Nicotine Is Associated with Improved Histological and Biochemical Indices of Oral Ulcer Repair in an Acetic Acid-Induced Rat Model.

Background and

Objectives

This study aimed to evaluate the association between systemic nicotine administration and histological and biochemical repair endpoints in an acetic acid-induced rat oral ulcer model. Materials and

Methods

Thirty-six male Wistar rats were assigned to control, oral ulcer + saline, and oral ulcer + nicotine (1 mg/kg/day, s.c.) groups. Oral ulcers were induced with 70% acetic acid. After 15 days, buccal mucosa and plasma samples were collected for histopathological and biochemical analyses. Epithelial thickness and fibrosis were assessed histologically, while malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), vascular endothelial growth factor-A (VEGF-A), and epidermal growth factor receptor (EGFR) were quantified.

Results

Relative to controls, ulcer induction was associated with reduced epithelial thickness and increased fibrosis, MDA, and TNF-α levels. Compared with the oral ulcer + saline group, the nicotine-treated group showed greater epithelial thickness, lower fibrosis, lower MDA and TNF-α levels, and higher VEGF-A and EGFR levels at the study endpoint. No significant difference in VEGF-A was observed between the control and oral ulcer + saline groups.

Conclusions

In this acetic acid-induced rat model, systemic nicotine administration was associated with improved endpoint histological and biochemical indices of oral ulcer repair. Because macroscopic wound closure, dose-response relationships, route comparisons, and direct mechanistic experiments were not included, these findings should be interpreted as preliminary preclinical associations rather than evidence of a direct causal effect of nicotine on wound healing.