Cytotoxicity of endodontic materials over 6-weeks ex vivo.

AIM: To test the hypothesis that extending the time of a traditional ex vivo cytotoxicity test helps to identify trends in the behaviour of root core materials and sealers, which could ultimately aid in predicting their clinical safety and performance. METHODOLOGY: Endodontic sealers and core specimens were initially tested in direct contact with L929 fibroblasts for 72 h. Cell response was estimated by measuring cellular succinate dehydrogenase activity relative to Teflon controls. Cytotoxicity (% of more active cells) was reassessed after 1, 3, 4 and 6 weeks, with the specimens stored in a physiologically balanced salt-solution between tests. RESULTS: Distinct trends in cytotoxicity among both core materials and sealers were observed over the 6-week test. Four of the six sealers and two of the three core materials showed cell viabilities of <30% of Teflon after 6 weeks (>70% cytotoxicity). CONCLUSIONS: The current results suggest that some endodontic materials have an elevated biological risk for extended intervals.

Initial cytotoxicity of novel titanium alloys.

We assessed the biological response to several novel titanium alloys that have promising physical properties for biomedical applications. Four commercial titanium alloys [Super-TIX(R) 800, Super-TIX(R) 51AF, TIMETAL(R) 21SRx, and Ti-6Al-4V (ASTM grade 5)] and three experimental titanium alloys [Ti-13Cr-3Cu, Ti-1.5Si and Ti-1.5Si-5Cu] were tested. Specimens (n = 6; 5.0 x 5.0 x 3.0 mm(3)) were cast in a centrifugal casting machine using a MgO-based investment and polished to 600 grit, removing 250 mum from each surface. Commercially pure titanium (CP Ti: ASTM grade 2) and Teflon (polytetrafluoroethylene) were used as positive controls. The specimens were cleaned and disinfected, and then each cleaned specimen was placed in direct contact with Balb/c 3T3 fibroblasts for 72 h. The cytotoxicity [succinic dehydrogenase (SDH) activity] of the extracts was assessed using the MTT method. Cytotoxicity of the metals tested was not statistically different compared to the CP Ti and Teflon controls (p > 0.05). These novel titanium alloys pose cytotoxic risks no greater than many other commonly used alloys, including commercially pure titanium. The promising short-term biocompatibility of these Ti alloys is probably due to their excellent corrosion resistance under static conditions, even in biological environments.

In vitro biological effects of sodium titanate materials.

UNLABELLED: Monosodium titanate (MST) particles effectively bind specific metals and are therefore promising compounds for delivery or sequestration of metals in biological contexts. Yet, the biological properties of MST are largely unexplored. Our previous study showed that the cytotoxicity of these compounds was mild, but the nature of the dose response curves suggested that residual titanates in culture may have interfered with the assay. In the current study, we assessed the importance of these artifacts, and extended our previous results using fibroblasts for biological evaluation. We also assessed the biological response to a new type of titanate (referred to as amorphous peroxo-titanate or APT) that shows more promising metal binding properties than MST. METHODS: The degree of titanate-induced interference in the MTT (mitochondrial activity assay) was estimated by means of cell-free assays with and without a final centrifugation step to remove residual titanate particulate. Cytotoxic responses to titanates were assessed by measuring succinate dehydrogenase activity (by MTT) in THP1 monocytes or L929 fibroblasts after 24-72 h exposures. Monocytic activation by APT was assessed by TNFalpha secretion (ELISA) from monocytes with or without lipopolysaccharide (LPS) activation. RESULTS: We confirmed that residual titanate particulates may alter the SDH activity assay, but that this effect is eliminated by adding a final centrifugation step to the standard MTT procedure. Addition of MST or APT at concentrations up to 100 mg/L altered succinate dehydrogenase activity by < 25% in both monocytes and fibroblasts. Fibroblasts displayed time-dependent adaptation to the MST. APT did not trigger TNFalpha secretion or modulate LPS-induced TNFalpha secretion from monocytes. CONCLUSIONS: Although further in vitro and in vivo assessment is needed, MST and APT exhibit biological properties that are promising for their use as agents to sequester or deliver metals in biological systems.

In vitro cytotoxicity of dental composites based on new and traditional polymerization chemistries.

