ReviewCurrent drug metabolism2009
The potential of p38 MAPK inhibitors to modulate periodontal infections.
Review in Current drug metabolism, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 58 citations in OpenAlex.
- Inflammatory bone loss and signaling pathways in periodontitis: mechanistic insights and emerging therapeutic strategies.Bone research · 2026Review
- Progesterone-induced activation of progesterone receptor alleviates alveolar bone resorption and inflammatory response in periodontitis.Clinical oral investigations · 2025Article
- Exploring the toxicological effects of DOTP exposure on periodontitis by combining molecular docking and molecular dynamics simulations.Scientific reports · 2025Article
- Regulating periodontal disease with smart stimuli-responsive systems: Antimicrobial activity, immunomodulation, periodontium regeneration.Materials today. Bio · 2025Review
- Mitogen-Activated Protein Kinases (MAPKs) and Enteric Bacterial Pathogens: A Complex Interplay.International journal of molecular sciences · 2023Review
- Salivary irisin level is higher and related with interleukin-6 in generalized periodontitis.Clinical oral investigations · 2023Article
- A high-throughput, 28-day, microfluidic model of gingival tissue inflammation and recovery.Communications biology · 2023Article
- Article
- Transcriptome landscape comparison of periodontium in developmental and renewal stages.Frontiers in endocrinology · 2023Article
- The pathogenic mechanism of oral bacteria and treatment with inhibitors.Clinical and experimental dental research · 2022Review
- Shared Molecular Mechanisms between Alzheimer's Disease and Periodontitis Revealed by Transcriptomic Analysis.BioMed research international · 2021Article
- Pleckstrin Levels Are Increased in Patients with Chronic Periodontitis and RegulatedFrontiers in immunology · 2021Article
- Deep Learning Reveals Key Immunosuppression Genes and Distinct Immunotypes in Periodontitis.Frontiers in genetics · 2021Article
- Functionalized nanoparticles containing MKP-1 agonists reduce periodontal bone loss.Journal of periodontology · 2019Article
- Roles of Mitogen-Activated Protein Kinases in Osteoclast Biology.International journal of molecular sciences · 2018Review
- The LPS-inducible lncRNA Mirt2 is a negative regulator of inflammation.Nature communications · 2017Article
- Plumbagin suppresses chronic periodontitis in rats via down-regulation of TNF-α, IL-1β and IL-6 expression.Acta pharmacologica Sinica · 2017Article
- TLR4-induced NF-κB and MAPK signaling regulate the IL-6 mRNA stabilizing protein Arid5a.Nucleic acids research · 2017Article
- Synthesis and biological evaluation of Chromenylurea and Chromanylurea derivatives as anti-TNF-α agents that target the p38 MAPK pathway.Molecules (Basel, Switzerland) · 2014Article
- Anti-inflammatory effects of cordycepin in lipopolysaccharide-stimulated RAW 264.7 macrophages through Toll-like receptor 4-mediated suppression of mitogen-activated protein kinases and NF-κB signaling pathways.Drug design, development and therapy · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Periodontal disease initiation and progression occurs as a consequence of the host immune inflammatory response to oral pathogens. The innate and acquired immune systems are critical for the proper immune response. LPS, an outer membrane constituent of periodontal pathogenic bacteria, stimulates the production of inflammatory cytokines IL-1beta, TNFalpha, IL-6 and RANKL either directly or indirectly. In LPS-stimulated cells, the induction of cytokine expression requires activation of several signaling pathways including the p38 MAPK pathway. This review will discuss the significance of the p38 MAPK pathway in periodontal disease progression and the potential therapeutic consequences of pharmacological antagonism of this pathway in the treatment of periodontal diseases.
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What OpenQuestion holds
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.