CCL20 / Chemokines, CC / Chemotaxis, Leukocyte / Dental Caries / Humans / Immunohistochemistry / Macrophage Inflammatory Proteins / Middle Aged / Pulpitis / Receptors, CCR6 / Receptors, Chemokine / T-Lymphocytes (Link to Publication Site) ● Publication site (DOI): 10.1097/01.don.0000143414.22112.57 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15671814 ● Search Scopus @ Elsevier (PMID): 15671814 ● Search Scopus @ Elsevier (DOI): 10.1097/01.don.0000143414.22112.57 (DOI: 10.1097/01.don.0000143414.22112.57, PubMed: 15671814)
21.	Takashi Matsuo, Toshiyuki Shirakami, Kazumi Ozaki, Tadashi Nakanishi, Hiromichi Yumoto and Shigeyuki Ebisu : An immunohistological study of the localization of bacteria invading root pulpal walls of teeth with periapical lesions, Journal of Endodontics, Vol.29, No.3, 194-200, 2003. (Summary) We immunohistologically examined the prevalence and localization of bacteria invading dentinal tubules of the roots of teeth with infected canals. Forty extracted teeth with apical lesions were selected and divided into two groups: a group of untreated teeth and a group of canal-enlarged teeth. The bacteria in the specimens were detected by Brown-Brenn stain and the labeled-streptavidin-biotin method with specific antisera for 16-bacteria. Seventy percent of the examined teeth showed bacteria invading the dentinal tubules of the roots. Fusobacterium nucleatum, Eubacterium alactolyticum, E. nodatum, Lactobacillus casei, and Peptostreptococcus micros were abundant. Even in the canal-enlarged group, invasion of bacteria was observed in 65% of teeth. This study revealed the actual condition of bacteria in infected root dentin and suggested that the canal-enlargement procedure could not completely remove all the bacteria in the infected dentinal tubules of the root. (Keyword) Adult / Aged / Bacteria / Coloring Agents / Dental Pulp / Dentin / Eubacterium / Fusobacterium nucleatum / Humans / Immune Sera / Immunoenzyme Techniques / Immunohistochemistry / Lactobacillus casei / Middle Aged / Peptostreptococcus / Periapical Diseases / Porphyromonas / Prevotella / Root Canal Preparation / Statistics, Nonparametric / Tooth Root (Link to Publication Site) ● Publication site (DOI): 10.1097/00004770-200303000-00008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12669880 ● Search Scopus @ Elsevier (PMID): 12669880 ● Search Scopus @ Elsevier (DOI): 10.1097/00004770-200303000-00008 (DOI: 10.1097/00004770-200303000-00008, PubMed: 12669880)
22.	Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Kanako Takahashi, Hiromichi Yumoto, Kazumi Ozaki and Takashi Matsuo : Macrophage Inflammatory Protein 3α-CC chemokine receptor 6 interactions play an important role in CD4⁺ T-cell accumulation in periodontal diseased tissue., Clinical and Experimental Immunology, Vol.128, No.3, 548-554, 2002. (Summary) The regulatory role of chemokines and chemokine receptors on specific lymphocyte recruitment into periodontal diseased tissue is poorly characterized. We observed that lymphocytes infiltrating inflamed gingival tissue expressed marked levels of CCR6. In periodontal diseased tissue, the expression of MIP-3alpha mRNA was detected by RT-PCR and further, MIP-3alpha was distributed in the basal layer of gingival epithelial cells, microvascular endothelial cells and the areas of inflammatory cells as shown by immunohistochemistry. Moreover, CCR6-expressing cells infiltrated into periodontal diseased tissue, and the proportion of CCR6-positive CD4+ T cells was significantly elevated in periodontal diseased tissue compared with peripheral blood in the same patients. Furthermore, gingival lymphocytes isolated from patients showed migration toward MIP-3alpha in an in vitro chemotaxis assay in which migration was abrogated by specific antibody to CCR6. Thus, these findings suggested that CCR6 and the corresponding chemokine, MIP-3alpha may have an important regulatory role in specific lymphocyte migration into inflamed periodontal tissue. (Keyword) CCR6 / MIP-3 alpha / periodontal disease / MONOCYTE CHEMOATTRACTANT PROTEIN-1 / INFLAMED HUMAN GINGIVA / IMMUNOHISTOLOGICAL ANALYSIS / SELECTIVE RECRUITMENT / INDUCIBLE EXPRESSION / BACTERIA / IMMUNITY / HEALTHY / LESIONS / SUBSETS (Link to Publication Site) ● Publication site (DOI): 10.1046/j.1365-2249.2002.01865.x (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12067311 ● Search Scopus @ Elsevier (PMID): 12067311 ● Search Scopus @ Elsevier (DOI): 10.1046/j.1365-2249.2002.01865.x (DOI: 10.1046/j.1365-2249.2002.01865.x, PubMed: 12067311)
