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氧化应激在慢性氟中毒大鼠牙齿移动过程中的调节作用。

The regulatory role of oxidative stress in the tooth movement process of rats with chronic fluorosis.

作者信息

Lai Lingyan, Chen Wanxin, Hao Yue, Chen Bo, Yang Hua

机构信息

Guizhou University of Traditional Chinese Medicine, Guiyang, 550000, China.

Department of Stomatology, Guizhou Provincial People's Hospital, Guiyang, 550000, China.

出版信息

BMC Oral Health. 2025 Aug 20;25(1):1344. doi: 10.1186/s12903-025-06599-7.

DOI:10.1186/s12903-025-06599-7
PMID:40836231
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12366193/
Abstract

BACKGROUND

Clinically, fluorosis patients exhibit delayed orthodontic tooth movement and compromised retention. Experimental studies in fluorosis-exposed rats demonstrate suppressed tooth movement, impaired periodontal angiogenesis, and downregulated VEGF/PI3K/AKT/eNOS signaling. Oxidative stress is critical in periodontal remodeling during orthodontic treatment, yet its role in fluorosis-related movement alterations remains unclear.

METHODS

Seventy 3-week-old Sprague-Dawley rats (body weight 60 ± 5 g) were randomly allocated into experimental groups. Ten rats served as a baseline group (0 day). The remaining 60 were randomized into three groups: control (C), orthodontic (O), and fluorosis orthodontic (FO), (n = 20 rats), subdivided into 3, 7, 14, and 21 days subgroups. C, O groups and blank baseline subgroup received purified water (fluoride < 0.08 mg/L, below the national standard of 1 mg/L), the FO group and fluorosis baseline subgroup drank 150 mg/L NaF water to establish a fluorosis model. After 3 months, orthodontic appliances were applied to O and FO groups. Fluoride accumulation (blood/urine), tooth movement rate and oxidative stress markers (SOD, CAT, MDA, and 8-OHdG) were analyzed.

RESULTS

1 FO group showed elevated blood/urine fluoride levels with C group (P < 0.05). Successful tooth movement was confirmed by interdental expansion.2 FO group exhibited slower tooth movement rate than O group (P < 0.05)0.3 Oxidative stress dynamics: Intergroup Difference: SOD and CAT levels were lowest in the FO group before 7 days, while MDA and 8-OHdG levels were highest in the FO group (P < 0.05), with differences narrowing in later stages.Intragroup Comparisons: SOD: C group: Levels initially increased, peaked at 14 days, and subsequently declined.O group: Levels consistently decreased over time.FO group: Levels exhibited a continuous upward trend.CAT: C group: Levels fluctuated in the early phase and sharply increased in the later phase.O group: Levels initially rose and then declined.FO group: Levels persistently increased throughout the study.MDA: C and FO groups: Levels continuously decreased.O group: Levels first increased, then decreased with fluctuations.8-OHdG: C group: Levels initially rose and later declined.O group: Levels fluctuated markedly.FO group: Levels first decreased and then slightly rebounded.

CONCLUSION

Fluorosis inhibits early-stage tooth movement (3-7 days) through aggravated oxidative stress, with diminishing effects over time as compensatory antioxidant mechanisms emerge.

摘要

背景

临床上,氟中毒患者表现出正畸牙齿移动延迟和固位受损。在氟暴露大鼠中进行的实验研究表明牙齿移动受到抑制、牙周血管生成受损以及VEGF/PI3K/AKT/eNOS信号下调。氧化应激在正畸治疗期间的牙周重塑中起关键作用,但其在氟中毒相关的移动改变中的作用仍不清楚。

方法

将70只3周龄的Sprague-Dawley大鼠(体重60±5g)随机分为实验组。10只大鼠作为基线组(0天)。其余60只随机分为三组:对照组(C)、正畸组(O)和氟中毒正畸组(FO),(每组n = 20只大鼠),再细分为3天、7天、14天和21天亚组。C组、O组和空白基线亚组饮用纯净水(氟含量<0.08mg/L,低于国家标准1mg/L),FO组和氟中毒基线亚组饮用150mg/L氟化钠水以建立氟中毒模型。3个月后,对O组和FO组施加正畸矫治器。分析氟积累(血液/尿液)、牙齿移动速率和氧化应激标志物(超氧化物歧化酶、过氧化氢酶、丙二醛和8-羟基脱氧鸟苷)。

结果

  1. FO组血液/尿液氟水平高于C组(P<0.05)。通过牙间隙扩大证实牙齿成功移动。2. FO组牙齿移动速率比O组慢(P<0.05)。3. 氧化应激动态变化:组间差异:7天前FO组超氧化物歧化酶和过氧化氢酶水平最低,而丙二醛和8-羟基脱氧鸟苷水平最高(P < 0.05),后期差异缩小。组内比较:超氧化物歧化酶:C组:水平最初升高,在14天达到峰值,随后下降。O组:水平随时间持续下降。FO组:水平呈持续上升趋势。过氧化氢酶:C组:水平在早期波动,后期急剧上升。O组:水平先上升后下降。FO组:水平在整个研究过程中持续上升。丙二醛:C组和FO组:水平持续下降。O组:水平先升高,然后波动下降。8-羟基脱氧鸟苷:C组:水平先上升后下降。O组:水平波动明显。FO组:水平先下降然后略有反弹。

结论

氟中毒通过加重氧化应激抑制早期牙齿移动(3 - 7天),随着补偿性抗氧化机制的出现,其作用随时间减弱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/7042f95e3c8c/12903_2025_6599_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/ceb7e6f90f05/12903_2025_6599_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/38804d07c426/12903_2025_6599_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/a7dded5fb669/12903_2025_6599_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/25cbd09b64ed/12903_2025_6599_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/7042f95e3c8c/12903_2025_6599_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/ceb7e6f90f05/12903_2025_6599_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/38804d07c426/12903_2025_6599_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/a7dded5fb669/12903_2025_6599_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/25cbd09b64ed/12903_2025_6599_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c6ed/12366193/7042f95e3c8c/12903_2025_6599_Fig5_HTML.jpg

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