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206 - Cellular Effects of Silver Diamine Fluoride in Oral Cells

Friday, May 22, 2026
4:40 PM - 4:55 PM PST
Has Audio

    Presenting Author(s)

  • Tori Bernard, DMD

    PGY2 Resident
    University of Tennessee Health Science Center (UTHSC)
    University of Tennessee Health Science Center
    Memphis, Tennessee, United States

    • Co-Author(s)

  • Ji Min Yochim, DMD, MS, PhD

    Assistant Professor, Research Director
    UTHSC College of Dentistry, Pediatric Dentistry and Community Oral Health
    UTHSC College of Dentistry, Pediatric Dentistry and Community Oral Health
    Memphis, Tennessee, United States

  • SR

    Sheeja Rajasingh, MSc, MPhil

    UTHSC College of Dentistry

  • Clarice S. Law-Eyre, DMD, MS

    Associate Professor and Chair
    UTHSC College of Dentistry
    UCLA School of Dentistry
    Memphis, Tennessee, United States

  • AA

    Ayman Al Dayeh, BDS, MDS, PhD

    UTHSC College of Dentistry

  • Rajasingh Johnson, MPhil, PhD, HCLD (he/him/his)

    Professor
    UTHSC College of Dentistry
    University of Tennessee Health Science Center
    Memphis, Tennessee, United States

    • Research Mentor(s)

  • Ji Min Yochim, DMD, MS, PhD

    Assistant Professor, Research Director
    UTHSC College of Dentistry, Pediatric Dentistry and Community Oral Health
    UTHSC College of Dentistry, Pediatric Dentistry and Community Oral Health
    Memphis, Tennessee, United States

    • Program Director(s)

  • Volk V. Vinall, DMD

    Program Director
    The University of Tennessee Health Science Center
    Memphis, Tennessee, United States

Abstract:


Purpose: Silver diamine fluoride (SDF) is widely used for its caries-arresting, antimicrobial, and remineralizing effects. However, its cytotoxic, inflammatory, and genotoxic effects on oral cells remain unclear. This study evaluated SDF’s impact on cell viability, inflammation, DNA integrity, and functional properties across varying concentrations.





Methods: Dental pulp stem cells (DPSCs), periodontal ligament fibroblasts (PDLFs), and gingival fibroblasts (GFs) were exposed to increasing concentrations of SDF. Cell viability and apoptosis were assessed by MTT and Annexin V assays. Inflammatory and DNA damage–related gene expression was analyzed by qRT-PCR. Wound closure and trans-well migration assays evaluated functional effects. To simulate dentin permeability, a trans-well system (0.4 µm pores) was used to test whether SDF diffuses and affects underlying cells.



Results: SDF exposure (0.005–0.01%, 24-48 h) caused a dose-dependent reduction in viability, confirming increased apoptosis across all cell types. qRT-PCR showed upregulation of inflammatory genes (IL-1β and COX2) and downregulation of DNA repair genes (RAD51, PARP1, and XRCC4). Functional assays demonstrated impaired wound closure and reduced cell migration. Notably, indirect exposure through the dentin-mimicking trans-well barrier also significantly reduced cell viability and wound healing.



Conclusion: SDF concentrations lower than those commonly used clinically, even when separated by a dentin-like barrier, can induce inflammation, apoptosis, impaired wound healing, and suppression of DNA repair pathways in oral cells including DPSCs. These findings emphasize potential cytotoxic and genotoxic risks associated with SDF and highlight the need to re-evaluate concentrations to balance therapeutic benefits with cellular safety in patients.







Identify Supporting Agency and Grant Number: None