Oral tissues are exposed to various stresses, including the reported release of dental monomers.  Stress proteins such as heat shock proteins play a key role in protecting and preventing cellular damage from cell stress. Objective:  To quantify the ability of dental monomers to induce heat shock protein-72 (HSP72) in THP-1 human monocytes. Methods: Cell cultures (n=6) were grown in RPMI1640 supplemented with 10%FCS and exposed to heat shock (43°C for 1 h) to induce HSP72 with or without HEMA (0, 2.5, 5, 10 mmol/L) or TEGDMA (0, 0.25, 0.5, 1 mmol/L). Monomer concentrations were below toxic levels. The cells were then allowed to recover at 37°C for 6 h before processing with SDS-PAGE. Controls contained no HEMA and/or no heat shock. HSP72 induction was detected by Western blotting, quantified with STORM, expressed as a percentage of the controls, and statistically analyzed with ANOVA/Tukey (a=0.05). Results: Both HEMA and TEGDMA significantly suppressed (* in table)

HEMA Conc (mmol/L)	0	2.5	5	10
HSP72 Induction (% control) (SD)	100 (8)	71 (4)*	58 (6)*	41 (2)*
TEGDMA Conc. (mmol/L)	0	0.25	0.5	1
HSP72 Induction (% control) (SD)	100 (8)	47 (4)*	69 (6)*	15 (1)*

HSP72induction by heat shock during the 7 h period.  TEGDMA was a more potent suppressor than HEMA.  Conclusions: HEMA and TEGDMA suppress  THP-1 monocytes' ability to express HSP72 at subtoxic concentrations.  Released dental monomers may affect cellular response to chemical or thermal stress. (Support: Grant-in-aid 13877349 MESSC Japan/MCG)  

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