ArticleJournal of clinical periodontology2013
Differential expression of mitogen activating protein kinases in periodontitis.
Article in Journal of clinical periodontology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Effects of P38 MAPK Pathway Inhibition on the Metabolism of Periodontal Ligament Fibroblasts During Inflammation.Journal of cellular and molecular medicine · 2026Article
- Article
- Senescent CD4International journal of molecular sciences · 2022Review
- Detection of Salivary miRNAs That Predict Chronic Periodontitis Progression: A Cohort Study.International journal of environmental research and public health · 2021Article
- Silencing matrix metalloproteinase-13 (Mmp-13) reduces inflammatory bone resorption associated with LPS-induced periodontal disease in vivo.Clinical oral investigations · 2021Article
- Functionalized nanoparticles containing MKP-1 agonists reduce periodontal bone loss.Journal of periodontology · 2019Article
- Detection of Salivary miRNAs Reflecting Chronic Periodontitis: A Pilot Study.Molecules (Basel, Switzerland) · 2019Article
- Current Status of Proteomic Technologies for Discovering and Identifying Gingival Crevicular Fluid Biomarkers for Periodontal Disease.International journal of molecular sciences · 2018Review
- A new albumin-depletion strategy improves proteomic research of gingival crevicular fluid from periodontitis patients.Clinical oral investigations · 2018Article
- Article
- Increased visfatin expression is associated with nuclear factor-kappa B and phosphatidylinositol 3-kinase in periodontal inflammation.Clinical oral investigations · 2017Article
- Mitogen-Activated Protein Kinase 2 Signaling Shapes Macrophage Plasticity in Aggregatibacter actinomycetemcomitans-Induced Bone Loss.Infection and immunity · 2017Article
- Mini but mighty: microRNAs in the pathobiology of periodontal disease.Periodontology 2000 · 2015Review
- Critical role of MKP-1 in lipopolysaccharide-induced osteoclast formation through CXCL1 and CXCL2.Cytokine · 2015Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
aimFollowing toll-like receptor (TLR) engagement, lipopolysaccharide (LPS) can stimulate the expression of pro-inflammatory cytokines thus activating the innate immune response. The production of inflammatory cytokines results, in part, from the activation of kinase-induced signalling cascades and transcriptional factors. Of the four distinct classes of mitogen-activated protein kinases (MAPK) described in mammals, p38, c-Jun N-terminal activated kinases (JNK1-3) and extracellular activated kinases (ERK1,2) are the best studied. Previous data have established that p38 MAPK signalling is required for inflammation and bone loss in periodontal disease pre-clinical animal models. MATERIALS &
methodsIn this study, we obtained healthy and diseased periodontal tissues along with clinical parameters and microbiological parameters. Excised fixed tissues were immunostained with total and phospho-specific antibodies against p38, JNK and ERK kinases.
resultsIntensity scoring from immunostained tissues was correlated with clinical periodontal parameters. Rank correlations with clinical indices were statistically significantly positive (p-value < 0.05) for total p38 (correlations ranging 0.49-0.68), phospho-p38 (range 0.44-0.56), and total ERK (range 0.52-0.59) levels, and correlations with JNK levels also supported association (range 0.42-0.59). Phospho-JNK and phospho-ERK showed no significant positive correlation with clinical parameters of disease.
conclusionThese data strongly implicate p38 MAPK as a major MAPK involved in human periodontal inflammation and severity.
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