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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
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Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
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Updated: Aug 31, 2025

Isolation of Mesenchymal Stem Cells from Human Alveolar Periosteum and Effects of Vitamin D on Osteogenic Activity of Periosteum-derived Cells
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Dec2 negatively regulates bone resorption in periodontitis.

Xiaoyan Li1, Lijia Guo2, Fuyuki Sato3

  • 1Laboratory of Tissue Regeneration and Immunology and Department of Periodontics, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, School of Stomatology, Capital Medical University, Beijing, China.

Journal of Periodontal Research
|August 22, 2022
PubMed
Summary

Differentiated embryo-chondrocyte 2 (Dec2) regulates periodontitis by modulating RANKL expression and osteoclastogenesis. Dec2 deficiency exacerbates bone loss in a mouse model of P. gingivalis-induced periodontitis.

Keywords:
P. gingivalisDec2RANKLalveolar bone resorptionimmunoregulationperiodontal inflammationtranscription factor

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Area of Science:

  • Immunology
  • Molecular Biology
  • Periodontal Disease Research

Background:

  • The role of transcription factor Differentiated embryo-chondrocyte 2 (Dec2) in inflammatory diseases like periodontitis remains unclear.
  • Investigating Dec2's impact on RANKL expression and osteoclastogenesis is crucial for understanding periodontitis progression.

Purpose of the Study:

  • To determine the effect of Dec2 on RANKL expression and osteoclastogenesis in the context of periodontitis.
  • To elucidate the mechanism by which Dec2 influences inflammatory responses in periodontitis.

Main Methods:

  • Utilized wild-type and Dec2 knockout mice to model periodontitis.
  • Assessed alveolar bone resorption using microcomputed tomography (CT).
  • Employed Western blot, flow cytometry, qPCR, immunohistochemistry, luciferase reporter, and ChIP assays to analyze inflammation, osteoclasts, and Dec2-RANKL interaction.

Main Results:

  • Dec2 knockout mice exhibited more severe alveolar bone resorption and active osteoclast differentiation.
  • Increased CD11b+ F4/80+ and CD4+ RANKL+ T cells were observed in Dec2 knockout mice.
  • Dec2 was confirmed to directly bind to the RANKL gene, indicating a regulatory role.

Conclusions:

  • Dec2 possesses immune regulatory capabilities that modulate P. gingivalis-induced periodontitis.
  • Dec2 influences periodontitis progression through its regulation of RANKL.