摘要
硝苯地平诱导的药物性牙龈增生(nifedipine-induced gingival overgrowth,NIGO)是指由长期服用高血压药物硝苯地平(nifedipine,NIF)引起的牙龈增生,是一种药物不良反应。NIGO具有发病率高,患者基数大的特点,是临床上最为常见的牙龈增生类型之一。既往关于NIGO病因的研究多聚焦于NIF的直接药理作用,但近年来的研究表明,炎症亦是NIGO的关键风险因素。菌斑是牙周炎症的核心始动因素,然而细菌在NIGO发病机制中的具体作用尚不明确。本文对相关研究进行综述,探讨细菌参与NIGO发病的潜在途径:①以NIF为代表的高血压药物可引起口腔菌群失调,导致牙周致病菌相对丰度增加。在宿主对细菌的免疫应答中,牙龈成纤维细胞释放的炎症趋化因子可与NIF产生协同效应,促进胶原过度生成或募集免疫细胞参与组织纤维化进程;②转化生长因子-β(transforming growth factor-β,TGF-β)在纤维化疾病中具有重要作用,细菌感染可显著上调TGF-β水平,进而促进上皮-间充质转化,或通过激活其下游信号通路直接参与牙龈纤维化;③细菌还可通过激活Wnt/β-catenin通路、干扰整合素α2β1表达、抑制miR-200调控细胞周期等多种途径,导致牙龈成纤维细胞增殖异常、胶原合成增多而降解减少,最终加剧NIGO。综上,细菌是NIGO发生发展中的重要因素,对接受NIF治疗的高血压患者进行口腔菌斑控制和健康管理,对预防和缓解NIGO具有重要临床意义。未来研究可聚焦NIGO患者口腔菌群与宿主免疫细胞间的相互作用,为NIGO的预防和治疗提供新的策略。
Nifedipine-induced gingival overgrowth(NIGO)refers to gingival hyperplasia caused by long-term use of the hypertensive drug nifedipine(NIF),and it is a drug adverse reaction.NIGO is characterized by a high incidence rate and a large patient base,and it is one of the most common types of gingival hyperplasia in clinical practice.Previous studies on the etiology of NIGO mainly focused on the pharmacological effects of NIF,while in recent years,it has been proposed that inflammation may also be a major risk factor for NIGO.Plaque is the initiating factor of periodontal inflammation.However,the role and mechanism of bacteria in the pathogenesis of NIGO remain unclear at present.Therefore,this article reviews relevant research and finds that bacteria may be involved in the pathogenesis of NIGO through the following pathways:①Hypertensive drugs represented by NIF can cause dysbiosis of the oral flora,increasing the relative abundance of periodontal pathogenic bacteria.The inflammatory chemokines released by fibroblasts in the immune response to bacteria can work in synergy with NIF to promote excessive collagen production or recruit immune cells to participate in tissue fibrosis.②Transforming growth factor-β(TGF-β)plays a significant role in fibrotic diseases.Bacterial infections can significantly increase the level of TGF-β,promoting epithelial-mesenchymal transition or allowing TGF-βand its downstream substances to directly participate in gingival fibrosis.③Bacteria can also cause massive proliferation of gingival fibroblasts,increased collagen synthesis and reduced degradation by activating the Wnt/β-catenin pathway,interfering with integrinα2β1 expression,and inhibiting miR-200 to alter the cell cycle,ultimately exacerbating NIGO.In conclusion,bacteria may be an important factor in aggravating NIGO,and oral health management for patients with hypertension should be given due attention.Future research can focus on the interaction between the oral microbiota and immune cells in NIGO patients,providing new strategies for their prevention and treatment.
作者
马心睿
张曦木
MA Xinrui;ZHANG Ximu(The Affiliated Stomatological Hospital of Chongqing Medical University&Chongqing Key Laboratory of Oral Diseases&Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education&Chongqing Municipal Health Commission Key Laboratory of Oral Biomedical Engineering,Chongqing 401147,China)
出处
《口腔疾病防治》
2026年第2期202-211,共10页
Journal of Prevention and Treatment for Stomatological Diseases
基金
重庆市教委科学技术研究重点项目(KJZD-K202500412)。
关键词
药物性牙龈增生
硝苯地平
口腔细菌
炎症
上皮间充质转化
细胞外基质
纤维化
口腔疾病
drug-induced gingival overgrowth
nifedipine
oral bacteria
inflammation
epithelial-mesenchymal transition
extracellular matrix
fibrosis
oral diseases