23.	Tadashi Nakanishi, Hirotoshi Shimizu, Yoshitaka Hosokawa and Takashi Matsuo : An immunohistological study on cyclooxygenase-2 in human dental pulp., Journal of Endodontics, Vol.27, No.6, 385-388, 2001. (Summary) Characteristics of cyclooxygenase-2 (COX-2) expressing cells in human dental pulp were immunohistologically studied. Extirpated pulpal tissues from extracted teeth were examined to elucidate the localization and distribution of COX-2. Pulpal tissues were examined by the labeled streptavidin biotin method using specific mouse monoclonal antibodies for COX-2. Cell types of the COX-2 expressing cells were also investigated by the double stain technique using both monoclonal antibodies for CD68/macrophage and anti-COX-2. COX-2 expressing cells could be found in all of the inflamed pulps, and these cells were mostly distributed close to the area of accumulation of inflammatory cells. COX-2 was mainly expressed in fibroblasts rather than macrophages. In contrast, COX-2 expressing cells were scarcely found in the normal pulps. These findings indicate that pulpal fibroblasts, as well as macrophages, may participate in the production of prostaglandin through COX-2 expression in pulpal inflammation, and might be involved in the pathogenesis of irreversible pulpitis. (Keyword) Adult / Antibodies, Monoclonal / Antigens, CD / Antigens, Differentiation, Myelomonocytic / Coloring Agents / Cyclooxygenase 2 / Dental Pulp / Fibroblasts / Fluorescent Dyes / Humans / Immunoenzyme Techniques / Immunohistochemistry / Isoenzymes / Macrophages / Membrane Proteins / Middle Aged / Peroxidases / Prostaglandin-Endoperoxide Synthases / Prostaglandins / Pulpitis (Link to Publication Site) ● Publication site (DOI): 10.1097/00004770-200106000-00003 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11487130 ● Search Scopus @ Elsevier (PMID): 11487130 ● Search Scopus @ Elsevier (DOI): 10.1097/00004770-200106000-00003 (DOI: 10.1097/00004770-200106000-00003, PubMed: 11487130)
24.	Takashi Matsuo, Tadashi Nakanishi, Hirotoshi Shimizu and Shigeyuki Ebisu : A clinical study of direct pulp capping applied to carious-exposed pulps, Journal of Endodontics, Vol.22, No.10, 551-556, 1996.
25.	Takashi Matsuo, Tadashi Nakanishi and Shigeyuki Ebisu : Immunoglobulins in periapical exudates of infected root canals: correlations with the clinical findings of the involved teeth, Endodontics & dental traumatology, Vol.11, No.2, 95-99, 1995.
26.	Tadashi Nakanishi, Takashi Matsuo and Shigeyuki Ebisu : Quantitative analysis of immunoglobulins and inflammatory factors in human pulpal blood from exposed pulps, Journal of Endodontics, Vol.21, No.3, 131-136, 1995.
27.	Takashi Matsuo, Shigeyuki Ebisu, Tadashi Nakanishi, Kouki Yonemura, Yasushi Harada and Hiroshi Okada : Interleukin-1 alpha and interleukin-1 beta periapical exudates of infected root canals: correlations with the clinical findings of the involved teeth, Journal of Endodontics, Vol.20, No.9, 432-435, 1994.
28.	Tadashi Nakanishi, Takashi Matsuo, 多川知里, 白神俊之 and Shigeyuki Ebisu : Diagnosis of Pulpitis Using Pulpal Blood, --- Establishment of the Method for Collection of Pulpal Blood ---, The Japanese Journal of Conservative Dentistry, Vol.36, No.5, 1404-1409, 1993. (Keyword) 歯髄炎 / 診断 / 歯髄血液
29.	Masahiro Yoshiyama, Kazumi Ozaki, Yuichiro Noiri, Kenya Kataoka, Tadashi Nakanishi, Reiko Ogimoto, Hideaki Nakae, Takashi Matsuo and Shigeyuki Ebisu : Treatment of Dentin Hypersensitivity-Effect of a Light-curing Resin Liner on Tubule Occlusion-, The Japanese Journal of Conservative Dentistry, Vol.34, No.1, 76-81, 1991. (Keyword) 象牙質知覚過敏症 / 象牙細管封鎖 / 光重合型レジンランナー
30.	yuichiro Noiri, Kazumi Ozaki, Tadashi Nakanishi, Kenya Ktaoka, Ichiro Amano and Masahiro Yoshiyama : Study on Adhesive Properties of Restorative Materials to Human Root Dentin, --- 1.Adhesive Properties of Resin Cement Used for Composite Resin Inlay Restoration to Human Coronal and Root Debtin ---, The Japanese Journal of Conservative Dentistry, Vol.33, No.3, 639-647, 1990. (Keyword) 歯根部象牙質 / 接着性 / レジセメント

Academic Paper (Unrefereed Paper):

1.	Takashi Matsuo, Tadashi Nakanishi, Hiromichi Yumoto, Kouji Hirao, Chihiro Shinohara and Toshihiko Tominaga : Conception of Infected Root Canal Treatment, Journal of Oral Health and Biosciences, Vol.28, No.2, 87-92, 2016. (Summary) It is a well-established fact that bacterial infection of the dental pulp ultimately results in the formation of apical periodontitis. And apical periodontitis may develop periapical leisons consisting granulomas and cysts. In this article, we show the pathologic condition of infected root canal systems and periapical lesions immunohistologically. We also describe the possible causes of refractory apical periodontitis that conventional root canal therapy could not work effectively. Finally,we explain our newly developing treatment for refractory apical periodontitis named electro-magnetic apical treatment, and illustrate clinical efficacy of this treatment. (Keyword) infected root canal treatment / refractory apical periodontitis / pathological condition (Tokushima University Institutional Repository) ● Metadata: 109873 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050845762395157248 (Tokushima University Institutional Repository: 109873, CiNii: 1050845762395157248)

