ReviewJournal of oral biosciences2020
Osteoclastogenesis in periodontal diseases: Possible mediators and mechanisms.
Review in Journal of oral biosciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
49 citing papers in PubMed, 90 citations in OpenAlex.
- MPRO3 Regulates Macrophage Polarization and OsteoclastogenesisJournal of microbiology and biotechnology · 2026Article
- Article
- LincRNA-EPS alleviates osteoclastogenesis under inflammatory microenvironment through preventing excessive iron metabolism.Cell death & disease · 2026Article
- Porphyromonas gingivalis-Derived Virulence Lipids Accelerate Osteoclastogenesis Independently of High Mobility Group Box Protein-1 Canonical Signaling.Molecular oral microbiology · 2026Article
- Bone and Infections: An Osteoimmunological Interplay.International journal of molecular sciences · 2026Review
- Impact of smoking and periodontitis on salivary IL-39, IL-41, IL-1β, and TNF-α levels: a cross-sectional analysis.BMC oral health · 2026Article
- Inflammatory bone loss and signaling pathways in periodontitis: mechanistic insights and emerging therapeutic strategies.Bone research · 2026Review
- Toll-like receptor engaged in activation and osteoimmuno-cytokines production by unswitched memory B cells during periodontitis.Odontology · 2026Article
- Generation of osteoclast-like cells from human peripheral blood mononuclear cells using NFATc1 modified RNA.PloS one · 2026Article
- Article
- GWAS for Periodontitis Phenotypes Using Multi-Ancestry All of Us Research Platform.medRxiv : the preprint server for health sciences · 2025Article
- Postbiotics Derived fromNutrients · 2025Article
- An Off-the-Shelf Artificial Blood Clot Hydrogel Neutralizing Multiple Proinflammatory Mediators for Pro-Regenerative Periodontitis Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Effect of natural compounds on NRF2/KEAP1 signaling in periodontitis: a potential use to prevent age-related disorders.Molecular biology reports · 2025Review
- Therapeutic Potential of Tanshinones in Osteolytic Diseases: From Molecular and Cellular Pathways to Preclinical Models.Dentistry journal · 2025Review
- Regulating periodontal disease with smart stimuli-responsive systems: Antimicrobial activity, immunomodulation, periodontium regeneration.Materials today. Bio · 2025Review
- Emerging therapeutic strategies targeting bone signaling pathways in periodontitis.Journal of periodontal research · 2025Review
- Article
- Oral biofluid levels of Activin-A and interleukin-1beta in stage III periodontitis.Clinical oral investigations · 2024Article
- The Effect of the Root Bark ofAntioxidants (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundPeriodontitis is the inflammation of the tooth-supporting structures and is one of the most common diseases of the oral cavity. The outcome of periodontal infections is tooth loss due to a lack of alveolar bone support. Osteoclasts are giant, multi-nucleated, and bone-resorbing cells that are central for many osteolytic diseases, including periodontitis. Receptor activator of nuclear factor-kB ligand (RANKL) is the principal factor involved in osteoclast differentiation, activation, and survival. However, under pathological conditions, a variety of pro-inflammatory cytokines secreted by activated immune cells also contribute to osteoclast differentiation and activity. Lipopolysaccharide (LPS) is a vital component of the outer membrane of the Gram-negative bacteria. It binds to the Toll-like receptors (TLRs) expressed in many cells and elicits an immune response. HIGHLIGHTS: The presence of bacterial LPS in the periodontal area stimulates the secretion of RANKL as well as other inflammatory mediators, activating the process of osteoclastogenesis. RANKL, either independently or synergistically with LPS, can regulate osteoclastogenesis, while LPS alone cannot. MicroRNA, IL-22, M1/M2 macrophages, and memory B cells have recently been shown to modulate osteoclastogenesis in periodontal diseases.
conclusionIn this review, we summarize the mechanism of osteoclastogenesis accompanying periodontal diseases at the cellular level. We discuss a) the effects of LPS/TLR signaling and other cytokines on RANKL-dependent and -independent mechanisms involved in osteoclastogenesis; b) the recently identified role of several endogenous factors such as miRNA, IL-22, M1/M2 macrophages, and memory B cells in regulating osteoclastogenesis during periodontal pathogenesis.
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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.