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The study used an orthodontic tooth movement model and an in vitro stretching model and found that tension activates glycolysis in periodontal ligament fibroblasts and increases H3K18la. CUT&Tag showed that H3K18la is enriched at the CXCL1 promoter, promoting CXCL1 expression. Inhibiting glycolysis can reduce H3K18la and CXCL1. CXCL1 enhances macrophage oxidative phosphorylation and promotes M2 polarization through CXCR2. In vivo, inhibiting glycolysis or blocking the CXCL1/CXCR2 axis disrupts the immune microenvironment and affects bone formation.
Results
Orthodontic tension induces glycolysis in periodontal ligament fibroblasts, leading to lactate accumulation and increased H3K18la. H3K18la is enriched at the CXCL1 promoter, upregulating CXCL1. CXCL1, through CXCR2, promotes macrophage oxidative phosphorylation and M2 polarization. In vivo, 3PO inhibits H3K18la and CXCL1, reduces CXCR2-positive macrophage infiltration, and suppresses bone formation. Cxcr2 knockout impairs M2 polarization and bone deposition on the tension side. These results indicate that the glycolysis-H3K18la-CXCL1 axis helps shape a pro-resorption immune microenvironment and promotes alveolar bone formation.
Original Source:
Journal of Advanced Research
Pub Date: 2026-10-01
DOI: 10.1016/j.jare.2026.01.012
Yan Zhang, Chong Chen, Chibuike C. Udenigwe, Zhaojun Zheng, Yuanfa Liu
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