DNA damage‐inducible transcript 3 deficiency promotes bone resorption in murine periodontitis models.

Background and Objective: Periodontitis is a multifactorial inflammatory disease that leads to the destruction of supporting structures of the teeth. DNA damage‐inducible transcript 3 (DDIT3) plays crucial roles in cell survival and differentiation. DDIT3 regulates bone mass and osteoclastogenesis i...

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Publicado en:Journal of Periodontal Research Vol. 58; no. 4; pp. 841 - 852
Autores principales: Luo, Yao, Yang, Beining, Dong, Wei, Yu, Wenqian, Jia, Meie, Wang, Jiawei
Formato: diagnostic images pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell Aug2023
Acceso en línea:Ver este registro en EBSCOhost
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      jid:
        00223484
        8E9
      jtl: Journal of Periodontal Research
      issn: 00223484
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    pubinfo:
      dt: Aug2023
      vid: 58
      iid: 4
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1111/jre.13142
        164722919
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      tig:
        atl: DNA damage‐inducible transcript 3 deficiency promotes bone resorption in murine periodontitis models.
      aug:
        au:
          Luo, Yao
          Yang, Beining
          Dong, Wei
          Yu, Wenqian
          Jia, Meie
          Wang, Jiawei
        affil: The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei‐MOST) and Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, China
      sug:
        subj:
          Periodontitis Complications
          Bone Resorption Risk Factors
          Transcription Factors Deficiency
          Transcription Factors Physiology
          Animal Studies
          Models, Biological
          Mice
          Clustered Regularly Interspaced Short Palindromic Repeats
          Gene Expression
          Periodontium Metabolism
          Polymerase Chain Reaction
          Immunohistochemistry
          Alveolar Process
          Phenotype
          Tomography, X-Ray Computed Methods
          Microscopy
          Osteoclasts Physiology
          Histology
          Staining and Labeling
          Osteoclasts Metabolism
          Acid Phosphatase Analysis
          Macrophages Analysis
          Inflammation Risk Factors
          Osteogenesis
          Alveolar Bone Loss Risk Factors
          Cytokines Metabolism
          Biological Markers Metabolism
          In Vitro Studies
          Funding Source
      ab: Background and Objective: Periodontitis is a multifactorial inflammatory disease that leads to the destruction of supporting structures of the teeth. DNA damage‐inducible transcript 3 (DDIT3) plays crucial roles in cell survival and differentiation. DDIT3 regulates bone mass and osteoclastogenesis in femur. However, the role of DDIT3 in periodontitis has not been elucidated. This research aimed to explore the role and mechanisms of DDIT3 in periodontitis. Methods: DDIT3 gene knockout (KO) mice were generated using a CRISPR/Cas9 system. Experimental periodontitis models were established to explore the role of DDIT3 in periodontitis. The expression of DDIT3 in periodontal tissues was detected by quantitative real‐time polymerase chain reaction (qRT‐PCR) and immunohistochemistry (IHC). The alveolar bone phenotypes were observed by micro‐CT and stereomicroscopy. The inflammation levels and osteoclast activity were examined by histological staining, immunostaining, and qRT‐PCR. Bone marrow‐derived macrophages (BMMs) were isolated to confirm the effects of DDIT3 on osteoclast formation and function in vitro. Results: The increased expression of DDIT3 in murine inflamed periodontal tissues was detected. DDIT3 knockout aggravated alveolar bone loss and enhanced expression levels of inflammatory cytokines in murine periodontitis models. Increased osteoclast formation and higher expression levels of osteoclast‐specific markers were observed in the inflamed periodontal tissues of KO mice. In vitro, DDIT3 deficiency promoted the formation of tartrate‐resistant acid phosphatase (TRAP)‐positive multinucleated osteoclasts and the bone resorption activity of mature osteoclasts. Conclusions: Our results demonstrate that DDIT3 deletion aggravated alveolar bone loss in experimental periodontitis through enhanced inflammatory reactions and osteoclastogenesis. The anti‐inflammation and the inhibition of bone loss by DDIT3 in murine periodontitis provides a potential novel therapeutic strategy for periodontitis.
      pubtype: Academic Journal
      doctype:
        diagnostic images
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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