ArticleMediators of inflammation2014
LPS from P. gingivalis and hypoxia increases oxidative stress in periodontal ligament fibroblasts and contributes to periodontitis.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 147 citations in OpenAlex.
- Immunoproteomic insights into inflammatory diseases of the critically endangered black rhinoceros (Diceros bicornis).Scientific reports · 2026Article
- The Hypoxostat Model: A Conceptual Framework Linking Hypoxia, Oxidative Stress and Periodontal Breakdown Under Orthodontic Load.Antioxidants (Basel, Switzerland) · 2026Article
- Yoda1-activated Piezo1 enhances mitophagy in human gingival fibroblasts to promote maxillofacial wound repair.Frontiers in pharmacology · 2026Article
- N-acetylcysteine restores osteogenesis in human periodontal ligament stem cells by attenuating HIF-1α-driven oxidative stress and glycolytic reprogramming.Journal of dental sciences · 2026Article
- Interaction between methylated arginine metabolites and oxidative stress in periodontitis: a cross-sectional study.BMC oral health · 2025Observational
- The Role of Reactive Oxygen Species (ROS) in Periodontitis: A Potential Therapeutic Target.Immunity, inflammation and disease · 2025Review
- LOR Regulated by METTL3 Alleviates Lipopolysaccharides-Induced Periodontitis Injury.Journal of microbiology and biotechnology · 2025Article
- Activation of the Nrf2 Signaling Pathway as a Therapeutic Strategy Against Periodontal Disease: A Narrative Review.Dentistry journal · 2025Review
- Article
- Clinical Response Characteristics of Salivary Proteins in the Management Strategy of Diabetes-Associated Periodontitis.Journal of proteome research · 2025Article
- Review
- Role of periodontal ligament fibroblasts in periodontitis: pathological mechanisms and therapeutic potential.Journal of translational medicine · 2024Review
- Investigation of Oxidative-Stress Impact on Human Osteoblasts During Orthodontic Tooth Movement Using an In Vitro Tension Model.International journal of molecular sciences · 2024Article
- Deciphering 3D periodontal fibroblast-macrophage crosstalk in bioactive nanoparticle-guided immunomodulation for treating traumatic dental avulsion.Bioactive materials · 2024Article
- Modulation of NRF2/KEAP1 Signaling by Phytotherapeutics in Periodontitis.Antioxidants (Basel, Switzerland) · 2024Review
- The Impact of a Topical Oxygen-Releasing Gel (blueMedicina (Kaunas, Lithuania) · 2024Article
- International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis.Autophagy · 2024Review
- Therapeutic Effects of Hinokitiol through Regulating the SIRT1/NOX4 against Ligature-Induced Experimental Periodontitis.Antioxidants (Basel, Switzerland) · 2024Article
- Er:YAG laser suppresses pro-inflammatory cytokines expression and inflammasome in human periodontal ligament fibroblasts with Porphyromonas gingivalis-lipopolysaccharide stimulation.Journal of dental sciences · 2024Article
- Cytokines in gingivitis and periodontitis: from pathogenesis to therapeutic targets.Frontiers in immunology · 2024Review
13 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress is characterized by an accumulation of reactive oxygen species (ROS) and plays a key role in the progression of inflammatory diseases. We hypothesize that hypoxic and inflammatory events induce oxidative stress in the periodontal ligament (PDL) by activating NOX4. Human primary PDL fibroblasts were stimulated with lipopolysaccharide from Porphyromonas gingivalis (LPS-PG), a periodontal pathogen bacterium under normoxic and hypoxic conditions. By quantitative PCR, immunoblot, immunostaining, and a specific ROS assay we determined the amount of NOX4, ROS, and several redox systems. Healthy and inflamed periodontal tissues were collected to evaluate NOX4 and redox systems by immunohistochemistry. We found significantly increased NOX4 levels after hypoxic or inflammatory stimulation in PDL cells (P < 0.001) which was even more pronounced after combination of the stimuli. This was accompanied by a significant upregulation of ROS and catalase (P < 0.001). However, prolonged incubation with both stimuli induced a reduction of catalase indicating a collapse of the protective machinery favoring ROS increase and the progression of inflammatory oral diseases. Analysis of inflamed tissues confirmed our hypothesis. In conclusion, we demonstrated that the interplay of NOX4 and redox systems is crucial for ROS formation which plays a pivotal role during oral diseases.
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