ArticleGeroScience2021
Contribution of Porphyromonas gingivalis lipopolysaccharide to experimental periodontitis in relation to aging.
Article in GeroScience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 44 citations in OpenAlex.
- The Role ofAntibiotics (Basel, Switzerland) · 2026Review
- Immunosenescence and Bone Homeostasis: From Mechanisms of Homeostasis Disruption to Therapeutic Opportunities in Age-Related Skeletal Disorders.International journal of molecular sciences · 2026Review
- Porphyromonas gingivalis-Derived Virulence Lipids Accelerate Osteoclastogenesis Independently of High Mobility Group Box Protein-1 Canonical Signaling.Molecular oral microbiology · 2026Article
- Modulation of the Immune-Inflammatory Microenvironment by Implant Material Properties in Peri-Implantitis.International journal of molecular sciences · 2026Review
- Porphyromonas gingivalis-derived extracellular vesicles aggravate bone destruction in rheumatoid arthritis by promoting Syk-dependent osteoclastogenesis.International journal of oral science · 2026Article
- Article
- Hyperfunctional Neutrophils in Aged Mice Are Linked to Enhanced Bone Loss in Ligature-Induced Periodontitis.Dentistry journal · 2025Article
- Platr3/NUDT21/NF-κB Axis Mediates P. gingivalis-Suppressed Cementoblast Mineralization.Inflammation · 2025Article
- [Research Advances in the Replication of Animal Models for Periodontal Diseases].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Review
- Associations between immune-inflammatory markers, age, and periodontal status: a cross-sectional study.Odontology · 2024Article
- Proteomic analysis of P. gingivalis-Lipopolysaccharide induced neuroinflammation in SH-SY5Y and HMC3 cells.GeroScience · 2024Article
- Experimental models for peri-implant diseases: a narrative review.Clinical oral investigations · 2024Review
- Effects of IL-34 and anti-IL-34 neutralizing mAb on alveolar bone loss in a ligature-induced model of periodontitis.Molecular oral microbiology · 2024Article
- Article
- Osteoclasts and osteoarthritis: Novel intervention targets and therapeutic potentials during aging.Aging cell · 2024Review
- Recent Clinical Treatment and Basic Research on the Alveolar Bone.Biomedicines · 2023Review
- [The Relationship Between Oral Microbiota and Chronic Obstructive Pulmonary Disease].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Review
- A GP130-Targeting Small Molecule, LMT-28, Reduces LPS-Induced Bone Resorption around Implants in Diabetic Models by Inhibiting IL-6/GP130/JAK2/STAT3 Signaling.Mediators of inflammation · 2023Article
- Article
- Hsa_circ_0099630 knockdown induces the proliferation and osteogenic differentiation and attenuates the apoptosis of porphyromonas gingivalis lipopolysaccharide-induced human periodontal ligament fibroblasts.Annals of translational medicine · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Aging is associated with increased prevalence and severity of pathogenic outcomes of periodontal disease, including soft tissue degeneration and bone loss around the teeth. Although lipopolysaccharide (LPS) derived from the key periodontal pathogen Porphyromonas gingivalis (Pg) plays an important role in the promotion of inflammation and osteoclastogenesis via toll-like receptor (TLR)4 signaling, its pathophysiological role in age-associated periodontitis remains unclear. This study investigated the possible effects of Pg-LPS on RANKL-primed osteoclastogenesis and ligature-induced periodontitis in relation to aging using young (2 months old) and aged (24 months old) mice. To the best of our knowledge, our results indicated that expression of TLR4 was significantly diminished on the surface of osteoclast precursors isolated from aged mice compared with that of young mice. Furthermore, our data demonstrated that the TLR4 antagonist (TAK242) dramatically decreased the numbers of tartrate-resistant acid phosphatase positive (TRAP+) osteoclasts differentiated from RANKL-primed young osteoclast precursors (OCPs) compared with those isolated from aged mice in response to Pg-LPS. In addition, using a ligature-induced periodontitis mouse model, we demonstrated that Pg-LPS elevated (1) secretion of senescence-associated secretory phenotype (SASP) markers, including the pro-inflammatory cytokines TNF-α, IL-6, and IL-1β, as well as osteoclastogenic RANKL, and (2) the number of OCPs and TRAP+ osteoclasts in the periodontal lesion induced in young mice. In contrast, Pg-LPS had little, or no, effect on the promotion of periodontitis inflammation induced in aged mice. Altogether, these results indicated that periodontal disease in older mice occurs in a manner independent of canonical signaling elicited by the Pg-LPS/TLR4 axis.
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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.