ArticleJournal of signal transduction2012
MAPK usage in periodontal disease progression.
Article in Journal of signal transduction, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 59 citations in OpenAlex.
- Non-Invasive Physical Plasma Regulates COX-2 via EP2/EP4 Expression in Periodontal Ligament Cells Under Inflammatory Conditions.International journal of molecular sciences · 2026Article
- Mechanistic insights into anti-parkinson effect of baicalein: from neuroinflammation and cell death to neurogenesis and synaptic plasticity.Molecular biology reports · 2026Review
- Effects of P38 MAPK Pathway Inhibition on the Metabolism of Periodontal Ligament Fibroblasts During Inflammation.Journal of cellular and molecular medicine · 2026Article
- Inflammatory bone loss and signaling pathways in periodontitis: mechanistic insights and emerging therapeutic strategies.Bone research · 2026Review
- Smart Nanogel Systems for Periodontitis Management: A Review of Microenvironment-Targeted Therapies.International journal of nanomedicine · 2026Review
- Effects of Zanthoxyli Pericarpium Extracts on Ligature-Induced Periodontitis and Alveolar Bone Loss in Rats.Antioxidants (Basel, Switzerland) · 2025Article
- Featured Immune Characteristics of Periodontitis and Primary Sjögren's Syndrome Revealed by Single-Cell Transcriptome Analyses.Journal of cellular and molecular medicine · 2025Article
- Article
- Exploring the role of oral bacteria in oral cancer: a narrative review.Discover oncology · 2025Review
- Multi-dimensional role of AGEs in periodontitis: from matrix remodeling to neuro-immune crosstalk.Frontiers in immunology · 2025Review
- SARS-CoV-2, periodontal pathogens, and host factors: The trinity of oral post-acute sequelae of COVID-19.Reviews in medical virology · 2024Review
- Dexamethasone Suppresses IL-33-exacerbated Malignant Phenotype of U87MG Glioblastoma CellsAnti-cancer agents in medicinal chemistry · 2024Article
- Genomic DNA Extracted fromFood science of animal resources · 2023Article
- Sequential anti-inflammatory and osteogenic effects of a dual drug delivery scaffold loaded with parthenolide and naringin in periodontitis.Journal of periodontal & implant science · 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
- Therapeutic and Metagenomic Potential of the Biomolecular Therapies against Periodontitis and the Oral Microbiome: Current Evidence and Future Perspectives.International journal of molecular sciences · 2022Review
- 7-Ketocholesterol-Induced Micro-RNA-107-5p Increases Number and Activity of Osteoclasts by Targeting MKP1.International journal of molecular sciences · 2022Article
- Evaluation of the protective effects of non-thermal atmospheric plasma on alveolar bone loss in experimental periodontitis.Clinical oral investigations · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
In periodontal disease, host recognition of bacterial constituents, including lipopolysaccharide (LPS), induces p38 MAPK activation and subsequent inflammatory cytokine expression, favoring osteoclastogenesis and increased net bone resorption in the local periodontal environment. In this paper, we discuss evidence that the p38/MAPK-activated protein kinase-2 (MK2) signaling axis is needed for periodontal disease progression: an orally administered p38α inhibitor reduced the progression of experimental periodontal bone loss by reducing inflammation and cytokine expression. Subsequently, the significance of p38 signaling was confirmed with RNA interference to attenuate MK2-reduced cytokine expression and LPS-induced alveolar bone loss. MAPK phosphatase-1 (MKP-1), a negative regulator of MAPK activation, was also critical for periodontal disease progression. In MPK-1-deficient mice, p38-sustained activation increased osteoclast formation and bone loss, whereas MKP-1 overexpression dampened p38 signaling and subsequent cytokine expression. Finally, overexpression of the p38/MK2 target RNA-binding tristetraprolin (TTP) decreased mRNA stability of key inflammatory cytokines at the posttranscriptional level, thereby protecting against periodontal inflammation. Collectively, these studies highlight the importance of p38 MAPK signaling in immune cytokine production and periodontal disease progression.
Identifiers
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.