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The frontiers of orthodontically induced inflammatory root resorption: mechanism, treatment, and future prospects
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DOI：10.1016/j.joen.2026.06.005.png)
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Abstract
En 中文
Orthodontically induced inflammatory root resorption (OIIRR) is a common complication of orthodontic therapy, characterized by sterile inflammatory degradation of dental hard tissues on the root surface. Its pathogenesis involves complex interplay of biomechanical forces and molecular pathways within the periodontal microenvironment. Key mechanisms include inflammatory signaling via IL-6, IL-1β, and IL-18, mechanotransduction through Piezo1 and sphingosine-1-phosphate (S1P), cell-to-cell communication via exosomes and ligand-receptor interactions, and disruptions in osteogenic pathways including Wnt/β-catenin and EphB4/ephrinB2. Programmed cell death (pyroptosis, ferroptosis), mitochondrial dysfunction, autophagy, and post-transcriptional regulation by non-coding RNAs further contribute to osteoclast differentiation. Current predictive strategies focus on biomarkers in gingival crevicular fluid (GCF). Therapeutic interventions under investigation include anti-inflammatory agents, low-intensity pulsed ultrasound, laser and photobiomodulation (PBM) therapy, and bioactive substances such as lithium chloride (LiCl), exosomes, and intermittent parathyroid hormone (iPTH). Prognostically, mild to moderate OIIRR rarely compromises long-term tooth survival, whereas severe resorption requires individualized risk assessment. Notably, endodontically treated teeth exhibit significantly less OIIRR than vital pulp teeth, as root canal therapy eliminates pulp-derived pro-resorptive signaling (CH25H/25-HC, NF-κB, MMPs), offering a clinically relevant strategy for high-risk cases. This review synthesizes current knowledge on OIIRR mechanisms and emerging treatments, providing a framework for prevention and targeted therapy.
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