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Updated: May 14, 2026

Establishment of a Murine Pulp Exposure Model with a Novel Mouth-Gag for Pulpitis Research
Published on: October 27, 2023
Temporal histological and immunohistochemical characterization of experimental dental pulp inflammation in rats
Julissa Denisse Arguello Alvarado1, Rafaela Ricci1, Romulo de Oliveira Sales-Junior1
1Department of Preventive and Restorative Dentistry, School of Dentistry, São Paulo State University (UNESP), Araçatuba, Brazil.
Objective:
To establish a temporal histological and immunohistochemical profile in a rat model of pulpitis by assessing cytokine immunoreactivity at the root canal orifice over time.
Design:
This experimental animal study included 28 male Wistar rats allocated to seven groups based on the time elapsed after pulp exposure: D0, D1, D2, D3, D4, D5, D6 (0-6 days). Pulp inflammation was induced in maxillary first molars, and hemimaxillae were processed for histological and immunohistochemical analyses. Cytokines (IL-17, TGF-β, IL-6, IL-1β, IL-10 and TNF-α) were evaluated using the immunoperoxidase technique, and immunoreactivity was semi-quantitatively scored. Inflammatory infiltrate was assessed histologically. Data were analyzed using Kruskal-Wallis and post hoc tests (α = 0.05).
Results:
Histological analysis demonstrated a progressive increase in inflammation and tissue damage over time, ranging from absence or mild inflammatory changes in D0-D1 to complete necrosis at D6 (p < 0.05). Immunohistochemical analysis revealed detectable immunoreactivity for TGF-β and IL-17 at the earliest time points (D0-D1), while no significant temporal differences were observed among cytokines from D0 to D2 (p > 0.05). From D3 onwards, all cytokines exhibited a significant increase in immunoreactivity compared to D0 (p < 0.05), with sustained elevated expression through D6.
Conclusion:
Pulp inflammation was associated with time-dependent histological alterations and cytokine immunoreactivity at the root canal orifice. Early TGF-β and IL-17 expression was observed at initial time points, while a progressive increase in cytokine immunoreactivity from D3 onwards marked the development of an established inflammatory response and subsequent tissue damage.
