TEGDMA releasing in resin composites with different filler contents and its correlation with mitochondrial mediated cytotoxicity in human gingival fibroblasts

Abstract

Compositions of resin composite exhibit cytotoxicity, especially Triethylene‐glycol‐dimethacrylate (TEGDMA), yet the underlying mechanisms and its relationship with filler content are poorly understood. Here, specimens of five composites (VITA LC, VITA ZETA, Z350, Filtek P60, and AP‐X), containing different filler size and weight, were immersed into culture medium for 72 h. After TEGDMA quantification, the resin composite eluates were used to incubate HGFs. Cellular viability was evaluated. Total reactive oxygen species (ROS) and mitochondrial ROS were detected to assess oxidative stress. Adenosine triphosphate and cytochrome c oxidase (CcO) activity, mitochondrial membrane potential and morphology, mitochondrial biogenesis regulators were analyzed to evaluate mitochondrial functions. Results showed that TEGDMA release negatively correlated to filler size and weight of tested composites. Although cell viability reduction was not significant, total and mitochondrial ROS production showed a positive relationship with the amount of TEGDMA in composite eluates. Furthermore, the expression of mitochondrial biogenesis markers and mitochondrial fusion protein, were markedly elevated in TEGDMA rich eluates, especially in VITA‐LC group, shown as elongated mitochondrial morphology and aberrant mitochondrial functions. Overall, TEGDMA could elute easier from those resin composites with less filler content and cause oxidative stress in HGFs via mitochondria dysregulation. These data can be instructive to optimize the synthesis of resin composites from the perspective of biocompatibility. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 1132–1142, 2019.

Bioenergetic Impairment of Triethylene Glycol Dimethacrylate- (TEGDMA-) Treated Dental Pulp Stem Cells (DPSCs) and Isolated Brain Mitochondria are Amended by Redox Compound Methylene Blue

“…It was reported that TEGDMA adversely affects cellular metabolism, signaling, differentiation, and dentinogenesis, while it also interferes with wound healing and tissue repair [28,40,[68][69][70][71]; it induces oxidative stress [46][47][48], apoptosis and/or necrosis [42,43,49,72]. Due to its amphiphilic character, TEGDMA can penetrate the membranes of human gingival fibroblast and human oral epithelium of the mouth, resulting in an inflammatory response [73].…”

“…It has been described that inhibition of CI is accompanied by excessive ROS production which can induce cell damage and apoptosis in a dose-dependent manner [76,77]. In line with these observations, Liu et al revealed that 72 h TEGDMA exposure gave rise to cell death and increased ROS formation in human gingival fibroblasts [47]. Furthermore, in a mouse preodontoblast cell line mDPC6T, TEGDMA decreased cell viability, and induced excessive ROS formation [49].…”

“…It was reported earlier that TEGDMA exhibited some of these deleterious effects via mitochondrial impairment [45][46][47][48][49].…”

“…A previous study indicated that TEGDMA treatment suppressed the activity of Complex III (CIII) in mouse dental papilla cells [49]. TEGDMA released from resin composites stimulated the mitochondrial production of ROS and induced alterations in morphology of mitochondria [47].…”

Biodegradation of Dental Resin-Based Composite—A Potential Factor Affecting the Bonding Effect: A Narrative Review

“…Meanwhile, UDMA changes the normal morphology of dental pulp cells, lengthening or shortening normal spindle cells and reducing their activity [ 95 ]. Moreover, oxidative stress of gingival fibroblasts and pre-odontoblasts is initiated by TEGDMA through mitochondrial dysfunction [ 96 , 97 ]. The above are examples of the toxic effects of monomers on cells.…”