UNLABELLED: The biological response to dental restorative polymer composites is mediated by the release of unpolymerized residual monomers. Several new composite formulations claim to reduce unpolymerized residual mass. The current study assessed the cytotoxic responses to several of these new formations and compared them with more traditional formulations. Our hypothesis predicted that if these new polymerization chemistries reduce unpolymerized residual mass, the cytotoxicity of these materials also should be reduced relative to traditional formulations. METHODS: Materials (HerculiteXRV, Premise, Filtek Supreme, CeramxDuo, Hermes, and Quixfil) were tested in vitro in direct contact with Balb mouse fibroblasts, initially, then after aging in artificial saliva for 0, 1, 3, 5, or 8 weeks. The toxicity was determined by using the MTT assay to the estimate SDH activity. Knoop hardness of the materials also was measured at 0 and 8 weeks to determine whether surface breakdown of the materials in artificial saliva contributed to cytotoxic responses. RESULTS: Materials with traditional methacrylate chemistries (Herculite, Premise, Filtek Supreme) were severely (>50%) cytotoxic throughout the 8-week interval, but materials with newer chemistries or filling strategies (Hermes, CeramXDuo, and Quixfil) improved over time of aging in artificial saliva. Hermes showed the least cytotoxicity at 8 weeks, and was statistically equivalent to Teflon negative controls. Hardness of the materials was unaffected by exposure to artificial saliva. CONCLUSIONS: Newer polymerization and filling strategies for dental composites show promise for reducing the release of unpolymerized components and cytotoxicity.

Intra- and extracellular reactive oxygen species generated by blue light.

Blue light from dental photopolymerization devices has significant biological effects on cells. These effects may alter normal cell function of tissues exposed during placement of oral restorations, but recent data suggest that some light-induced effects may also be therapeutically useful, for example in the treatment of epithelial cancers. Reactive oxygen species (ROS) appear to mediate blue light effects in cells, but the sources of ROS (intra- versus extracellular) and their respective roles in the cellular response to blue light are not known. In the current study, we tested the hypothesis that intra- and extracellular sources of blue light-generated ROS synergize to depress mitochondrial function. Normal human epidermal keratinocytes (NHEK) and oral squamous cell carcinoma (OSC2) cells were exposed to blue light (380-500 nm; 5-60 J/cm(2)) from a dental photopolymerization source (quartz-tungsten-halogen, 550 mW/cm(2)). Light was applied in cell-culture media or balanced salt solutions with or without cells present. Intracellular ROS levels were estimated using the dihydrofluorescein diacetate (DFDA) assay; extracellular ROS levels were estimated using the leucocrystal violet assay. Cell response was estimated using the MTT mitochondrial activity assay. Blue light increased intracellular ROS equally in both NHEK and OSC2. Blue light also increased ROS levels in cell-free MEM or salt solutions, and riboflavin supplements increased ROS formation. Extracellularly applied ROS rapidly (50-400 muM, <1 min) increased intracellular ROS levels, which were higher and longer-lived in NHEK than OSC2. The type of cell-culture medium significantly affected the ability of blue light to suppress cellular mitochondrial activity; the greatest suppression was observed in DMEM-containing or NHEK media. Collectively, the data support our hypothesis that intra- and extracellularly generated ROS synergize to affect cellular mitochondrial suppression of tumor cells in response to blue light. However, the identity of blue light targets that mediate these changes remain unclear. These data support additional investigations into the risks of coincident exposure of tissues to blue light during material polymerization of restorative materials, and possible therapeutic benefits.

Adsorption of biometals to monosodium titanate in biological environments.

