Abstract Background Early-life adversity (ELA) has been linked to accelerated biological development. This study aimed to explore the cumula
Abstract Background Early-life adversity (ELA) has been linked to accelerated biological development. This study aimed to explore the cumulative effects of different dimensions of early-life adversity (ELA) on accelerating biological aging, as indicated by the accelerated eruption of the second permanent molar (M2). Methods Participants were drawn from an ongoing cohort of 1,448 children aged 7–12 years who were recruited following a 2-year follow-up and 1,191 children were ultimately included in this study. A multi-informant assessment of exposure to threat-related, deprivation-related, and unpredictability-related ELA was performed at baseline. Statistical analyses were performed via an accelerated failure time (AFT) model. Results The analysis revealed that parents of 1,558 children (mean [SD] age, 9.2 [1.3] years) reported exposure to different types of ELA dimensions (threat, deprivation, and unpredictability) in their offspring. During a 2-year follow-up, three waves of physical and dental examinations were administered to the participants. The M2 accelerated eruption rate was 13.4% (209/1,558) at baseline and increased to 34.7% (444/1,280) at wave 3, with no significant sex difference (boys: 25.8%, girls: 26.3%). Deprivation-related (HR = 1.07, 95%CI: 1.12–2.29, P = 0.046) and unpredictability-related ELA (HR = 1.15, 95%CI: 1.06–1.25, P = 0.001) were found to be associated with M2 accelerated eruption over a two-year follow-up period, whereas threat-related ELA showed no such association. Notably, high ELA exposure in each dimension resulted in an increased risk of M2 accelerated eruption. These associations remained stable after controlling for covariates. Conclusions The findings suggest that ELA-induced acceleration of biological aging can be detected at the time of molar eruption in a dimension-specific and dose-specific manner. These results emphasize the importance of considering the different dimensions and levels of ELA exposure when evaluating its impact on biological aging.