S. Ratanasathien

Bio: S. Ratanasathien is an academic researcher from University of Michigan. The author has contributed to research in topics: UDMA & Dentin. The author has an hindex of 1, co-authored 1 publications receiving 283 citations.

Cytotoxic Interactive Effects of Dentin Bonding Components on Mouse Fibroblasts

Abstract: Previous studies have shown a wide range of pulpal reactions to dentin bonding systems and a poor correlation between in vitro and in vivo toxicity of dentin bonding agents. Because dentin bonding agents are composed of multiple components which may diffuse through dentin, we hypothesized that these components may cause cytotoxicity through interactive (synergistic) effects. We investigated the cytotoxicities of four dentin bonding components--HEMA, Bis-GMA, TEGDMA, and UDMA--and interactive effects for three binary combinations of the dentin bonding components--HEMA and Bis-GMA, Bis-GMA and TEGDMA, and TEGDMA and UDMA. Cytotoxicities to Balb/c 3T3 mouse fibroblasts were measured by the MTT assay. Concentrations which caused 50% toxicity compared with controls (TC50 values) were compared, and the interactive effects were determined by evaluation of the differences between observed and expected MTT activities of the cells. The ranks of toxicity of the dentin bonding components in terms of TC50 values were as follows: Bis-GMA > UDMA > TEGDMA >>> HEMA (least toxic) after 24- and 72-hour exposures. As binary combinations, the three combinations of dentin bonding components interacted in three ways--synergism, additivism, and antagonism--which were influenced by the concentrations of both components. The longer period of exposure resulted in a significant increase in the cytotoxicity of the dentin bonding components and combinations. The findings indicate that both exposure time and the interactions between the dentin bonding components may be important parameters in determining the cytotoxicity of dentin bonding agents in vivo.

Cytotoxic effects of acrylates and methacrylates: Relationships of monomer structures and cytotoxicity

Abstract: Thirty-nine acrylates and methacrylates that had been used in dental resin materials were evaluated by a cytotoxicity test, and the relationships between their structures and cytotoxicity were studied to predict cytotoxic levels of dental resin materials in order to develop new low-toxic resin materials All the acrylates evaluated were more toxic than corresponding methacrylates In both the acrylates and methacrylates, a hydroxyl group seemed to enhance cytotoxicity Dimethacrylates with 14 or fewer oxyethylene chains showed similar cytotoxicity while dimethacrylates with 23 oxyethylene chains showed lower cytotoxicity The cytotoxicity ranking of monomers widely used in dental resin materials was bisphenol A bis 2-hydroxypropyl methacrylate (bisGMA) > urethane dimethacrylate (UDMA) > triethyleneglycol dimethacrylate (3G) > 2-hydroxyethyl methacrylate (HEMA) > methyl methacrylate (MMA) In acrylates, methacrylates, and ethylmethacrylates with either substituents, the lipophilicity of substituents affected their cytotoxicity, and an inverse correlation between IC50 and logP was observed These results will be useful in developing new resin materials with low toxic monomer compositions

Biocompatibility of Resin-Modified Filling Materials

Abstract: Increasing numbers of resin-based dental restorations have been placed over the past decade. During this same period, the public interest in the local and especially systemic adverse effects caused by dental materials has increased significantly. It has been found that each resin-based material releases several components into the oral environment. In particular, the comonomer, triethyleneglycol di-methacrylate (TEGDMA), and the 'hydrophilic' monomer, 2-hydroxy-ethyl-methacrylate (HEMA), are leached out from various composite resins and 'adhesive' materials (e.g., resin-modified glass-ionomer cements [GICs] and dentin adhesives) in considerable amounts during the first 24 hours after polymerization. Numerous unbound resin components may leach into saliva during the initial phase after polymerization, and later, due to degradation or erosion of the resinous restoration. Those substances may be systemically distributed and could potentially cause adverse systemic effects in patients. In addition, absorption of organic substances from unpolymerized material, through unprotected skin, due to manual contact may pose a special risk for dental personnel. This is borne out by the increasing numbers of dental nurses, technicians, and dentists who present with allergic reactions to one or more resin components, like HEMA, glutaraldehyde, ethyleneglycol di-methacrylate (EGDMA), and dibenzoyl peroxide (DPO). However, it must be emphasized that, except for conventional composite resins, data reported on the release of substances from resin-based materials are scarce. There is very little reliable information with respect to the biological interactions between resin components and various tissues. Those interactions may be either protective, like absorption to dentin, or detrimental, e.g., inflammatory reactions of soft tissues. Microbial effects have also been observed which may contribute indirectly to caries and irritation of the pulp. Therefore, it is critical, both for our patients and for the profession, that the biological effects of resin-based filling materials be clarified in the near future.

In vitro and in vivo studies on the toxicity of dental resin components: a review

Abstract: In vitro and in vivo studies have clearly identified that some components of restorative composite resins, adhesives, and resin-modified glass ionomer cements are toxic. The mechanisms of cytotoxicity are related firstly to the short-term release of free monomers occurring during the monomer–polymer conversion. Secondly, long-term release of leachable substances is generated by erosion and degradation over time. In addition, ion release and proliferation of bacteria located at the interface between the restorative material and dental tissues are also implicated in the tissue response. Molecular mechanisms involve glutathione depletion and reactive oxygen species (ROS) production as key factors leading to pulp or gingival cell apoptosis. Experimental animal approaches substantiate the occurrence of allergic reactions. There is a large gap between the results published by research laboratories and clinical reports.

Keys to clinical success with pulp capping: a review of the literature

Abstract: Clinical Relevance Confusion and misconceptions surround direct and indirect pulp capping. This review of the literature provides evidence-based recommendations to guide clinicians in their decision-making process when they encounter a situation requiring pulp capping.