Review, Commentary:

1.	Daisuke Takegawa, Kazuhide Yonekura, Hitomi Kuramoto, Yumika Ida, Yuki Hosokawa, Ikuko Hosokawa, Yoshitaka Hosokawa, Toshiyuki Suge, Tadashi Nakanishi and Keiichi Hosaka : Clinical Key Points of Class II Direct Composite Restoration, Journal of Oral Health and Biosciences, Vol.36, No.1, 8-12, Sep. 2023. (Keyword) dental care (Tokushima University Institutional Repository) ● Metadata: 118637 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050579289345785472 (Tokushima University Institutional Repository: 118637, CiNii: 1050579289345785472)
2.	Hitomi Kuramoto and Tadashi Nakanishi : Possibility of applying caffeic acid phenethyl ester to the treatment of pulpitis, Medical Science Digest, Vol.48, No.11, 48-49, Oct. 2022. (Keyword) pulpitis / caffeic acid phenethyl ester / vascular endothelial growth factor / anti-inflammatory effect / vital pulp therapy
3.	Takashi Matsuo and Tadashi Nakanishi : 深在性う蝕への対応と歯髄の免疫応答, The Japanese Journal of Conservative Dentistry, Vol.62, No.1, 1-7, Feb. 2019. (Keyword) 深在性う蝕 / pulpitis / 免疫応答 (Link to Publication Site) ● Publication site (DOI): 10.11471/shikahozon.62.1 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.11471/shikahozon.62.1 (DOI: 10.11471/shikahozon.62.1)
4.	Hiromichi Yumoto, Kouji Hirao, Yuki Hosokawa, Hitomi Kuramoto, Daisuke Takegawa, Tadashi Nakanishi and Takashi Matsuo : The Roles of Odontoblasts in Dental Pulp Innate Immunity, Japanese Dental Science Review, Vol.54, No.3, 105-117, Aug. 2018. (Summary) Odontoblasts located in the outermost layer of dental pulp form a natural barrier between mineralized tissues, dentin, and soft tissues, dental pulp, of the vital tooth, and they first recognize caries-related pathogens and sense external irritations. Therefore, odontoblasts possess a specialized innate immune system to fight oral pathogens invading into dentin. Generally, the rapid initial sensing of microbial pathogens, especially pathogen-associated molecular patterns (PAMPs) shared by microorganisms, are mediated by pattern recognition receptors (PRRs), such as Toll-like receptor and the nucleotide-binding oligomerization domain (NOD). The innate immune responses in odontoblasts initiated by sensing oral pathogens provide host protective events, such as inflammatory reactions, to produce a variety of pro-inflammatory mediators, including chemokines and cytokines. These attract various inflammatory cells and cause antibacterial reactions, such as the production of defensins, to kill microorganisms in the proximal region of the odontoblast layer. This review focuses on innate immunity, especially cellular and molecular mechanisms regarding the sensing of PAMPs from oral pathogens by PRRs, in odontoblasts and provides information for future studies for the development of novel therapeutic strategies, including diagnosis and treatment, to prevent exceeding dental pulp inflammation and preserve the dental pulp tissues. (Tokushima University Institutional Repository) ● Metadata: 112960 (Link to Publication Site) ● Publication site (DOI): 10.1016/j.jdsr.2018.03.001 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 30128058 ● Summary page in Scopus @ Elsevier: 2-s2.0-85044379499 (Tokushima University Institutional Repository: 112960, DOI: 10.1016/j.jdsr.2018.03.001, PubMed: 30128058, Elsevier: Scopus)
5.	Tadashi Nakanishi and Takashi Matsuo : 感染根管における細菌感染の実態, The Nippon Dental Review, Vol.77, No.11, 45-58, Nov. 2017.
6.	Takashi Matsuo and Tadashi Nakanishi : 歯髄炎の病態形成における細菌侵襲と歯髄の反応性, The Nippon Dental Review, Vol.73, No.6, 9-11, Jun. 2013. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1524232504494800512 (CiNii: 1524232504494800512)
7.	Takashi Matsuo, Kazumi Ozaki, Tadashi Nakanishi, Hiromichi Yumoto, Kanako Takahashi, Kouji Hirao and Daisuke Takegawa : Pulp pathosis and its diagnosis, The Journal of Japan Endodontic Association, Vol.34, No.2, 67-76, May 2013. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680166022016 (CiNii: 1390282680166022016)
8.	Tadashi Nakanishi : 歯髄炎の病態形成における細菌侵襲と歯髄の反応性, The Japanese Journal of Conservative Dentistry, Vol.53, No.5, 489-491, Oct. 2010.
9.	Takashi Matsuo and Tadashi Nakanishi : Pharmacologic Control of Dental Pain, the Quintessence, Vol.22, No.6, 147-161, Jun. 2003. (Keyword) 歯痛 / 薬剤 / 象牙質知覚過敏 / 歯髄炎
10.	Yoshitaka Hosokawa, Tadashi Nakanishi and Takashi Matsuo : Expresion of Chemokines in periodontitis, Clinical Immunology, Vol.38, No.2, 151-156, Feb. 2002.
11.	Tadashi Nakanishi, Kanako Takahashi, Yoshitaka Hosokawa, Kazumi Ozaki and Takashi Matsuo : Bacterial irritation and pulpal response in pulpitis, Shikoku Dental Research, Vol.14, No.2, 255-263, 2002. (Keyword) 歯髄炎 / う蝕関連細菌 / 免疫担当細胞 / プロスタグランディン / cytokine
12.	Takashi Matsuo, Tadashi Nakanishi and Keiko Fujinaka : Pathology of Apical Periodontitis Refractory to endod, 現代の根管治療の診断科学, 91-97, 1999.

