ReviewInternational journal of molecular sciences2024
The Potential Regulatory Role of Ferroptosis in Orthodontically Induced Inflammatory Root Resorption.
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- PGE2 regulates ferroptosis and osteogenesis of MC3T3-E1 cells via NOS2.Scientific reports · 2026Article
- Cell Death in Orthodontic Tooth Movement: Recent Advances and Emerging Insights.International journal of molecular sciences · 2026Review
- Inhibition of NCOA4/FTH1-mediated ferritinophagy attenuates ferroptosis in PDLCs and alleviates orthodontically induced inflammatory root resorption.Progress in orthodontics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
People, in increasing numbers, are seeking orthodontic treatment to correct malocclusion, while some of them are suffering from orthodontically induced inflammatory root resorption (OIIRR). Recent evidence suggests that the immune-inflammatory response occurring during bone remodeling may be responsible for OIIRR. Ferroptosis, a new type of programmed cell death (PCD), has been found to have a close interrelation with inflammation during disease progression. While ferroptosis has been extensively studied in bone-related diseases, its role in OIIRR is poorly understood. Considering that the tooth root shares a lot of similar characteristics with bone, it is reasonable to hypothesize that ferroptosis contributes to the development of OIIRR. Nevertheless, direct evidence supporting this theory is currently lacking. In this review, we introduced ferroptosis and elucidated the mechanisms underlying orthodontic tooth movement (OTM) and OIIRR, with a special focus on the pivotal role inflammation plays in these processes. Additionally, we covered recent research exploring the connections between inflammation and ferroptosis. Lastly, we emphasized the important regulatory function of ferroptosis in bone homeostasis. Further investigations are required to clarify the modulation mechanisms of ferroptosis in OIIRR and to develop novel and potential therapeutic strategies for the management of OIIRR.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.