Dec2 negatively regulates bone resorption in periodontitis. (22nd August 2022)

• Record Type: Journal Article
• Authors: Li, Xiaoyan; Guo, Lijia; Sato, Fuyuki; Kitayama, Toshiyasu; Tewari, Nitesh; Makishima, Makoto; Hamada, Nobushiro; Liu, Yi; Bhawal, Ujjal K.
• Is Part Of: Journal of periodontal research. Volume 57:Number 5(2022)
• Page Start: 1056
• Page End: 1069
• Publication Date: 2022-08-22
• Subjects: alveolar bone resorption -- Dec2 -- immunoregulation -- P. gingivalis -- periodontal inflammation -- RANKL -- transcription factor; Periodontics -- Periodicals; 617.632
• DOI: 10.1111/jre.13046
• Languages: English
• ISSNs: 0022-3484

Abstract

Abstract: Background and Objectives: The potential role of the transcription factor Differentiated embryo‐chondrocyte 2 (Dec2) in the progression of inflammatory diseases such as periodontitis has been unclear. Here, the effect of Dec2 on the expression of RANKL and on osteoclastogenesis was determined. Material and Methods: Wild‐type (WT) and Dec2 knockout (KO) mice as a model for periodontitis were used to assess alveolar bone resorption by microcomputed tomography (CT). Western blot, flow cytometry, quantitative real‐time PCR, and immunohistochemical analyses were utilized to detect inflammation and osteoclasts. Luciferase reporter and Chromatin immunoprecipitation (ChIP) assays examined the interaction between Dec2 and RANKL. Results: Micro‐CT showed that the alveolar bone resorption of Dec2 KO mice was more severe than WT mice after treatment with P. gingivalis . Immunohistochemistry and Tartrate‐resistant acid phosphatase staining showed active osteoclast differentiation in Dec2 KO mice. There was an increase in CD11b + F4/80 + and CD4 + RANKL + T cells in Dec2 KO mice treated with P. gingivalis . Moreover, inflammatory and immune markers were expressed at significantly higher levels in gingival mononuclear cells in Dec2 KO mice. Furthermore, luciferase reporter and ChIP assays confirmed the direct binding of Dec2 protein to the RANKL gene. Conclusion: Dec2 has an immune regulation ability that modulates P. gingivalis ‐induced periodontitis via RANKL.