ArticleThe American journal of pathology2006
B and T lymphocytes are the primary sources of RANKL in the bone resorptive lesion of periodontal disease.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 256 papers.
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Who cites it
256 citing papers in PubMed, 553 citations in OpenAlex.
- Trial
- Critical role of AKT protein in myeloma-induced osteoclast formation and osteolysis.The Journal of biological chemistry · 2013Trial
- Osteoprotegerin and receptor activator of NF-kappaB ligand as biomarkers for bone resorption-related disorders.World journal of experimental medicine · 2026Review
- LPS-Induced TNF-α and IL-1 Signaling in Periodontitis: Molecular Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Targeting IFN-I driven tertiary lymphoid structures halts B cell-mediated bone loss in periodontitis.International journal of oral science · 2026Article
- Interleukin-38 promotes alveolar bone repair in periodontitis by suppressing the nuclear factor kappa B pathway.Stem cell research & therapy · 2026Article
- Hijacking the bone niche: mechanistic insights into bone metastasis in breast cancer.Bone research · 2026Review
- Myeloid-Derived Grancalcin Promotes Periodontal Inflammation and Pathological Bone Remodeling in Periodontitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- EBV promotes alveolar trabecula resorption via extracellular vesicle remodeling by group IIA secreted phospholipase AJournal of lipid research · 2026Article
- Cell signaling and transcriptional regulation of osteoclast lineage commitment, differentiation, bone resorption and diseases.Cell discovery · 2026Review
- Osteoporosis After Menopause and After Drug Therapy: The Molecular Mechanism of Bone Loss and Its Treatment.International journal of molecular sciences · 2026Review
- MMPs at Work: Deciphering Their Role in the Cellular Mechanisms of Orthodontic Tooth Movement.International journal of molecular sciences · 2026Review
- Removal of CD5 on T cells alters their differentiation and cytokine production in anFrontiers in immunology · 2026Article
- Periodontitis and systemic diseases: insights into the correlation, mechanisms, and clinical implications.Frontiers in immunology · 2026Review
- Type H Vessels Are Progressively Lost in a Mouse Model of Periodontitis: A 3D Tissue-clearing Analysis of Alveolar Bone.Operative dentistry, endodontology and periodontology · 2025Article
- Diminished osteoprotegerin production by gingival fibroblasts from periodontitis patients is associated with their reduced ability to suppress osteoclastogenesis.Scientific reports · 2025Article
- Chronic stress and the IL-10-mediated immunoregulatory loop in the pathogenesis of periodontitis.Clinical science (London, England : 1979) · 2025Review
- Unraveling the mechanisms of bone diseases: targeting dendritic cells in osteoimmunology for internal homeostasis balance.Bone research · 2025Review
- Bone marrow neutrophil progenitors suppress osteoclast formation in murine cortical and trabecular bone.Blood · 2025Article
196 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
Receptor activator of nuclear factor-kappaB (RANKL)-mediated osteoclastogenesis plays a pivotal role in inflammatory bone resorption. The aim of this study was to identify the cellular source of RANKL in the bone resorptive lesions of periodontal disease. The concentrations of soluble RANKL, but not its decoy receptor osteoprotegerin, measured in diseased tissue homogenates were significantly higher in diseased gingival tissues than in healthy tissues. Double-color confocal microscopic analyses demonstrated less than 20% of both B cells and T cells expressing RANKL in healthy gingival tissues. By contrast, in the abundant mononuclear cells composed of 45% T cells, 50% B cells, and 5% monocytes in diseased gingival tissues, more than 50 and 90% of T cells and B cells, respectively, expressed RANKL. RANKL production by nonlymphoid cells was not distinctly identified. Lymphocytes isolated from gingival tissues of patients induced differentiation of mature osteoclast cells in a RANKL-dependent manner in vitro. However, similarly isolated peripheral blood B and T cells did not induce osteoclast differentiation, unless they were activated in vitro to express RANKL; emphasizing the osteoclastogenic potential of activated RANKL-expressing lymphocytes in periodontal disease tissue. These results suggest that activated T and B cells can be the cellular source of RANKL for bone resorption in periodontal diseased gingival tissue.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.