Related Experiment Video
Updated: Jun 17, 2026
Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model
Published on: February 17, 2023
Crack Cocaine Smoke Induces Tissue Degeneration in Rat Submandibular Glands by Toll-like Signaling Pathway
Lorrany da Silva Avanci1, Daniel Vitor de Souza1, Gabriel Carvalhal de Aguiar1
1Department of Biosciences, Institute of Health and Society, Federal University of Sao Paulo UNIFESP, Rua Silva Jardim, 136, Room 332, Vila Mathias, Santos 11050-020, SP, Brazil.
Background:
This study investigated the impact of crack cocaine smoke exposure on the submandibular salivary gland of Wistar rats.
Methods:
The animals were distributed into four groups: control (CTRL); 25 mg exposure (CK25); 50 mg exposure (CK50); and 100 mg exposure (CK100). The animals were exposed to crack cocaine smoke once a day for five consecutive days.
Results:
Exposure to crack cocaine smoke-induced histopathological changes in submandibular salivary glands in all groups under exposure. The immunohistochemical analysis demonstrates that exposure to crack cocaine smoke led to an increase in BCL-2 and P16 expression in all groups exposed to crack cocaine (p < 0.05). The analysis of Ki-67 expression revealed a significant increase in immunoreactive cells across all exposure groups (p < 0.05). Although MYD88 expression was observed in all crack cocaine-exposed groups, only the group treated with the highest dose (100 mg) exhibited a statistically significant increase compared to the control group (p < 0.05).
Conclusions:
In summary, this study demonstrates that exposure to crack cocaine smoke-induced tissue degeneration in the submandibular salivary gland, increasing cellular senescence and promoting compensatory cell proliferation in Wistar rats.
