IADR Abstract Archives

Mechanism of HEMA Mediated Apoptosis in Dental Pulp Stromal Cells

Objective: The use of resins, resin based materials, primers and bonding agents in dentistry are becoming increasingly common. While the use of these materials is beneficial to the health and appearance of patients, they carry potential risks such as damage to the cells (cytotoxicity) and allergic reactions. Most dentin bonding techniques use a primer containing 2-hydroxyethylmethacrylate (HEMA). The objective of this study is to evaluate the effects of HEMA on dental pulpal stromal cells (DPSCs) and odontoblasts, and establish the pathway of HEMA mediated apoptosis.

Materials and Methods: Dual staining with FITC- Annexin V and Propidium iodide and Propidium iodide staining of ethanol fixed cells were used to assess HEMA mediated apoptosis. Alkaline Phosphatase (ALP) staining was used as a functional assay for odotoblasts. The changes in the mitochondrial membrane potential were assessed by staining with DiOC6 and the levels of Caspases 9 and 3 were studied using Western blot and flow cytometric analysis. Nuclear extracts were used to measure the levels of mobilized NFkB in untreated and HEMA treated cells.

Results: HEMA induced significant apoptosis in DPSCs and a variety of other cell types. DPSCs differentiated into odontoblasts were relatively more resistant to HEMA mediated apoptosis. Odontoblasts treated with HEMA showed decreased ALP staining which corresponded to loss of function. The induction of apoptosis by HEMA is primarily through the intrinsic pathway of cell death due to a decrease in mitochondrial membrane potential and in elevation of Caspases 3 and 9. HEMA also mediated decrease of Nuclear-Factor-Kappa-B (NFkB).

Conclusion: Activation of intrinsic death pathway in DPSCs by HEMA may decrease the regenerative capacity of undifferentiated DPSCs and odontoblasts eventually contributing to hypersensitivity and loss of viable teeth. HEMA mediated decrease in NFkB activation may be the primary step in induction of apoptosis.

Supported by RO1- DE 10331:08 from NIH-NIDCR.


AADR/CADR Annual Meeting
2006 AADR/CADR Annual Meeting (Orlando, Florida)
Orlando, Florida
2006
59
Pharmacology, Therapeutics, & Toxicology
  • Paranjpe, Avina  ( University of California at Los Angeles, Los Angeles, CA, USA )
  • Hume, Wyatt  ( University of California at Los Angeles, Los Angeles, CA, USA )
  • Jewett, Anahid  ( University of California at Los Angeles, Los Angeles, CA, USA )
    • Oral Session
    Clinical Pharmacology and Toxicology
    03/08/2006