Int Endod J. 2021 Aug 10. doi: 10.1111/iej.13606. Online ahead of print.
ABSTRACT
AIM: To evaluate if treatment with resiniferatoxin (RTX) is capable of lowering the plasma levels of PGE2 and TNF-α, as well as histopathological parameters in inflammation of pulp tissue in a mouse experimental model.
METHODOLOGY: Ten groups of six BALB/c mice were formed as follows: healthy group (HC ), healthy group treated with RTX (HRTX ), two groups with pulp inflammation at 14 and 18 hours (PI14 /PI18 ); six groups with pulpal inflammation plus treatment with Ibuprofen (IBU14 /IBU18 ), dexamethasone (DEX14 /DEX18 ) and resiniferatoxin (RTX14 /RTX18 ) at 14 and 18 hours, respectively. Pulpal inflammation was induced through occlusal exposure of the pulp of the maxillary first molar. The plasma levels of PGE2 and TNF-α and the histological parameters of the pulp tissue of the HC and HRTX groups were evaluated at the time of acquiring the animals. In the other groups, the plasma levels of PGE2 and TNF-α and the histopathological parameters were evaluated at 14 and 18 hours after pulp damage. Plasma levels of PGE2 and TNF-α were quantified by ELISA assay and the histopathological parameters were evaluated by H/E staining. Statistical significance was determined by one-way analysis of variance (ANOVA) to test for overall differences between group means.
RESULTS: A significant increase (*p<0.05) in plasma levels of PGE2 and TNF-α occurred 14 and 18 hours after pulp damage. In addition, treatment with RTX significantly decreased (*p<0.05) the plasma levels of PGE2 and TNF-α at 14 and 18 hours after pulp damage, as well as the infiltrate of inflammatory cells at 18 hours after pulp damage, similarly to treatment with ibuprofen and dexamethasone.
CONCLUSION: It was possible to detect systemic levels of PGE2 and TNF-α at 14 and 18 hours after pulp damage. Likewise, treatment with RTX was associated with an anti-inflammatory effect similar to treatment with ibuprofen and dexamethasone. These findings place resiniferatoxin as a therapeutic alternative in the treatment of inflammatory diseases in Dentistry.
PMID:34375451 | DOI:10.1111/iej.13606