Monosodium titanate (MST) is an inorganic sorbent/ion exchanger developed for the removal of radionuclides from nuclear wastes. We investigated the ability of MST to bind Cd(II), Hg(II), Au(III), or the Au-organic compound auranofin to establish the utility of MST for applications in environmental decontamination or medical therapy (drug delivery). Adsorption isotherms for MST were determined at pH 7-7.5 in water or phosphate-buffered saline. The extent of metal binding was determined spectroscopically by measuring the concentrations of the metals in solution before and after contact with the MST. Cytotoxic responses to MST were assessed using THP1 monocytes and succinate dehydrogenase activity. Monocytic activation by MST was assessed by TNFalpha secretion (ELISA) with or without lipopolysaccharide (LPS) activation. MST adsorbed Cd(II), Hg(II), and Au(III) under conditions similar to those in physiological systems. MST exhibited the highest affinity for Cd(II) followed by Hg(II) and Au (III). MST (up to 100 mg/L) exhibited only minor (<25% suppression of succinate dehydrogenase) cytotoxicity and did not trigger TNFalpha secretion nor modulate LPS-induced TNFalpha secretion from monocytes. MST exhibits high affinity for biometals with no significant biological liabilities in these introductory studies. MST deserves further scrutiny as a substance with the capacity to decontaminate biological environments or deliver metals or metal compounds for therapeutic applications.

Au(III), Pd(II), Ni(II), and Hg(II) alter NF kappa B signaling in THP1 monocytic cells.

The transcription factor NFkappaB plays a key role in the tissue inflammatory response. Metal ions released into tissues from biomaterials (e.g., Au, Pd, Ni, Hg) are known to alter the binding of NFkappaB proteins to DNA, thereby modulating the effect of NFkappaB on gene activation and, ultimately, the tissue response to biomaterials. Little is known about the effect of these metals on key signaling steps prior to NFkappaB-DNA binding such as transcription factor activation or nuclear translocation, yet these steps are equally important to modulation of the pathway. Oxidative stress is known to alter NFkappaB proteins and is suspected to play a role in metal-induced NFkappaB signaling modulation. Our aim in the current study was to assess the effects of sublethal levels of Ni, Hg, Pd, and Au ions on NFkappaB activation and nuclear translocation in the monocyte, which is acknowledged as an important orchestrator of the biological response to materials and the pathogenesis of chronic disease. Sublethal concentrations of Au(III), Ni(II), Hg(II), and Pd(II) were added to cultures of human THP1 monocytic cells for 72 h. In parallel cultures, lipopolysaccharide (LPS) was added for the last 30 min to activate the monocytic cells. Then cellular cytoplasmic and nuclear proteins were isolated, separated by electrophoresis, and probed for IkappaBalpha degradation (activation) and NFkappaB p65 translocation. Protein levels were digitally quantified and statistically compared. The levels of reactive oxygen species (ROS) in the monocytic cells were measured as a possible mechanism of metal-induced NFkappaB modulation. Only Au(III) activated IkappaBalpha degradation by itself. Au(III) and Pd(II) enhanced LPS-induced IkappaBalpha degradation, but Hg(II) and Ni(II) suppressed it. Au(III), Ni(II), and Pd(II) activated p65 nuclear translocation without LPS, and all but Ni(II) enhanced LPS-induced translocation. Collectively, the results suggest that these metal ions alter activation and translocation of NFkappaB, each in a unique way at unique concentrations. Furthermore, even when these metals had no overt effects on signaling by themselves, all altered activation of signaling by LPS, suggesting that the biological effects of these metals on monocytic function may only be manifest upon activation. None of the metal ions elevated levels of ROS at 72 h, indicating that ROS were probably not direct modulators of the NFkappaB activation or translocation at this late time point.

Anti-rheumatic gold compounds as sublethal modulators of monocytic LPS-induced cytokine secretion.

The objective of this study was to quantify the ability of sublethal concentrations of several gold compounds to differentially modulate the monocytic secretion of key cytokines that are important in the etiology of rheumatic diseases. Human THP1 monocytic cells were exposed to the anti-rheumatic drugs auranofin (AF), gold sodium thiomalate (GSTM) or HAuCl4 (Au(III)) for 24-72 h. Succinate dehydrogenase (SDH) activity of the monocytes was used to determine sublethal concentrations. Monocytes were then exposed to sublethal concentrations of gold compounds for 72 h, and the activator lipopolysaccharide (LPS) was added (or not) to cultures for the last 6h. The secretion of IL6, IL8, IL10, and TNFalpha were measured in cell supernatants using ELISA. Cytokine secretion was compared among concentrations and gold compounds. SDH experiments established a sublethal concentration range of 0-75 microM for GSTM and Au(III) and 0-0.5 microM for AF. In cytokine experiments, none of the compounds alone activated secretion of any of the cytokines, but all differentially (50-440%, p<0.05) increased LPS-induced secretion of IL6 and IL8 over TNFalpha and IL10. In conclusion, sublethal concentrations of AF, GSTM, and Au(III) all may differentially modulate activation of monocytic cells, and this differential modulation may be important in the mechanisms of action of these compounds.

