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可摘局部义齿对口腔内促氧化剂/抗氧化剂平衡和氧化还原敏感炎症生物标志物 NF-κB 的影响:一项干预性随访研究。

The Influence of Removable Complete Denture on Pro-Oxidant Antioxidant Balance and Redox-Sensitive Inflammation Biomarker NF-ĸB in the Oral Cavity: An Interventional Follow-Up Study.

机构信息

Department of Prosthodontics, Medical Faculty, University of Niš, Nis, Nis region, Serbia.

Department of Biochemistry, Medical Faculty, University of Niš, Nis, Nis region, Serbia.

出版信息

Clin Exp Dent Res. 2024 Oct;10(5):e70007. doi: 10.1002/cre2.70007.

DOI:10.1002/cre2.70007
PMID:39295455
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11411146/
Abstract

OBJECTIVES

Oxidative stress, an imbalance between the body's natural antioxidant defenses and the production of reactive oxygen species (ROS), can result in serious oral diseases, including oral cancer, periodontal diseases, and oral lichen planus, through the activation of the redox-sensitive transcription factors and inflammation. The purpose of this study was to assess the potential effects of a removable complete denture on the levels of oxidative stress markers, such as lipid peroxidation (MDA), advanced oxidation protein products (AOPP), and catalase, and the quantitative expression of the redox-sensitive transcription factor NF-κB p65 subunit.

MATERIALS AND METHODS

This interventional follow-up study enrolled 40 participants of both sexes aged 28-78 years, with a median age of 56 years, where unstimulated saliva was collected before denture placement, immediately after the denture placement, and 24 h, 7 days, and 30 days after the denture placement. The most prominent ROS overproduction was reported on the seventh day (p < 0.05), followed by a significant fall in antioxidative defense.

RESULTS

The NF-κB p65 subunit, whose expression pattern was highest in the same time period on the seventh day, serves as a signaling molecule for redox imbalance due to ROS production. Over the next 30 days, its levels remained moderately increased compared to the basal value, which may influence pro-inflammatory pathways and the integrity of oral tissue components. These alterations may be induced by the dentures, which can produce high pressures on the supporting tissues or by the synthetic materials used for producing the dentures.

CONCLUSION

Our research may help to clarify the potential pathways by which oxidative stress and redox-sensitive inflammatory mediators, as well as mechanical and chemical irritants, may serve as risk factors for premalignant lesions in the mouth. Further research on this topic is required to understand the molecular mechanisms behind the relationship between inflammation and oral premalignant lesions caused by mechanical and chemical irritation.

摘要

目的

氧化应激是指机体的天然抗氧化防御系统与活性氧(ROS)产生之间的失衡,可通过激活氧化还原敏感转录因子和炎症,导致严重的口腔疾病,包括口腔癌、牙周病和口腔扁平苔藓。本研究旨在评估可摘全口义齿对氧化应激标志物水平的潜在影响,如脂质过氧化(MDA)、晚期氧化蛋白产物(AOPP)和过氧化氢酶,以及氧化还原敏感转录因子 NF-κB p65 亚单位的定量表达。

材料与方法

本干预性随访研究纳入了 40 名年龄在 28-78 岁之间的男女参与者,中位年龄为 56 岁,在戴义齿前、戴义齿后即刻、戴义齿后 24 小时、7 天和 30 天采集非刺激性唾液。第 7 天报告了最显著的 ROS 过度产生(p<0.05),随后抗氧化防御显著下降。

结果

NF-κB p65 亚单位的表达模式在第 7 天最高,作为 ROS 产生导致氧化还原失衡的信号分子。在接下来的 30 天内,与基础值相比,其水平仍保持中度升高,这可能影响促炎途径和口腔组织成分的完整性。这些变化可能是由义齿对支持组织产生的高压力或义齿制造中使用的合成材料引起的。

结论

我们的研究可能有助于阐明氧化应激和氧化还原敏感炎症介质以及机械和化学刺激物作为口腔癌前病变危险因素的潜在途径。需要进一步研究这一主题,以了解炎症与机械和化学刺激引起的口腔癌前病变之间的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17eb/11411146/d461610b9dcd/CRE2-10-e70007-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17eb/11411146/d461610b9dcd/CRE2-10-e70007-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17eb/11411146/d461610b9dcd/CRE2-10-e70007-g001.jpg

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Clin Exp Dent Res. 2020 Aug;6(4):439-447. doi: 10.1002/cre2.296. Epub 2020 Jun 16.
2
Inflammation, NF-κB, and Chronic Diseases: How are They Linked?炎症、核因子κB与慢性病:它们是如何关联的?
Crit Rev Immunol. 2020;40(1):1-39. doi: 10.1615/CritRevImmunol.2020033210.
3
Salivary biomarkers of inflammation and oxidative stress in healthy adults.健康成年人的炎症和氧化应激的唾液生物标志物。
Arch Oral Biol. 2019 Jan;97:215-222. doi: 10.1016/j.archoralbio.2018.10.026. Epub 2018 Oct 24.
4
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Arch Oral Biol. 2018 Aug;92:8-17. doi: 10.1016/j.archoralbio.2018.04.018. Epub 2018 May 1.
5
Insulin-Leptin Axis, Cardiometabolic Risk and Oxidative Stress in Elderly with Metabolic Syndrome.代谢综合征老年人的胰岛素-瘦素轴、心血管代谢风险与氧化应激
Exp Clin Endocrinol Diabetes. 2018 Feb 8. doi: 10.1055/s-0043-123825.
6
The Role of Chronic Mucosal Trauma in Oral Cancer: A Review of Literature.慢性黏膜创伤在口腔癌中的作用:文献综述
Indian J Med Paediatr Oncol. 2017 Jan-Mar;38(1):44-50. doi: 10.4103/0971-5851.203510.
7
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Sci Rep. 2017 Feb 8;7:41971. doi: 10.1038/srep41971.
8
Potential Co-Relation Between Chronic Periodontitis And Cancer - An Emerging Concept.慢性牙周炎与癌症之间的潜在关联——一个新兴概念。
Gulf J Oncolog. 2016 Jan;1(20):20-4.
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10
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