ArticleJournal of dental research2023
Increased STAT3 Activation in Periodontitis Drives Inflammatory Bone Loss.
Article in Journal of dental research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Strontium-incorporated thermoresponsive hydrogel platform co-delivering graphene oxide-mannose nanocomplexes: An osteoimmunomodulatory strategy for periodontitis therapy.Materials today. Bio · 2026Article
- Article
- IL-6/STAT3-Mediated miR-181a-5p in Bone Marrow-Derived Mesenchymal Stem Cells Regulates Th17/Treg Balance in Experimental Periodontitis.International dental journal · 2026Article
- IL-22 synergizes with IL-17 to promote mucosal inflammation and bone loss.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Long Non-coding RNA TLX1NB Regulates Inflammatory Response in Periodontitis by Interacting With Matrix Metalloproteinase 8.Inflammation · 2026Article
- Interferon-JAK-STAT Axis in Bone Metabolism.Current osteoporosis reports · 2026Review
- Thyroid dysfunction alters gut microbiota composition and alveolar bone levels in female mice.Physiological reports · 2026Article
- Inflammatory bone loss and signaling pathways in periodontitis: mechanistic insights and emerging therapeutic strategies.Bone research · 2026Review
- NOX2 exacerbates periodontitis via JAK2-STAT3-mediated ferroptosis of gingival epithelial cells.Frontiers in immunology · 2026Article
- Transcriptional regulation of human follicular dendritic cell-secreted protein gene by interleukin-6.Odontology · 2025Article
- Annexin levels in GCF determine the imbalance of periodontal inflammatory regulation.Scientific reports · 2024Article
- Quantum graph embedding of transcription factor-gene networks reveals key modules in periodontal bone inflammation: Comparative analysis of GAE and GAN.Journal of oral biology and craniofacial researchArticle
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Authors and funding
11 authors.
Funding
Abstract
Periodontitis is one of the most prevalent human inflammatory diseases. It is characterized by periodontal tissue destruction, progressively driven by the host response. In this regard, cytokines associated with tissue destruction, such as interleukin (IL)-6 and IL-23, use a common signaling pathway mediated by STAT3. This transcription factor is also needed for IL-17A production, a key mediator in periodontitis pathogenesis. Although several studies have reported increased activation of STAT3 in experimental periodontitis, a detailed characterization of STAT3 activation in human gingival tissues and its involvement in alveolar bone loss has yet to be explored. Using a cross-sectional study design, we detected increased proportions of pSTAT3-positive cells during periodontitis compared with health, particularly in epithelial cells and T cells. Other cell types of hematopoietic and nonhematopoietic origin also display STAT3 activation in gingival tissues. We detected increased STAT3 phosphorylation and expression of STAT3-related genes during experimental periodontitis. Next, we evaluated the role of STAT3 in alveolar bone destruction using a mouse model of STAT3 loss of function (mut-
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