Dental adhesive compounds alter glutathione levels but not glutathione redox balance in human THP-1 monocytic cells.

The use of hydrophilic dental monomers in dentin bonding agents has vastly improved resin-dentin bond strengths, but incomplete polymerization of these monomers and their leaching into adjacent (pulpal) oral tissues has raised concerns about their biocompatibility. The sublethal effects of these resins are virtually unknown, but their electrophilic nature led to the hypothesis that they may alter cellular oxidative stress pathways. Glutathione balance between reduced (GSH) and oxidized (GSSG) is a major mechanism by which cells maintain redox balance and was therefore the focus of the current investigation. THP-1 human monocytic cells were exposed to hydroxyethyl methacrylate (HEMA), benzoyl peroxide (BPO), camphorquinone (CQ), or triethyelene glycol dimethacrylate (TEGDMA) for 24 h at sublethal doses, then GSH and GSSG levels were measured by means of Ellman's method adapted for cell culture. The results indicate that these dental resin compounds act at least partly via oxidative stress by increasing GSH levels at sublethal concentrations. However, the GSH-GSSG ratio was relatively unaffected. Only BPO altered the GSH-GSSG ratio at 24 h, again at sublethal levels (7.5-15 micromol/L). The results support the hypothesis that resin monomers act, at least in part, via oxidative stress, and that oxidative-stress pathways should be one focus of future investigations of monomer biocompatibility.

Fatigue of dental ceramics in a simulated oral environment.

Fatigue in ceramics refers to the subcritical growth of cracks, aided by the combined influence of water and stress. The dynamic fatigue (constant stressing rate) method was used to obtain subcritical crack growth parameters for three dental ceramics: a feldspathic porcelain, an aluminous porcelain, and a fine-grain, polycrystalline core material. The constant stressing rate experiments were carried out at 37 degrees C for all three ceramics in distilled water, and, for the feldspathic porcelain, in artificial saliva as well. Considerable differences were found in the value of the crack growth exponent (n) among the three ceramics. The feldspathic porcelain was lowest in n-value, while the fine-grain ceramic had the highest n-value. No differences were found for the feldspathic porcelain with respect to n measured in water and in the artificial saliva. Lifetime prediction curves in 37 degrees C water, constructed from the n-values and inert strengths, showed that fatigue failure within five years is a good possibility for feldspathic porcelain specimens at stress levels which can reasonably be anticipated to occur in the oral environment. Little likelihood of failure was perceived for the fine-grain ceramic. The aluminous porcelain was intermediate between these two materials with respect to failure probability.

Isothermal anneal effect on microcrack density around leucite particles in dental porcelain.

Because of the large differential in thermal expansion coefficient between leucite and the surrounding glass matrix, microcracks form around the leucite crystallites during the manufacture of dental porcelain frits. These microcracks decouple leucite from the surrounding glass matrix and affect the bulk thermal expansion of the porcelain frit (Binns, 1983). The purpose of this study was to determine if the microcrack density in a dental porcelain decreased as a result of isothermal heat treatment. Ten specimens of a commercial dental porcelain that had previously exhibited an increase in thermal expansion as a function of isothermal heat treatment were prepared and divided into two groups. The experimental group was heated to 750 degrees C and held for 16 minutes at that temperature. The control group received no anneal. The mean microcrack densities were determined by quantitative stereology to be 575 cm2/cm3 +/- 75 cm2/cm3 (mean +/- SEM) for the control group (no anneal) and 231 cm2/cm3 +/- 25 cm2/cm3 for the experimental group (16-minute anneal at 750 degrees C). The specimens annealed at 750 degrees C had a significantly lower microcrack density (p < 0.001) than those that received no anneal. A model was developed to estimate the effect of microcracking on thermal expansion of the porcelain, and a 6% increase in the coefficient of thermal expansion of the porcelain was predicted from this model as a result of this decrease in microcrack density.

