The role and research progress of bacteria in nifedipine-induced gingival hyperplasia
10.12016/j.issn.2096-1456.202550389
- Author:
MA Xinrui
1
;
ZHANG Ximu
1
Author Information
1. 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
- Publication Type:Review
- Keywords:
drug-induced gingival overgrowth;
nifedipine;
oral bacteria;
inflammation;
epithelial-mesenchymal transition;
extracellular matrix;
fibrosis;
oral diseases
- From:
Journal of Prevention and Treatment for Stomatological Diseases
2026;34(2):202-211
- CountryChina
- Language:Chinese
-
Abstract:
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: ① Hypertensive 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. ② Transforming 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-β and its downstream substances to directly participate in gingival fibrosis. ③ Bacteria can also cause massive proliferation of gingival fibroblasts, increased collagen synthesis and reduced degradation by activating the Wnt/β-catenin pathway, interfering with integrin α2β1 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.
- Full text:202602051129279524细菌在硝苯地平诱导的药物性牙龈增生中的作用及研究进展.pdf
