ArticleJournal of clinical periodontology2018
Osteocytes play an important role in experimental periodontitis in healthy and diabetic mice through expression of RANKL.
Article in Journal of clinical periodontology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 73 citations in OpenAlex.
- Insights into taurine therapy for periodontitis: Targeting osteocyte ferroptosis to mitigate obesity-exacerbated bone damage.Redox biology · 2026Article
- Periodontitis Induces B Cell-Macrophage Crosstalk to Exacerbate Glucose Dysregulation in Obesity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Role of Cytokines in Bone Diseases and Their Therapeutic Application.ImmunoTargets and therapy · 2026Review
- Mitochondrial dysfunction as a key player in aggravating periodontitis among diabetic patients: review of the current scope of knowledge.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Role of Masticatory Force in Modulating Jawbone Immunity and Bone Homeostasis: A Review.International journal of molecular sciences · 2025Review
- Oral cell lysates reduce osteoclastogenesis in murine bone marrow cultures.Cytotechnology · 2025Article
- Panax notoginseng saponins alleviate alveolar bone loss and reprogram macrophages in diabetic periodontitis rats.Journal of applied oral science : revista FOB · 2025Article
- Connection between oral health and chronic diseases.MedComm · 2025Review
- Inflammation and mechanical force-induced bone remodeling.Periodontology 2000 · 2024Review
- Gingival fibroblasts produce paracrine signals that affect osteoclastogenesis in vitro.Bone reports · 2024Article
- An update on periodontal inflammation and bone loss.Frontiers in immunology · 2024Review
- Inflammatory Processes Affecting Bone Health and Repair.Current osteoporosis reports · 2023Review
- Ageing and Inflammation: What Happens in Periodontium?Bioengineering (Basel, Switzerland) · 2023Review
- Interleukin-22 Inhibits Apoptosis of Gingival Epithelial Cells Through TGF-β Signaling Pathway During Periodontitis.Inflammation · 2023Article
- Osteocyte RANKL Drives Bone Resorption in Mouse Ligature-Induced Periodontitis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Regulation of the Osteocyte Secretome with Aging and Disease.Calcified tissue international · 2023Review
- Resveratrol Alleviates Diabetic Periodontitis-Induced Alveolar Osteocyte Ferroptosis Possibly via Regulation of SLC7A11/GPX4.Nutrients · 2023Article
- Osteoimmunology in Periodontitis and Orthodontic Tooth Movement.Current osteoporosis reports · 2023Review
- Type 1 diabetes mellitus leads to gingivitis and an early compensatory increase in bone remodeling.Journal of periodontology · 2023Article
- Diabetes mellitus promotes susceptibility to periodontitis-novel insight into the molecular mechanisms.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 4 countries.
Funding
Abstract
aimPeriodontitis results from bacteria-induced inflammation. A key cytokine, RANKL, is produced by a number of cell types. The cellular source of RANKL critical for periodontitis has not been established.
methodsWe induced periodontal bone loss by oral inoculation of Porphyromonas gingivalis and Fusobacterium nucleatum in both normoglycaemic and streptozotocin-induced type 1 diabetic mice. Experimental transgenic mice had osteocyte-specific deletion of floxed receptor activator of nuclear factor kappa-B ligand (RANKL) mediated by DMP-1-driven Cre recombinase. Outcomes were assessed by micro-CT, histomorphometric analysis, immunofluorescent analysis of RANKL and tartrate-resistant acid phosphatase staining for osteoclasts and osteoclast activity.
resultsOral infection stimulated RANKL expression in osteocytes of wild-type mice, which was increased by diabetes and blocked in transgenic mice. Infected wild-type mice had significant bone loss and increased osteoclast numbers and activity, which were further enhanced by diabetes. No bone loss or increase in osteoclastogenesis or activity was detected in transgenic mice with RANKL deletion in osteocytes that were normoglycaemic or diabetic.
conclusionsThis study demonstrates for the first time the essential role of osteocytes in bacteria-induced periodontal bone loss and in diabetes-enhanced periodontitis.
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