ArticleOral diseases2026
Th17/IL-17A Drives Alveolar Bone Loss via the JAK/STAT3-RANKL Axis in the Periodontal Ligament.
Article in Oral diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Recent Advances in Microenvironment-Responsive Materials for Periodontitis Therapy.International journal of molecular sciences · 2026Review
- The Osteoimmune Axis: Immune-Mechanical Crosstalk in Periodontal Bone Remodeling.Biomolecules · 2026Article
- MicroRNAs in periodontal disease: from pathogenic mechanisms and RANKL/OPG regulation to nanoparticle delivery and personalized medicine.Frontiers in immunology · 2026Review
- RANKL-convergent osteoimmune network framework in osteoporosis: integrating macrophage activation, T-cell imbalance, and cytokine crosstalk.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
objectivesTh17 cells play a critical role in alveolar bone loss, which is closely associated with osteoclast maturation during periodontitis. Previous studies have established that periodontal ligament cells (PDLCs) are a significant source of receptor activator of nuclear factor-κB ligand (RANKL), a pivotal osteoclast-inducing cytokine. However, the mechanisms by which IL-17A promotes osteoclast activation via the PDL-mediated pathways are poorly understood. This study investigates how IL-17A promotes RANKL production in PDLCs and evaluates the therapeutic potential of targeting the JAK/STAT3 pathway in periodontitis.
methodsA ligature-induced periodontitis (LIP) model was established and alveolar bone loss was assessed using micro-CT and TRAP staining. The molecular mechanisms were investigated using bioinformatic analysis, western blotting, and immunohistochemistry. The efficacy of anti-IL-17A (αIL-17A) and tofacitinib in inhibiting alveolar bone loss was evaluated through intraperitoneal injection.
resultsRANKL was predominantly expressed in the PDL during periodontitis. IL-17A enhanced osteoclast activity in RAW264.7 cells co-cultured with PDLCs. IL-17A upregulated RANKL expression in PDLCs through STAT3 activation. Tofacitinib significantly inhibited alveolar bone loss by suppressing Th17 cell differentiation and osteoclast activation.
conclusionsIL-17A promoted RANKL expression through JAK/STAT3 activation in PDLCs. Tofacitinib, a clinically available JAK inhibitor, significantly attenuated alveolar bone loss in periodontitis.
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