Proceeding of International Conference:

1.	Tadashi Nakanishi : Dental Pulp Responses to Dental Caries, Dentisphere 4; International Scientific Meeting 5th ASEAN Plus Tokushima Joint International Conference, Nov. 2019.
2.	Yuki Hosokawa, Hiromichi Yumoto, Kouji Hirao, Hitomi Kuramoto, Tadashi Nakanishi, Daisuke Takegawa and Takashi Matsuo : Anti-inflammatory effects of polyphenols on rat odontoblastic cells, 95th General Session & Exhibition of the International Association for Dental Research (San Francisco), Mar. 2017.
3.	Daisuke Takegawa, Tadashi Nakanishi, Kouji Hirao, Hiromichi Yumoto, Yuki Hosokawa and Takashi Matsuo : Interferon-gamma modulates the innate immune response in odontoblast-like cells, 95th General session and exhibition of the IADR, Mar. 2017.
4.	Tadashi Nakanishi, Daisuke Takegawa, Kouji Hirao, Hiromichi Yumoto, Yuki Hosokawa and Takashi Matsuo : Effect of interleukin-17A on CCL20 production from odontoblast-like cells, 95th General session and exhibition of the IADR, Mar. 2017.
5.	Tadashi Nakanishi, Daisuke Takegawa, Hiromichi Yumoto, Kouji Hirao and Takashi Matsuo : Interleukin-17 Regulates Inflammatory Mediator Expression in IL-1beta-stimulated Dental Pulp Cells, 93th General Session & Exhibition of the International Association for Dental Research, Boston (USA), Mar. 2015.
6.	Tadashi Nakanishi, Daisuke Takegawa, Kouji Hirao, Hiromichi Yumoto, Kanako Takahashi and Takashi Matsuo : Prostaglandin F2a Regulates Cytokine Expression in Dental Pulp Cells, 91th General Session & Exhibition of the IADR, Seattle, USA, Mar. 2013.
7.	Daisuke Takegawa, Tadashi Nakanishi, Kouji Hirao, Hiromichi Yumoto, Kanako Takahashi and Takashi Matsuo : Interferon-g modulates the innate immune response of dental pulp cells, 91th General Session & Exhibition of the IADR, Seattle, USA, Mar. 2013.
8.	Tadashi Nakanishi, Kouji Hirao, Takegawa Daisuke, Hiromichi Yumoto, Kanako Takahashi and Takashi Matsuo : Catechins suppress cyclooxygenase-2 expression in human dental pulp cells, 88th General Session and Exhibition of the IADR, Jul. 2010.
9.	Takegawa Daisuke, Tadashi Nakanishi, Kouji Hirao, Hiromichi Yumoto, Kanako Takahashi and Takashi Matsuo : Interferon-gamma enhances toll-like receptor ligand-induced cytokine production in pulpal cells, 88th General Session and Exhibition of the IADR, Jul. 2010.
10.	Kayo Mukai, Tadashi Nakanishi, Hiromichi Yumoto, Kanako Takahashi, Kouji Hirao and Takashi Matsuo : Effects of Catechins on Cytokine Production in Human Odontoblast-like Cells, 86th General Session and Exhibition of the International Association for Dental Research, Jul. 2008.
11.	Kouji Hirao, Hiromichi Yumoto, Tadashi Nakanishi, Kanako Takahashi, Kayo Mukai, Miho Yoneda and Takashi Matsuo : Functional Analysis of Pattern Recognition Receptor Expression in Pulpal Cells, 86th General Session and Exhibition of the International Association for Dental Research, Jul. 2008.
12.	Kayo Mukai, Tadashi Nakanishi, Yoshitaka Hosokawa, Kanako Takahashi and Takashi Matsuo : Inhibitory effects of catechins on inflammatory reactions in pulp fibroblasts, 84th General Session & Exhibition of the IADR, Brisbane, Jun. 2006.
13.	Tadashi Nakanishi, Jean Eastcott, Martin A Taubman and Toshihisa Kawai : Characteristics of regulatory dendritic cells induced by gingival epithelial cells, 35th Annual Meeting & Exhibition of the AADR, Orlando, Mar. 2006.
14.	Tadashi Nakanishi, Jean Eastcott, Martin A Taubman and Toshihisa Kawai : Induction of regulatory dendritic cells by gingival epithelial cells, 83rd General session of IADR (International Association for Dental Research), Baltimore, Mar. 2005.
15.	Tadashi Nakanishi, Tomohiko Adachi, Kanako Takahashi and Takashi Matsuo : Expression of interferon-gamma -inducible protein 10/CXCL10 in inflamed dental pulp, 82th General Session of the IADR(INternational Association of Dental Research), Honolulu, Mar. 2004.
16.	Kanako Takahashi, Tadashi Nakanishi, Tomohiko Adachi, Natsuko Ida, Hideaki Nakae and Takashi Matsuo : Effects of Streptococcus mutans on MIP-3 α production by macrophages, 82th General Session of the IADR(INternational Association of Dental Research), Honolulu, Mar. 2004.
17.	Daisuke Yamaguchi, Tadashi Nakanishi, Kanako Takahashi, Hideaki Nakae and Takashi Matsuo : Expression of macrophage inflammatory protein-3alpha/CCL20 in human gingival epithelial cells, 81th General Session of the IADR(INternational Association of Dental Research), エルサレム, Jun. 2003.
18.	Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Hiromichi Yumoto and Takashi Matsuo : LARC-CCR6 Interactions play an important role in CD4+ T cell accumulation in periodontal diseased tissue, 80th General Session and Exhibition of the International Association for Dental Research, San Diego(USA), Mar. 2002.
