ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2023
Osteocyte RANKL Drives Bone Resorption in Mouse Ligature-Induced Periodontitis.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 25 citations in OpenAlex.
- TRABD2A promotes osteogenic differentiation of human periodontal ligament stem cells by modulating TNF-α and IL-1β.Organogenesis · 2026Article
- Article
- Estradiol Enhances Alveolar Bone Resorption by Promoting Osteoclast Differentiation in Experimental Periodontitis.Dentistry journal · 2026Article
- Periodontitis as a Model for Inflammatory Uncoupling of Bone Remodeling.Journal of periodontal research · 2026Review
- Periodontitis induces skeletal muscle atrophy by increasing circulating levels of activin A.Nature communications · 2026Article
- Upregulation of senescence-associated gene expression levels in human gingival tissue affected by periodontitis.Journal of periodontology · 2026Article
- Article
- V-ATPase and Lysosomal Energy Sensing in Periodontitis and Medicine-Related Osteonecrosis of the Jaw.Biomolecules · 2025Review
- Role of CXCL10 released from osteocytes in response to TNF-α stimulation on osteoclasts.Scientific reports · 2025Article
- A study on the association between smoking, periodontal inflammation and alveolar bone resorption in patients with chronic periodontitis based on biomarkers: a meta-analysis.Frontiers in medicine · 2025Article
- Fracture-Induced Immunological Cascades Trigger Rapid Systemic Bone Loss via Osteocyte-Regulated Osteoclastogenesis.ImmunoTargets and therapy · 2025Article
- Mechanisms and therapeutic perspectives of mitochondrial dysfunction of macrophages in periodontitis.Frontiers in cellular and infection microbiology · 2025Review
- Inflammation and mechanical force-induced bone remodeling.Periodontology 2000 · 2024Review
- Fumarate Restrains Alveolar Bone Restoration via Regulating H3K9 Methylation.Journal of dental research · 2024Article
- Type VI Collagen Deficiency Causes Enhanced Periodontal Tissue Destruction.Journal of dental research · 2024Article
- Loss-of-functionJBMR plus · 2024Article
- Unraveling ferroptosis in osteogenic lineages: implications for dysregulated bone remodeling during periodontitis progression.Cell death discovery · 2024Article
- Inhibition of RANKL improves the skeletal phenotype of adenine-induced chronic kidney disease in mice.JBMR plus · 2024Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Mouse ligature-induced periodontitis (LIP) has been used to study bone loss in periodontitis. However, the role of osteocytes in LIP remains unclear. Furthermore, there is no consensus on the choice of alveolar bone parameters and time points to evaluate LIP. Here, we investigated the dynamics of changes in osteoclastogenesis and bone volume (BV) loss in LIP over 14 days. Time-course analysis revealed that osteoclast induction peaked on days 3 and 5, followed by the peak of BV loss on day 7. Notably, BV was restored by day 14. The bone formation phase after the bone resorption phase was suggested to be responsible for the recovery of bone loss. Electron microscopy identified bacteria in the osteocyte lacunar space beyond the periodontal ligament (PDL) tissue. We investigated how osteocytes affect bone resorption of LIP and found that mice lacking receptor activator of NF-κB ligand (RANKL), predominantly in osteocytes, protected against bone loss in LIP, whereas recombination activating 1 (RAG1)-deficient mice failed to resist it. These results indicate that T/B cells are dispensable for osteoclast induction in LIP and that RANKL from osteocytes and mature osteoblasts regulates bone resorption by LIP. Remarkably, mice lacking the myeloid differentiation primary response gene 88 (MYD88) did not show protection against LIP-induced bone loss. Instead, osteocytic cells expressed nucleotide-binding oligomerization domain containing 1 (NOD1), and primary osteocytes induced significantly higher Rankl than primary osteoblasts when stimulated with a NOD1 agonist. Taken together, LIP induced both bone resorption and bone formation in a stage-dependent manner, suggesting that the selection of time points is critical for quantifying bone loss in mouse LIP. Pathogenetically, the current study suggests that bacterial activation of osteocytes via NOD1 is involved in the mechanism of osteoclastogenesis in LIP. The NOD1-RANKL axis in osteocytes may be a therapeutic target for bone resorption in periodontitis. © 2023 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).
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