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Войти в исследования Journal of endodontics · 2026
The Frontiers of Orthodontically Induced Inflammatory Root Resorption: Mechanism, Treatment, and Future Prospects.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Lin Xinping, Chen Sihang, Cai Jiayi, Cai Jingwen, Chen Linxin, Chen Zhonghan, Huang Pengcheng, Chen Zongfei, Cai Senxin, Xu Linyu, Wang Han
Аннотация
INTRODUCTION: Orthodontically induced inflammatory root resorption (OIIRR) is a frequent complication of orthodontic treatment, featured by sterile inflammatory destruction of root hard tissues, which arises from the crosstalk between biomechanical forces and molecular pathways in the periodontal microenvironment.
METHODS: A literature review was conducted to analyze the key mechanisms, biomarkers, and potential interventions involved in OIIRR.
RESULTS: Multiple factors contribute to OIIRR, including inflammatory signaling (interleukin [IL]-6, IL-1β, IL-18), mechanotransduction (Piezo1, sphingosine-1-phosphate), intercellular communication, dysregulated osteogenic pathways (Wnt/β-catenin, EphB4/ephrinB2), programmed cell death, mitochondrial dysfunction, autophagy, and noncoding RNAs, all of which promote osteoclast differentiation. Gingival crevicular fluid biomarkers are used for prediction, while anti-inflammatory agents, low-intensity pulsed ultrasound, laser therapy and bioactive substances are under investigation. Mild to moderate OIIRR has no impact on tooth survival, and endodontically treated teeth show less OIIRR due to the elimination of pulp-derived pro-resorptive signals.
CONCLUSIONS: The complex network of signaling and cellular processes governs OIIRR progression. Biomarkers, targeted therapies and endodontic management provide effective strategies for the clinical control of OIIRR.
METHODS: A literature review was conducted to analyze the key mechanisms, biomarkers, and potential interventions involved in OIIRR.
RESULTS: Multiple factors contribute to OIIRR, including inflammatory signaling (interleukin [IL]-6, IL-1β, IL-18), mechanotransduction (Piezo1, sphingosine-1-phosphate), intercellular communication, dysregulated osteogenic pathways (Wnt/β-catenin, EphB4/ephrinB2), programmed cell death, mitochondrial dysfunction, autophagy, and noncoding RNAs, all of which promote osteoclast differentiation. Gingival crevicular fluid biomarkers are used for prediction, while anti-inflammatory agents, low-intensity pulsed ultrasound, laser therapy and bioactive substances are under investigation. Mild to moderate OIIRR has no impact on tooth survival, and endodontically treated teeth show less OIIRR due to the elimination of pulp-derived pro-resorptive signals.
CONCLUSIONS: The complex network of signaling and cellular processes governs OIIRR progression. Biomarkers, targeted therapies and endodontic management provide effective strategies for the clinical control of OIIRR.