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Updated: Oct 25, 2026
Establishment of a Murine Pulp Exposure Model with a Novel Mouth-Gag for Pulpitis Research
Published on: October 27, 2023
Establishment and comprehensive characterization of a murine model of post-traumatic oral mucosal injury
Ningning Xue1, Yihang Xie1, Chenyue Zhang1
1State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Chinese Academy of Medical Sciences, Research Unit of Oral Carcinogenesis and Management, West China Hospital of Stomatology, Sichuan University, Chengdu, Sichuan, 610041, China.
Objective:
Oral mucosal injury is commonly accompanied by local inflammation and tissue repair, yet experimental models that enable reproducible investigation of these dynamic processes remain limited. This study aimed to establish and comprehensively characterize a reproducible murine model of chemically induced oral mucosal injury and to evaluate its responsiveness to topical anti-inflammatory treatment.
Methods:
Oral mucosal injury was induced in male C57BL/6 mice by repeated chemical cauterization of the dorsal tongue mucosa. Lesion development and healing were monitored by macroscopic observation. Histopathological examination was performed to assess epithelial injury and inflammatory cell infiltration. Transcriptomic profiling, quantitative PCR, immunohistochemistry, and Western blotting were used to characterize inflammation-related molecular responses. The model's therapeutic responsiveness was assessed with topical dexamethasone.
Results:
Repeated chemical cauterization produced reproducible oral mucosal ulcerative injury with a defined course of lesion formation and spontaneous healing. Histopathological analysis demonstrated epithelial disruption, inflammatory cell infiltration, and subsequent tissue regeneration during healing. Transcriptomic analysis revealed significant enrichment of inflammatory and immune-related pathways, and molecular analyses supported increased activation of the NF-κB, STAT3, and STING signaling pathways. Expression of the pro-inflammatory mediators TNF-α, IL-6, and IL-1β was also increased in the lesion tissues. Topical dexamethasone significantly accelerated macroscopic injury healing and was accompanied by attenuation of NF-κB-, STAT3-, and STING-related inflammatory signaling.
Conclusions:
We established a reproducible murine model of post-traumatic oral mucosal injury that exhibits clinical, histopathological, and molecular features. This model provides a practical platform for investigating local inflammatory responses and tissue repair following oral mucosal injury and for evaluating potential pharmacological and targeted interventions.
