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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

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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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Related Experiment Video

Updated: Jul 19, 2025

Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model
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Osteocyte RANKL Drives Bone Resorption in Mouse Ligature-Induced Periodontitis.

Mizuho Kittaka1,2, Tetsuya Yoshimoto1,2, Marcus E Levitan1,2

  • 1Department of Biomedical Sciences and Comprehensive Care, Indiana University School of Dentistry, Indianapolis, IN, USA.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
|August 8, 2023
PubMed
Summary
This summary is machine-generated.

Osteocytes play a key role in periodontitis-related bone loss by activating osteoclastogenesis via the NOD1-RANKL pathway. This study reveals critical time points and mechanisms for therapeutic targeting in periodontitis bone resorption.

Keywords:
LIGATURE-INDUCED PERIODONTITISNOD1OSTEOCLASTSOSTEOCYTESRANKL

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Area of Science:

  • Bone Biology
  • Periodontology
  • Immunology

Background:

  • Ligature-induced periodontitis (LIP) is a model for studying alveolar bone loss.
  • The specific role of osteocytes in LIP and optimal evaluation parameters remain unclear.

Purpose of the Study:

  • To investigate the temporal dynamics of bone loss and osteoclastogenesis in LIP.
  • To elucidate the role of osteocytes in LIP-induced bone resorption.
  • To identify key molecular pathways involved in LIP pathogenesis.

Main Methods:

  • Time-course analysis of bone volume (BV) loss and osteoclast induction over 14 days in mice.
  • Genetic manipulation of osteocyte-specific RANKL expression and analysis of RAG1-deficient mice.
  • Investigation of the role of MYD88 and NOD1 signaling in osteocytes during LIP.

Main Results:

  • Osteoclast induction peaked on days 3-5, followed by peak BV loss on day 7, with bone recovery by day 14.
  • Osteocyte-derived RANKL is crucial for LIP-induced bone loss; T/B cells are dispensable.
  • Bacterial activation of osteocytes via NOD1 signaling promotes RANKL expression and osteoclastogenesis.

Conclusions:

  • LIP involves stage-dependent bone resorption and formation, emphasizing critical time point selection for evaluation.
  • Osteocytes, through the NOD1-RANKL axis, are key mediators of bacterial-induced osteoclastogenesis in periodontitis.
  • Targeting the osteocytic NOD1-RANKL pathway presents a potential therapeutic strategy for periodontitis-associated bone loss.