19.	Tadashi Nakanishi, Kanako Takahashi, Yoshitaka Hosokawa, Daisuke Yamaguchi, Chihiro Shinohara, Hiromichi Yumoto and Takashi Matsuo : Expression of macrophage inflammatory protein-3 α in human pulpitis, 80th General SEssion ofthe IADR(International Association of Dental Research), San Diego(USA), Mar. 2002.
20.	Tadashi Nakanishi, Kanako Takahashi, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : An immunohistological study on the localization of selected bacteria and chemokines in human deep-carious teeth, The International Conference on Dentin/Pulp complexs, Chiba, Jul. 2001.
21.	Hiromichi Yumoto, Daisuke Yamaguchi, Yoshitaka Hosokawa, Chihiro Shinohara, Tadashi Nakanishi, Hirotoshi Shimizu, Masayoshi Yamada, Hideaki Nakae and Takashi Matsuo : Expression of IL-18 and IL-18 receptor in human periodontally diseased tissue, Modern Periodontology New Directions in 21st Century-, Kanagawa(Japan), Jun. 2001.

Proceeding of Domestic Conference:

1.	MIEDA Katsuhiro, Tadashi Nakanishi, Hitomi Kuramoto, Yoshitaka Hosokawa, Ikuko Hosokawa, Daisuke Takegawa and Keiichi Hosaka : Sudachitinがヒト歯髄細胞の炎症メディエーター発現に与える影響, 日本歯科保存学会 2023年度春季学術大会(第158回), Jun. 2023.
2.	Hitomi Kuramoto, Tadashi Nakanishi, Daisuke Takegawa, MIEDA Katsuhiro and Keiichi Hosaka : Caffeic acid phenethyl ester (CAPE) がマウス骨芽細胞様細胞の組織修復関連因子発現に与える影響, 日本歯科保存学会 2023年度春季学術大会(第158回), Jun. 2023.
3.	三枝克啓, Tadashi Nakanishi, Hitomi Kuramoto, Daisuke Takegawa and Keiichi Hosaka : Interleukin-22 がヒト歯髄細胞の炎症性メディエーター発現に及ぼす影響, 第4回象牙質歯髄治療学会学術大会, May 2023.
4.	Hitomi Kuramoto, Tadashi Nakanishi, Daisuke Takegawa, Yuki Hosokawa, Katsuhiro Mieda and Keiichi Hosaka : The effects of Caffeic acid phenethyl ester (CAPE) on VEGF production in dental pulp cells, 日本歯科保存学会2021年度秋季学術大会(第155回), Oct. 2021.
5.	Hitomi Kuramoto, Kouji Hirao, Yuki Hosokawa, Daisuke Takegawa, Hiromichi Yumoto and Tadashi Nakanishi : ラット象牙芽細胞(KN-3)におけるVEGFの石灰化誘導作用, 日本歯科保存学会 2019年度秋季学術大会(第151回) (福岡), Nov. 2019.
6.	Daisuke Takegawa, Tadashi Nakanishi, Kouji Hirao, Hiromichi Yumoto, Yuki Hosokawa, Hitomi Kuramoto and Takashi Matsuo : Effects of interferon-γ on innate host responses in cultured odontoblast-like cells stimulated with NOD ligands, 第150回日本歯科保存学会 2019年度春季学術大会, Jun. 2019.
7.	Hitomi Kuramoto, Hiromichi Yumoto, Kouji Hirao, Yuki Hosokawa, Tadashi Nakanishi, Daisuke Takegawa and Takashi Matsuo : Caffeic Acid Phenetyl Ester (CAPE)の象牙芽細胞と骨芽細胞におけるVEGF産生誘導機序の解析, 第148回日本歯科保存学会春季学術大会, Jun. 2018.
8.	Hitomi Kuramoto, Hiromichi Yumoto, Kouji Hirao, 細川由樹, Tadashi Nakanishi, Daisuke Takegawa and Takashi Matsuo : Caffeic Acid Phenethyl Ester (CAPE)のラット象牙芽細胞(KN-3)におけるVEGF産生に与える影響, 日本歯科保存学会2017年度春季学術大会(第146回), Jun. 2017.
9.	Tadashi Nakanishi, Daisuke Takegawa, Kouji Hirao, Hiromichi Yumoto, 細川由樹 and Takashi Matsuo : Interleukin-17がラット象牙芽細胞様細胞(KN-3)のCCL20産生に及ぼす影響, 日本歯科保存学会 2015年度秋季学術大会(第143回), Nov. 2015.
10.	細川由樹, Hiromichi Yumoto, Kouji Hirao, Tadashi Nakanishi, Daisuke Takegawa and Takashi Matsuo : 象牙芽細胞が有するMincleを介した視細胞認識機構とその歯髄炎症反応における役割, 日本歯科保存学会 2015年度秋季学術大会(第143回), Nov. 2015.
11.	Kouji Hirao, Hiromichi Yumoto, 細川由樹, Tadashi Nakanishi, Daisuke Takegawa and Takashi Matsuo : ラット象牙芽細胞(KN-3)の自然免疫反応におけるシグナル伝達経路の解析, 日本歯科保存学会2015年度春季学術大会(第142回), Jun. 2015.
12.	細川由樹, Hiromichi Yumoto, Kouji Hirao, Tadashi Nakanishi, Daisuke Takegawa and Takashi Matsuo : ラット象牙芽細胞(KN-3)に対するカテキンとカフェイン酸の抗炎症作用, 日本歯科保存学会2015年度春季学術大会(第142回), Jun. 2015.
