ArticleLasers in medical science2026
Exploring the effect of Er, Cr: YSGG laser combined with GBR on osteogenesis at extraction sockets in rats with severe periodontitis via the Wnt/β-catenin pathway.
Article in Lasers in medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Alveolar bone defects following tooth extraction in severe periodontitis pose significant clinical challenges. This study evaluates the synergistic osteogenic effect of Er, Cr: YSGG laser combined with guided bone regeneration (GBR) in rat extraction sockets and explores the underlying Wnt/β-catenin pathway mechanism. Fifty Sprague-Dawley rats were randomized into five groups (n = 10/group): Control (extraction only), Laser (Er, Cr: YSGG laser irradiation only), GBR (Bio-Oss bone graft + barrier membrane), Laser+Bone Graft (laser irradiation + Bio-Oss without membrane), and Laser + GBR (laser irradiation + Bio-Oss + barrier membrane). At 4 and 8 weeks post-operation, CBCT quantified bone volume fraction (BV/TV) and bone mineral density (BMD). Histological staining was used to evaluate new bone formation. ELISA and qPCR analyzed osteogenic markers (β-catenin, Runx2, BMP-2) and the Wnt pathway inhibitor (DKK-1). MSD assays quantified β-catenin nuclear translocation and the p-GSK-3β/GSK-3β ratio to assess pathway activation. The Laser + GBR group demonstrated the highest BV/TV and BMD at 8 weeks, with complete scaffold degradation, dense trabeculae, and minimal inflammatory infiltration on histology. ELISA and qPCR confirmed the highest expression of β-catenin, Runx2, and BMP-2 alongside the lowest DKK-1 levels in this group at both time points. MSD detection revealed the highest β-catenin nuclear translocation rate and the lowest p-GSK-3β/GSK-3β ratio, indicating robust Wnt/β-catenin pathway activation. Er, Cr: YSGG laser synergizes with GBR to enhance alveolar bone regeneration, likely by suppressing DKK-1, inhibiting GSK-3β activity, and promoting β-catenin nuclear translocation, thereby activating the Wnt/β-catenin pathway and upregulating downstream osteogenic genes. This combination represents a promising strategy for post-extraction bone defect repair.Clinical Trial Number: Not applicable.
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