Hou Ruxia, Yang Jitong, Li Xixi, Wang Xinmei, Du Wenxin, Kang Wen, Liu Jiajia, Yang Tingting, Li Junming, Wang Xiangyu, Liu Junyu, Zhao Bin
Department of Pediatric and Preventive Dentistry, School and Hospital of Stomatology, Shanxi Medical University, Taiyuan, 030001, China.
Shanxi Province Key Laboratory of Oral Diseases Prevention and New Materials, Taiyuan, 030001, China.
Arch Toxicol. 2025 Mar 11. doi: 10.1007/s00204-025-04011-5.
Tobacco smoking involves the use of devices such as pipes, cigars, or cigarettes to inhale and exhale smoke from burning tobacco leaves, primarily to ingest nicotine and other substances. The impact of oxidative stress from smoking on periodontitis and its underlying mechanisms remains poorly understood. Previous research has shown that smoking activates oxidative stress responses, generating harmful oxidative substances and free radicals that induce periodontitis. Although traditionally recognized as a key pathway, recent studies suggest additional mechanisms are involved. The study aims to conduct a comprehensive review of the literature on periodontitis induced by oxidative stress from smoking, exploring potential mechanisms involving microorganisms, inflammation, immunity, cellular responses, and saliva. The primary objective is to compare and elucidate the various mechanisms by which traditional tobacco smoke and electronic cigarettes induce oxidative stress and lead to periodontitis and summarize the similarities or differences between the two. In addition, this article explores the different effects of smoking on oxidative stress and periodontitis under different conditions of nicotine presence and nicotine content. This comprehensive review contributes to our evolving understanding of how traditional tobacco smoke and electronic cigarettes affect periodontitis through different pathways and components, emphasizing that oxidative stress is an important factor in smoking-induced periodontitis. The insights gained from this study may help develop targeted interventions for the different pathways of the impact of traditional tobacco smoke and electronic cigarettes in clinical practice, to prevent or treat smoking-induced periodontitis and ultimately safeguard public oral health.
吸烟涉及使用烟斗、雪茄或香烟等器具来吸入和呼出燃烧烟草叶产生的烟雾,主要是为了摄取尼古丁和其他物质。吸烟引起的氧化应激对牙周炎的影响及其潜在机制仍知之甚少。先前的研究表明,吸烟会激活氧化应激反应,产生有害的氧化物质和自由基,从而诱发牙周炎。尽管传统上认为这是一条关键途径,但最近的研究表明还涉及其他机制。该研究旨在对吸烟引起的氧化应激导致牙周炎的文献进行全面综述,探索涉及微生物、炎症、免疫、细胞反应和唾液的潜在机制。主要目的是比较和阐明传统烟草烟雾和电子烟诱发氧化应激并导致牙周炎的各种机制,并总结两者之间的异同。此外,本文探讨了在不同尼古丁存在条件和尼古丁含量下,吸烟对氧化应激和牙周炎的不同影响。这一全面综述有助于我们不断深入了解传统烟草烟雾和电子烟如何通过不同途径和成分影响牙周炎,强调氧化应激是吸烟诱发牙周炎的一个重要因素。从这项研究中获得的见解可能有助于在临床实践中针对传统烟草烟雾和电子烟影响的不同途径制定有针对性的干预措施,以预防或治疗吸烟诱发的牙周炎,最终保障公众口腔健康。