13.	Takashi Matsuo, Tadashi Nakanishi, Hiromichi Yumoto, Chihiro Shinohara and Kouji Hirao : 感染根管治療の考え方, 四国歯学会(第46回例会), Mar. 2015.
14.	Tadashi Nakanishi, Daisuke Takegawa, Kouji Hirao, Hiromichi Yumoto and Takashi Matsuo : Interleukin-17がヒト歯髄線維芽細胞の炎症メディエーター発現に及ぼす影響, 日本歯科保存学会2014年度秋季学術大会(第141回), Oct. 2014.
15.	Kouji Hirao, Hiromichi Yumoto, Tadashi Nakanishi, Chihiro Shinohara, Kanako Takahashi, Daisuke Takegawa, 細川由樹 and Takashi Matsuo : ラット象牙芽細胞様細胞(KN3)における細菌関連病原因子刺激に対する自然免疫反応の解析, 日本歯科保存学会2014年度春季学術大会(第140回), Jun. 2014.
16.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : The effect of catechin on CCL11 production from TNF-alpha -stimulated human gingival fibroblasts, The Japanese Journal of Conservative Dentistry, Jun. 2012.
17.	Tadashi Nakanishi, Daisuke Takegawa, Kouji Hirao, Hiromichi Yumoto, Kanako Takahashi and Takashi Matsuo : prostaglandin F2aは歯髄細胞における炎症性メディエーター発現を調節する, 第136回日本歯科保存学会春季学術大会, Jun. 2012.
18.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi and Takashi Matsuo : The effect of TWEAK on CCL20 production on IL-1beta-stimulated human gingival fibroblasts, The Japanese Journal of Conservative Dentistry, Oct. 2011.
19.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : The effect of theaflavin on IL-6 production in TNFSF14-stimulated human gingival fibroblasts, The Japanese Journal of Conservative Dentistry, Jun. 2011.
20.	武川大輔, Tadashi Nakanishi, Kouji Hirao, Hiromichi Yumoto, Kanako Takahashi and Takashi Matsuo : ヒト培養歯髄細胞の自然免疫応答に対するインターフェロンγの影響, 第134回日本歯科保存学会春季学術大会, Jun. 2011.
21.	Shindo Satoru, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Oncostatin Mが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす紅茶ポリフェノールの影響, Journal of the Japanese Association of Periodontology, May 2011.
22.	Shindo Satoru, Yoshitaka Hosokawa, Hosokawa Ikuko, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : Oncostatin Mが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす紅茶ポリフェノールの影響, Journal of the Japanese Association of Periodontology, May 2011.
23.	Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : The effect of catechin on IL-6 production from TNFSF14-stimulated human gingival fibroblasts, The Japanese Journal of Conservative Dentistry, Oct. 2010.
24.	Tadashi Nakanishi, 武川大輔, Kouji Hirao, Hiromichi Yumoto, Kanako Takahashi and Takashi Matsuo : ヒト歯髄細胞におけるサイトカイン発現に対するProstaglandin F2alpha の影響, 日本歯科保存学会2010年度秋季学術大会(第133回), Oct. 2010.
25.	Yoshitaka Hosokawa, Hosokawa Ikuko, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : The effect of catechin on IL-6 production from TNFSF14-stimulated human gingival fibroblasts, The Japanese Journal of Conservative Dentistry, Oct. 2010.
26.	Hashimoto Reina, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : IL-1betaが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす緑茶カテキンの影響, Journal of the Japanese Association of Periodontology, Sep. 2010.
27.	Hashimoto Reina, Yoshitaka Hosokawa, Ikuko Hosokawa, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : IL-1betaが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす緑茶カテキンの影響, Journal of the Japanese Association of Periodontology, Sep. 2010.
28.	Hashimoto Reina, Yoshitaka Hosokawa, Hosokawa Ikuko, Kazumi Ozaki, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : IL-1betaが誘導するヒト歯肉線維芽細胞のCXCL10産生に及ぼす緑茶カテキンの影響, Journal of the Japanese Association of Periodontology, Sep. 2010.
29.	Kouji Hirao, Hiromichi Yumoto, Kayo Mukai, Kanako Takahashi, Tadashi Nakanishi and Takashi Matsuo : カテキンは細菌やその構成成分に対する培養歯髄細胞の反応を調節する, 第127回日本歯科保存学会秋季学術大会, Nov. 2007.
30.	Hiromichi Yumoto, Kouji Hirao, Kanako Takahashi, Kayo Mukai, Tadashi Nakanishi and Takashi Matsuo : 培養歯髄細胞におけるPattern Recognition Receptor (PRR)を介した接着分子の発現, 第127回日本歯科保存学会秋季学術大会, Nov. 2007.
31.	Kayo Mukai, Tadashi Nakanishi, Yoshitaka Hosokawa, Kanako Takahashi and Takashi Matsuo : カテキンが歯髄由来線維芽細胞の炎症性サイトカインおよび接着分子の発現誘導に与える影響, 第27回日本歯内療法学会学術大会, Jul. 2006.
32.	Kayo Mukai, Tadashi Nakanishi, Yoshitaka Hosokawa, Kanako Takahashi, 足立智彦 and Takashi Matsuo : カテキンが歯髄由来線維芽細胞の炎症性サイトカインおよび接着分子の発現誘導に与える影響, 第124回日本歯科保存学会春季学術大会, May 2006.
