Senescence on Dental Pulp Cells: Effects on Morphology, Migration, Proliferation, and Immune Response

Introduction: Evidence indicates that senescence can affect essential dental pulp functions, such as defense capacity and repair, consequently affecting the successes of conservative endodontic treatments. This study aims to evaluate the effects of senescence on the morphology, migration, proliferation, and immune response of human dental pulp cells. Methods: Cells were treated with doxorubicin to induce senescence, confirmed by b-galactosidase staining. Morphological changes, cellular proliferation, and migration were evaluated by scanning electron microscopy, trypan blue cells, and the scratch method, respectively. Modifications in the immune response were evaluated by measuring the genes for pro-inflammatory cytokines tumor necrosis factor alpha and interleukin (IL)-6 and anti-inflammatory cytokines transforming growth factor beta 1 and IL-10 using the real time polymerase chain reaction assay. Results: An increase in cell size and a decrease in the number of extensions were observed in senescent cells. A reduction in the proliferative and migratory capacity was also found in senescent cells. In addition, there was an increase in the gene expression of inflammatory cytokines tumor necrosis factor alpha and IL-6 and a decrease in the gene expression of IL-10 and transforming growth factor beta -1, suggesting an exacerbated inflammatory situation associated with immunosuppression. Conclusions: Cellular senescence is possibly a condition that affects prognoses of conservative endodontic treatments, as it affects primordial cellular functions related to this treatment. (J Endod 2024;50:362-369.) SIGNIFICANCE This study reveals that senescence in dental pulp cells causes morphological alterations, reduced cell function, and an exacerbated inflammatory and immunosuppressive response, potentially complicating conservative endodontic prognosis. Managing senescence is crucial for better treatment outcomes in endodontics.