Single-cell spatial atlas of smoking-induced changes in human gingival tissues.
10.1038/s41368-025-00385-5
- Author:
Yong ZHANG
1
;
Zongshan SHEN
1
;
Jiayu YANG
1
;
Junxian REN
1
;
Chi ZHANG
1
;
Lingping TAN
1
;
Li GAO
1
;
Chuanjiang ZHAO
2
Author Information
1. Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, China.
2. Hospital of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou, China. zhaochj@mail.sysu.edu.cn.
- Publication Type:Journal Article
- MeSH:
Humans;
Gingiva/cytology*;
Smoking/adverse effects*;
Male;
Periodontitis/pathology*;
Single-Cell Analysis;
Female;
Adult;
Middle Aged;
Macrophages;
Fibroblasts;
Endothelial Cells;
Case-Control Studies;
Chemokine CXCL12/metabolism*
- From:
International Journal of Oral Science
2025;17(1):60-60
- CountryChina
- Language:English
-
Abstract:
Smoking is a well-established risk factor for periodontitis, yet the precise mechanisms by which smoking contributes to periodontal disease remain poorly understood. Recent advances in spatial transcriptomics have enabled a deeper exploration of the periodontal tissue microenvironment at single-cell resolution, offering new opportunities to investigate these mechanisms. In this study, we utilized Visium HD single-cell spatial transcriptomics to profile gingival tissues from 12 individuals, including those with periodontitis, those with smoking-associated periodontitis, and healthy controls. Our analysis revealed that smoking disrupts the epithelial barrier integrity, induces fibroblast alterations, and dysregulates fibroblast-epithelial cell communication, thereby exacerbating periodontitis. The spatial analysis showed that endothelial cells and macrophages are in close proximity and interact, which further promotes the progression of smoking-induced periodontal disease. Importantly, we found that targeting the endothelial CXCL12 signalling pathway in smoking-associated periodontitis reduced the proinflammatory macrophage phenotype, alleviated epithelial inflammation, and reduced alveolar bone resorption. These findings provide novel insights into the pathogenesis of smoking-associated periodontitis and highlight the potential of targeting the endothelial-macrophage interaction as a therapeutic strategy. Furthermore, this study establishes an essential information resource for investigating the effects of smoking on periodontitis, providing a foundation for future research and therapeutic development for this prevalent and debilitating disease.