33.	足立智彦, Kouji Hirao, Hiromichi Yumoto, Kanako Takahashi, 向井佳代, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : 歯髄組織および細菌刺激THP-1細胞におけるCXCR3 ligands(特にIP-10)の発現解析, 第123回秋季日本歯科保存会, Nov. 2005.
34.	向井佳代, Tadashi Nakanishi, Yoshitaka Hosokawa, Kanako Takahashi, 足立智彦 and Takashi Matsuo : Toll-like receptor リガンドによる歯髄由来繊維芽細胞のIL-8, VEGF, 接着分子発現誘導, 第122回春季日本歯科保存学会, Jun. 2005.
35.	足立智彦, Tadashi Nakanishi, Kanako Takahashi and Takashi Matsuo : 歯髄線維芽細胞における細菌由来因子によるIP-10発現, 第122回春季日本歯科保存学会, Jun. 2005.
36.	Kayo Mukai, Tadashi Nakanishi, Yoshitaka Hosokawa, Kanako Takahashi, 足立智彦 and Takashi Matsuo : Toll-like receptor リガンドによる歯髄線維芽細胞のIL-8，VEGF，接着分子の発現誘導, 第122回日本歯科保存学会春季学術大会, Jun. 2005.
37.	足立智彦, Tadashi Nakanishi, Kanako Takahashi and Takashi Matsuo : 歯髄炎の病態形成におけるIP-10の役割, 第33回日本免疫学会総会, Dec. 2003.
38.	Kanako Takahashi, Tadashi Nakanishi, 足立智彦, 位田夏子, Hideaki Nakae and Takashi Matsuo : THP-1細胞からのサイトカイン産生におけるStrepptococcus mutansの影響について, 第33回日本免疫学会総会, Dec. 2003.
39.	足立智彦, Tadashi Nakanishi, Kanako Takahashi, 向井佳代 and Takashi Matsuo : 歯髄炎におけるCXCL10の発現に関する研究, 第119回秋季日本歯科保存学会, Nov. 2003.
40.	Kanako Takahashi, Tadashi Nakanishi, Daisuke Yamaguchi, Yoshitaka Hosokawa, Hiromichi Yumoto, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 歯髄炎の病態形成におけるLARCおよびCCR6の役割, 第32回日本免疫学会, Dec. 2002.
41.	Chihiro Shinohara, Tadashi Nakanishi, 末延慎司, Kazumi Ozaki and Takashi Matsuo : 抜歯に至った難治性根尖性歯周炎の1症例, 第116回日本歯科保存学会春季学会, Vol.45, 114, May 2002.
42.	Daisuke Yamaguchi, Yoshitaka Hosokawa, Chihiro Shinohara, Hiromichi Yumoto, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : 歯周炎病変局所におけるFractalkineおよびCX3CR1の発現, 第45回春季日本歯周病学会, Apr. 2002.
43.	Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Hirotoshi Shimizu, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 歯周炎病変局所におけるLARCおよびCCR6の発現, 第31回日本免疫学会, Dec. 2001.
44.	Daisuke Yamaguchi, Yoshitaka Hosokawa, Hiromichi Yumoto, Tadashi Nakanishi, Hideaki Nakae and Takashi Matsuo : 歯周炎病変局所におけるIL-18とその機能に関連する分子の発現について, 第31回日本免疫学会学術集会, Dec. 2001.
45.	Kanako Takahashi, Tadashi Nakanishi, Yoshitaka Hosokawa, Chihiro Shinohara, Hiromichi Yumoto, Kazumi Ozaki and Takashi Matsuo : 炎症歯髄におけるLARCおよびCCR6の発現, 第115回秋季日本歯科保存学会, Nov. 2001.
46.	Yoshitaka Hosokawa, Tadashi Nakanishi, Daisuke Yamaguchi, Hirotoshi Shimizu, Hiromichi Yumoto, Kazumi Ozaki and Takashi Matsuo : 歯周炎病変局所におけるLARCおよびCCR6の発現, 第44回秋季日本歯周病学会学術大会, Oct. 2001.
47.	Takashi Matsuo, Tadashi Nakanishi, Kanako Takahashi, Kazumi Ozaki and Hideaki Nakae : 歯髄炎の不可逆性化に関する臨床的および病理学的考察, 第14回「歯内療法の集い」, May 2001.
48.	Daisuke Yamaguchi, Yoshitaka Hosokawa, Hirotoshi Shimizu, Chihiro Shinohara, Hiromichi Yumoto, Tadashi Nakanishi and Takashi Matsuo : 歯周炎の病変局所におけるIL-18およびIL-18レセプターの発現, 第44回春季日本歯周病学会学術大会, Apr. 2001.
49.	Tadashi Nakanishi, Nozomi Matsuoka, Kanako Takahashi, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 深在う蝕における侵入細菌の局所と歯髄反応, 第113回秋季日本歯科保存学会, Nov. 2000.
50.	Yoshitaka Hosokawa, 山口大輔, 清水洋利, Tadashi Nakanishi, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 歯周炎の病巣局所におけるケモカインおよびケモカイン受容体の発現, 第30回日本免疫学会総会, Nov. 2000.
51.	Hirotoshi Shimizu, Yoshitaka Hosokawa, Daisuke Yamaguchi, Tadashi Nakanishi, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 歯周炎の病巣局所におけるリンパ球浸潤に対するケモカインの関与, 第29回日本免疫学会総会, Dec. 1999.
52.	Kazumi Ozaki, Tadashi Nakanishi, Keiko Fujinaka and Takashi Matsuo : 歯根部象牙質齲蝕誘発モデルの細菌学ならびに形態学的検索, 第110回日本歯科保存学会春季学会, May 1999.
