Work

Cellular senescence in the dental pulp and its implications for endodontics: a scoping review

Year: 2026

Type: article

Abstract: INTRODUCTION: Cellular senescence compromises pulp vitality and may negatively affect vital pulp therapy and regenerative endodontics. Exposure to dental materials may accelerate this process, highlighting the need for safer biomaterials and novel therapeutic strategies. OBJECTIVES: To map and analyze the scientific evidence on cellular senescence in dental pulp, focusing on triggers, biological consequences, and implications for endodontic therapies. MATERIALS AND METHODS: This scoping review was conducted following PRISMA-ScR guidelines (OSF registration: https://doi.org/10.17605/OSF.IO/5ARJH ). PubMed, EMBASE, Scopus, Web of Science, SciELO, and Cochrane Library were searched (1999–2026). RESULTS: From 1,391 records, 94 studies met the inclusion criteria. Most were in vitro (78%) and conducted in Asia (77.7%), mainly using human dental pulp stem cells. Senescence was primarily induced by oxidative stress (hydrogen peroxide), replicative exhaustion, and inflammatory stimuli like lipopolysaccharide. The most consistent markers were SA-β-gal activity and increased p16, p21, and p53 expression. Resin-based monomers, particularly TEGDMA, were associated with senescence induction via oxidative stress and DNA damage. Antioxidants and senolytic compounds reduced senescence markers and improved cell viability and proliferation in vitro. CONCLUSIONS: Oxidative stress and inflammation are key drivers of dental pulp senescence, and resin monomers may contribute to this process. Senescence assessment should be incorporated into biomaterial testing, and senotherapeutics represent potential adjuncts to improve regenerative endodontic outcomes. CLINICAL RELEVANCE: Identifying senescence-inducing factors may support safer material selection and biologically guided strategies to preserve pulp vitality and improve long-term outcomes.

Source: Clinical Oral Investigations

DOI: 10.1007/s00784-026-06822-x