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      The Genes Involved in Dentinogenesis

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      Author(s): a , b , c , c , a , a , d , a
      Publication date (Electronic, pub):
      Publication date (Electronic, collection):
      Journal: Organogenesis
      Publisher: Taylor & Francis
      Keywords: dentinogenesis, odontoblasts, Gene, signaling pathway

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          ABSTRACT

          The development and repair of dentin are strictly regulated by hundreds of genes. Abnormal dentin development is directly caused by gene mutations and dysregulation. Understanding and mastering this signal network is of great significance to the study of tooth development, tissue regeneration, aging, and repair and the treatment of dental diseases. It is necessary to understand the formation and repair mechanism of dentin in order to better treat the dentin lesions caused by various abnormal properties, whether it is to explore the reasons for the formation of dentin defects or to develop clinical drugs to strengthen the method of repairing dentin. Molecular biology of genes related to dentin development and repair are the most important basis for future research.

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          Deciduous autologous tooth stem cells regenerate dental pulp after implantation into injured teeth

          Shiyu Liu, Kun Xuan, Bei Li … (2018)
          Pulp necrosis arrests root development in injured immature permanent teeth, which may result in tooth loss. However, dental pulp regeneration and promotion of root development remains challenging. We show that implantation of autologous tooth stem cells from deciduous teeth regenerated dental pulp with an odontoblast layer, blood vessels, and nerves in two animal models. These results prompted us to enroll 40 patients with pulp necrosis after traumatic dental injuries in a randomized, controlled clinical trial. We randomly allocated 30 patients to the human deciduous pulp stem cell (hDPSC) implantation group and 10 patients to the group receiving traditional apexification treatment. Four patients were excluded from the implantation group due to loss at follow-up (three patients) and retrauma of the treated tooth (one patient). We examined 26 patients (26 teeth) after hDPSC implantation and 10 patients (10 teeth) after apexification treatment. hDPSC implantation, but not apexification treatment, led to regeneration of three-dimensional pulp tissue equipped with blood vessels and sensory nerves at 12 months after treatment. hDPSC implantation increased the length of the root (P < 0.0001) and reduced the width of the apical foramen (P < 0.0001) compared to the apexification group. In addition, hDPSC implantation led to regeneration of dental pulp tissue containing sensory nerves. To evaluate the safety of hDPSC implantation, we followed 20 patients implanted with hDPSCs for 24 months and did not observe any adverse events. Our study suggests that hDPSCs are able to regenerate whole dental pulp and may be useful for treating tooth injuries due to trauma.
          Article 0 comments Cited 145 times – based on 0 reviews     Review now
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            Mutations in AXIN2 cause familial tooth agenesis and predispose to colorectal cancer.

            Päivi Lahermo, S Pirinen, Irma Thesleff … (2004)
            Wnt signaling regulates embryonic pattern formation and morphogenesis of most organs. Aberrations of regulation of Wnt signaling may lead to cancer. Here, we have used positional cloning to identify the causative mutation in a Finnish family in which severe permanent tooth agenesis (oligodontia) and colorectal neoplasia segregate with dominant inheritance. Eleven members of the family lacked at least eight permanent teeth, two of whom developed only three permanent teeth. Colorectal cancer or precancerous lesions of variable types were found in eight of the patients with oligodontia. We show that oligodontia and predisposition to cancer are caused by a nonsense mutation, Arg656Stop, in the Wnt-signaling regulator AXIN2. In addition, we identified a de novo frameshift mutation 1994-1995insG in AXIN2 in an unrelated young patient with severe tooth agenesis. Both mutations are expected to activate Wnt signaling. The results provide the first evidence of the importance of Wnt signaling for the development of dentition in humans and suggest that an intricate control of Wnt-signal activity is necessary for normal tooth development, since both inhibition and stimulation of Wnt signaling may lead to tooth agenesis. Our findings introduce a new gene for hereditary colorectal cancer and suggest that tooth agenesis may be an indicator of cancer susceptibility.
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              Runx2, osx, and dspp in tooth development.

              Jeffrey H Chuang, Li Chen, J Gluhak … (2009)
              The transcription factors Runx2 and Osx are necessary for osteoblast and odontoblast differentiation, while Dspp is important for odontoblast differentiation. The relationship among Runx2, Osx, and Dspp during tooth and craniofacial bone development remains unknown. In this study, we hypothesized that the roles of Runx2 and Osx in the regulation of osteoblast and odontoblast lineages may be independent of one another. The results showed that Runx2 expression overlapped with Osx in dental and osteogenic mesenchyme from E12 to E16. At the later stages, from E18 to PN14, Runx2 and Osx expressions remained intense in alveolar bone osteoblasts. However, Runx2 expression was down-regulated, whereas Osx expression was clearly seen in odontoblasts. At later stages, Dspp transcription was weakly present in osteoblasts, but strong in odontoblasts where Osx was highly expressed. In mouse odontoblast-like cells, Osx overexpression increased Dspp transcription. Analysis of these data suggests differential biological functions of Runx2, Osx, and Dspp during odontogenesis and osteogenesis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Organogenesis
                Journal ID (iso-abbrev): Organogenesis
                Title: Organogenesis
                Publisher: Taylor & Francis
                ISSN (Print): 1547-6278
                ISSN (Electronic): 1555-8592
                Publication date (Electronic, pub): 13 January 2022
                Publication date (Electronic, collection): 2022
                Publication date PMC-release: 13 January 2022
                Volume: 18
                Issue: 1
                Pages: 1-19
                Affiliations
                [a ]Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital, Fudan University; , Shanghai, P. R. China
                [b ]Department of Prosthodontics, Shanghai Stomatological Hospital, Fudan University; , Shanghai, P. R. China
                [c ]Department of Stomatology, Huashan Hospital, Fudan University; , Shanghai, P. R. China
                [d ]Department of Endodontics, Shanghai Stomatological Hospital, Fudan University; , Shanghai, P. R. China
                Author notes
                CONTACT Shangfeng Liu Shangfeng_liu683@ 123456fudan.edu.cn Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital, Fudan University; , 365 Beijing Road, Shanghai 200001, P. R. China
                Xiaoling Wei xiaoling_wei@ 123456fudan.edu.cn Department of Endodontics, Shanghai Stomatological Hospital, Fudan University; , 365 Beijing Road, Shanghai 200001, P. R. China
                [*]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0002-2413-3946
                Article
                Publisher ID: 2022373
                DOI: 10.1080/15476278.2021.2022373
                PMC ID: 8865278
                PubMed ID: 35023442
                SO-VID: 81ec817e-2516-4824-a7f7-9aec61e9e4a0
                Copyright © © 2022 The Author(s). Published with license by Taylor & Francis Group, LLC.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Page count
                Figures: 0, Tables: 1, References: 163, Pages: 19
                Categories
                Subject: Review
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: dentinogenesis,odontoblasts,gene,signaling pathway
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: dentinogenesis, odontoblasts, gene, signaling pathway

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