Epigenetic studies, which can reflect biological aging, have shown that measuring DNA methylation (DNAm) levels provides new insights into the biological effects of social environment and socioeconomic position (SEP). This study explores how race, family structure, and SEP (income to poverty ratio) at birth influence youth epigenetic aging at age 15. Data were obtained from the Future of Families and Child Wellbeing Study (FFCWS) cohort, with GrimAge used as a measure of DNAm levels and epigenetic aging. Our analysis included 854 racially and ethnically diverse participants followed from birth to age 15. Structural equation modeling (SEM) examined the relationships among race, SEP at birth, and epigenetic aging at age 15, controlling for sex, ethnicity, and family structure at birth. Findings indicate that race was associated with lower SEP at birth and faster epigenetic aging. Specifically, income to poverty ratio at birth partially mediated the effects of race on accelerated aging by age 15. The effect of income to poverty ratio at birth on DNAm was observed in male but not female youth at age 15. Thus, SEP partially mediated the effect of race on epigenetic aging in male but not female youth. These results suggest that income to poverty ratio at birth partially mediates the effects of race on biological aging into adolescence. These findings highlight the long-term biological impact of early-life poverty in explaining racial disparities in epigenetic aging and underscore the importance of addressing economic inequalities to mitigate these disparities. Policymakers should focus on poverty prevention in Black communities to prevent accelerated biological aging and associated health risks later in life. Interventions aimed at eliminating poverty and addressing racial inequities could have significant long-term benefits for public health. Future research should explore additional factors contributing to epigenetic aging and investigate potential interventions to slow down the aging process. Further studies are needed to understand the mechanisms underlying these associations and to identify effective strategies for mitigating the impact of SEP and racial disparities on biological aging.

Objective: The study investigated the biological effects and molecular mechanisms of platelet-rich plasma (PRP) on periodontal bone regeneration. Methods: Electronic and manual searches were searched up to 1 October 2022 in the following databases: Pubmed, Scopus, Cochrane Library and Embase. [Platelet rich plasma or platelet or growth factors] and [periodontal] or [bone regeneration or bone defect or bone reconstruction] were used for searching. This study reviewed and analyzed published papers associated with PRP and periodontal bone defect restoration or bone regeneration or bone reconstruction. Results: Different growth factors exhibited varied biological characteristics and function. In-vitro studies, animal experiments and clinical studies confirmed that PRP displayed assorted role in periodontal bone defects repair. The growth factors secreted from PRP can promote new bone formation, soft tissue regeneration and wound healing. The fiber three-dimensional structure in PRP is conducive to the growth and migration of cells and provides strong support for the regeneration of periodontal soft and hard tissues. The anti-inflammatory characteristics of PRP are also closely related to the repair of periodontal bone defects. Conclusion: PRP played an important biological effect on periodontal bone regeneration. The mechanism is closely related to PRP promoting the growth, proliferation, differentiation and migration of periodontal ligament cells and osteoblasts, and the fiber stereo configuration of PRP and the anti-inflammatory effect of leukocytes.