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      Primary failure of tooth eruption: Etiology and management

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          Abstract

          Primary failure of eruption (PFE) is a rare disorder defined as incomplete tooth eruption despite the presence of a clear eruption pathway. PFE is known to be caused by rare variants in the parathyroid hormone 1 receptor gene ( PTH1R). Although several PTH1R variants have been reported, the etiology of PFE remains unclear. However, important studies that help elucidate the pathology of PFE have recently been published. The purpose of this review is to summarize current treatment options, clinical symptoms or phenotypes for diagnosis, genetic information including solid evidence in mouse disease models and disease-specific induced pluripotent stem cells, thus approaching the etiology of PFE from the perspective of the latest research.

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          Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors.

          Kazutoshi Takahashi, Shinya Yamanaka (2006)
          Differentiated cells can be reprogrammed to an embryonic-like state by transfer of nuclear contents into oocytes or by fusion with embryonic stem (ES) cells. Little is known about factors that induce this reprogramming. Here, we demonstrate induction of pluripotent stem cells from mouse embryonic or adult fibroblasts by introducing four factors, Oct3/4, Sox2, c-Myc, and Klf4, under ES cell culture conditions. Unexpectedly, Nanog was dispensable. These cells, which we designated iPS (induced pluripotent stem) cells, exhibit the morphology and growth properties of ES cells and express ES cell marker genes. Subcutaneous transplantation of iPS cells into nude mice resulted in tumors containing a variety of tissues from all three germ layers. Following injection into blastocysts, iPS cells contributed to mouse embryonic development. These data demonstrate that pluripotent stem cells can be directly generated from fibroblast cultures by the addition of only a few defined factors.
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            Induction of pluripotent stem cells from adult human fibroblasts by defined factors.

            Kazutoshi Takahashi, Koji TANABE, Mari Ohnuki … (2007)
            Successful reprogramming of differentiated human somatic cells into a pluripotent state would allow creation of patient- and disease-specific stem cells. We previously reported generation of induced pluripotent stem (iPS) cells, capable of germline transmission, from mouse somatic cells by transduction of four defined transcription factors. Here, we demonstrate the generation of iPS cells from adult human dermal fibroblasts with the same four factors: Oct3/4, Sox2, Klf4, and c-Myc. Human iPS cells were similar to human embryonic stem (ES) cells in morphology, proliferation, surface antigens, gene expression, epigenetic status of pluripotent cell-specific genes, and telomerase activity. Furthermore, these cells could differentiate into cell types of the three germ layers in vitro and in teratomas. These findings demonstrate that iPS cells can be generated from adult human fibroblasts.
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              Modulation of osteoclast differentiation and function by the new members of the tumor necrosis factor receptor and ligand families.

              T Suda, N Takahashi, N Udagawa … (1999)
              Osteoblasts/stromal cells are essentially involved in osteoclast differentiation and function through cell-to-cell contact (Fig. 8). Although many attempts have been made to elucidate the mechanism of the so-called "microenvironment provided by osteoblasts/stromal cells," (5-8) it has remained an open question until OPG and its binding molecule were cloned. The serial discovery of the new members of the TNF receptor-ligand family members has confirmed the idea that osteoclast differentiation and function are regulated by osteoblasts/stromal cells. RANKL, which has also been called ODF, TRANCE, or OPGL, is a member of the TNF ligand family. Expression of RANKL mRNA in osteoblasts/stromal cells is up-regulated by osteotropic factors such as 1 alpha, 25(OH)2D3, PTH, and IL-11. Osteoclast precursors express RANK, a TNF receptor family member, recognize RANKL through cell-to-cell interaction with osteoblasts/stromal cells, and differentiate into pOCs in the presence of M-CSF. RANKL is also involved in the survival and fusion of pOCs and activation of mature osteoclasts. OPG, which has also been called OCIF or TR1, is a soluble receptor for RANKL and acts as a decoy receptor in the RANK-RANKL signaling system (Fig. 8). In conclusion, osteoblasts/stromal cells are involved in all of the processes of osteoclast development, such as differentiation, survival, fusion, and activation of osteoclasts (Fig. 8). Osteoblasts/stromal cells can now be replaced with RANKL and M-CSF in dealing with the whole life of osteoclasts. RANKL, RANK, and OPG are three key molecules that regulate osteoclast recruitment and function. Further studies on these key molecules will elucidate the molecular mechanism of the regulation of osteoclastic bone resorption. This line of studies will establish new ways to treat several metabolic bone diseases caused by abnormal osteoclast recruitment and functions such as osteopetrosis, osteoporosis, metastatic bone disease, Paget's disease, rheumatoid arthritis, and periodontal bone disease.
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                Author and article information

                Contributors
                Tetsutaro Yamaguchi
                Journal
                Journal ID (nlm-ta): Jpn Dent Sci Rev
                Journal ID (iso-abbrev): Jpn Dent Sci Rev
                Title: The Japanese Dental Science Review
                Publisher: Elsevier
                ISSN (Print): 1882-7616
                ISSN (Electronic): 2213-6851
                Publication date PMC-release: 15 September 2022
                Publication date (Print): November 2022
                Publication date (Electronic): 15 September 2022
                Volume: 58
                Pages: 258-267
                Affiliations
                [a ]Department of Orthodontics, Kanagawa Dental University, Kanagawa, Japan
                [b ]Department of Bioinformatics and Genomics, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Ishikawa, Japan
                [c ]Department of Oral and Maxillofacial Surgery, Showa University School of Dentistry, Tokyo, Japan
                [d ]Department of Biochemistry, Showa University School of Dentistry, Tokyo, Japan
                [e ]University of Texas Health Science Center at Houston School of Dentistry, Houston, TX, USA
                Author notes
                [* ]Correspondence to: Department of Orthodontics, Kanagawa Dental University, 82 Inaoka-Cho, Yokosuka, Kanagawa 238-8580, Japan. t.yamaguchi@ 123456kdu.ac.jp
                Article
                Publisher Item ID: S1882-7616(22)00018-7
                DOI: 10.1016/j.jdsr.2022.08.002
                PMC ID: 9489741
                PubMed ID: 36159186
                SO-VID: 5d462633-c25a-4867-bbf1-7364abc9d016
                Copyright © © 2022 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 26 February 2022
                Date revision received : 1 July 2022
                Date accepted : 21 August 2022
                Categories
                Subject: Article

                Keywords: incomplete tooth eruption,animal model,disease-specific induced pluripotent stem cells,treatment
                Data availability:
                Keywords: incomplete tooth eruption, animal model, disease-specific induced pluripotent stem cells, treatment

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