53.	Hirotoshi Shimizu, Yoshitaka Hosokawa, Tadashi Nakanishi, Kazumi Ozaki and Hideaki Nakae : 歯周炎の病巣局所におけるVCAM-1,VLA-4を介する接着系の解析, 第28回日本免疫学会, Dec. 1998.
54.	Tadashi Nakanishi, Hirotoshi Shimizu, Kazumi Ozaki, Hideaki Nakae and Takashi Matsuo : 多形核白血球の集積化による歯髄組織破壊機構の解析, 第105回日本歯科保存学会春秋季学会, Nov. 1996.
55.	Takashi Matsuo, Tadashi Nakanishi, 片岡健哉, Kazumi Ozaki, 野杁由一郎, 大木元玲子, Hideaki Nakae, 吉山昌宏 and 恵比須繁之 : 覆髄法の適応範囲の拡大に関する臨床的検討, 第14回四国歯学会, Jul. 1991.
56.	Masahiro Yoshiyama, Kazumi Ozaki, Yuichiro Noiri, Kenya Kataoka, Tadashi Nakanishi, Reiko Ogimoto, Hideaki Nakae, Takashi Matsuo and Shigeyuki Ebisu : Treatment of Dentin Hypersensitivity, --- Effect of a Light-curing Resin Liner on Tubule Occlusion ---, 第93回日本歯科保存学会秋季学会, Sep. 1990.
57.	Kazumi Ozaki, 野杁由一郎, Tadashi Nakanishi, 片岡健哉 and 吉山昌宏 : コンポジットレジンの歯根部象牙質に対する接着性, 第92回日本歯科保存学会春季学会, Jun. 1990.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

ワサビ含有成分を歯周炎治療に用いるための基礎的研究～抗炎症作用に着目して～ (Project/Area Number: 22K09984 )
乳酸菌由来細胞外小胞を用いた歯周病治療戦略ーM1/M2マクロファージに着目してー (Project/Area Number: 22K09966 )
Basic study of the bioactive substances of a skin of citrus fruits for periodontal disease treatment (Project/Area Number: 19K10151 )
Basic research for using spice-containing ingredients in the treatment of periodontitis-Focusing on rosemary- (Project/Area Number: 18K09600 )
Elucidation of odontoblasts calcification and innate immune response in early pulpitis (Project/Area Number: 17K11709 )
Development of a new approach to the treatments in conservative dentistry based on a concept for home or visit care. (Project/Area Number: 17K11708 )
Analysis of leukocyte infiltration mechanism to participate in inflammatory bone resorption in periodontal lesion (Project/Area Number: 16K11834 )
role of melatonin in periodontal disease (Project/Area Number: 15K11392 )
Development of novel dental pulp preservation and calcification therapies by analyzing epigenetics and post-transcriptional regulation mechanism (Project/Area Number: 15K11117 )
The analysis of odontoblastic mechanism via innate immune system (Project/Area Number: 15K11116 )
Analysis of mechanism for pro-inflammatory and anti-inflammatory balance and role of Th17 cells in pulpitis (Project/Area Number: 15K11115 )
Application of electromagnetic wave irradiation to deep caries lesion. (Project/Area Number: 26462885 )
Analysis of Th17 cells migration and activation in periodontally diseased tissues (Project/Area Number: 25463219 )
Development of extracellular DNA-protein complex-targeting novel treatments and prevention for oral biofilm-related infectious diseases (Project/Area Number: 24592872 )
Analysis of a balance between pro-inflammatory and anti-inflammatory pulpal responses in the pathogenesis of pulpitis (Project/Area Number: 24592871 )
Development of a new comprehensive treatment for dental caries based on minimum intervention dentistry (Project/Area Number: 23390435 )
Endodontic therapeutic application of electro-magnetic wave irradiation for refractory periapical periodontitis and periapical biofilm (Project/Area Number: 21592423 )
Study on a therapeutic application of tea catechins to vital pulp treatment. (Project/Area Number: 20592228 )
Analysis of bacterial invasive lesion of refractory periapical periodontitis cases by genetic engineering technique (Project/Area Number: 18592092 )
Analysis of gingival epithelial cells and fibroblast using three-dimensional culture system mimic to periodontal pockets (Project/Area Number: 15592189 )
Study on the role of chemokines in the infiltration of inflammatory cells in dental pulp tissue destruction (Project/Area Number: 13672001 )
Analysis of the relationship between the invasion of dental caries-associated bacteria and the host response of dental pulp in human carious teeth with pulp exposure (Project/Area Number: 11671897 )
Bacterial Invasion of Infected Canals and Root Dentin of Human Teeth and Analysis of the Host-parasite Interaction at the Apex. - Elucidation of Pathogenesis of Refractory Cases-. (Project/Area Number: 10470406 )
歯髄組織破壊における多形核白血球浸潤の細胞傷害性に関する研究 (Project/Area Number: 08771701 )
ヒト歯周炎における炎症浸潤細胞の接着機構の研究 (Project/Area Number: 08672193 )
多形核白血球の集積化による歯髄組織破壊機構の解析 (Project/Area Number: 07771765 )
歯髄血液を用いた不可逆性歯髄炎の診断に関する研究 (Project/Area Number: 06771719 )
歯周組織破壊の進行過程における免疫担当細胞の動態 (Project/Area Number: 06671916 )
歯髄炎の非可逆性化に関与する炎症機構の解析 (Project/Area Number: 04671162 )
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Associate Professor : Nakanishi, Tadashi

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