Components of dentinal adhesives modulate heat shock protein 72 expression in heat-stressed THP-1 human monocytes at sublethal concentrations.

Few studies have investigated the ability of dental resins to induce cellular stress at sublethal concentrations. Cellular stress, especially in immune cells such as monocytes, may modulate the biological response to materials or the host's ability to respond to bacterially mediated inflammation. The current study examined the ability of sublethal concentrations of 2-hydroxylethylmethacrylate (HEMA) and triethyleneglycol dimethacrylate (TEGDMA) to induce heat shock protein 72 (HSP72) in human monocytes. HEMA and TEGDMA significantly suppressed heat-induced HSP72 expression, even at sublethal levels, but did not induce HSP72 by themselves. The results of the current study suggest that components released from dental resin could modulate the HSP stress response without altering cellular metabolic activity.

Blue light differentially modulates cell survival and growth.

Previous studies have reported that blue light (400-500 nm) inhibits cell mitochondrial activity. We investigated the hypothesis that cells with high energy consumption are most susceptible to blue-light-induced mitochondrial inhibition. We estimated cell energy consumption by population doubling time, and cell survival and growth by succinate dehydrogenase (SDH) activity. Six cell types were exposed to 5 or 60 J/cm(2) of blue light from quartz-tungsten-halogen (QTH), plasma-arc (PAC), or argon laser sources in monolayer culture. Post-light SDH activity correlated positively with population doubling time (R(2) = 0.91 for PAC, 0.76 for QTH, 0.68 for laser); SDH activity increased for cell types with the longest doubling times and was suppressed for cell types with shorter doubling times. Thus, light-induced exposure differentially affects SDH activity, cell survival, and growth, depending on cell energy consumption. Blue light may be useful as a therapeutic modulator of cell growth and survival.

Metal ions alter lipopolysaccharide-induced NF kappa B binding in monocytes.

Metals are components of a variety of biomaterials used in orthopedic and dental appliances; however, their biocompatibility with the surrounding tissues is not completely understood. Monocytes are important immune cells that respond to inflammatory stimuli by rapidly producing a variety of inflammatory proteins. Regulation of this response often involves activation of the transcription factor NF kappa B. The current study was designed to determine whether monocyte activation of NF kappa B in response to bacterial lipopolysaccharide (LPS) is affected by pretreatment with metal ions. Concentrations of metal ions that affected cell number after 24 h of exposure were first determined. Then THP-1 human monocytes were cultured for 2 h in media containing metal ions at concentrations below levels that altered cell growth. Parallel cultures were treated with 10 microg/mL Escherichia coli LPS, and all samples were cultured an additional 2 h. Nuclear proteins were extracted and normalized amounts were incubated with [(32)P]-end-labeled NF kappa B consensus oligonucleotide. NF kappa B-DNA complexes were identified and quantified by electrophoretic mobility shift analysis. The extent of NF kappa B-DNA complex formation after metal ion pretreatment with or without LPS induction was compared to no treatment or LPS-only treated controls. Finally, LPS-induced IL1 beta secretion was measured from palladium-treated and control cells. Concentrations were identified for each metal ion (Ag(+), Co(2+), Cu(2+), Hg(2+), Ni(2+), and Pd(2+)) that did not reduce cell number after 24 h of exposure (ranging from 5 microM for Ag(+) and Hg(2+) to 200 microM for Ni(2+)). Exposures of 2 h at these concentrations did not alter cell morphology, staining with trypan blue, or cell number. LPS exposure had no effect on cell number with or without metal ions after 2 h. When metal treatment alone was assessed, none of the metal ions had a significant effect on NF kappa B-DNA binding. However, pretreatment with Co(2+), Ni(2+), Ag(1+), Hg(2+), and Pd(2+) significantly decreased NF kappa B-DNA binding by 40-70% versus LPS alone. Only Cu(2+) had no effect on LPS-induced NF kappa B-DNA complex formation. Pd(2+) lowered, but did not abolish, IL1 beta secretion at concentrations comparable to those that altered NF kappa B-DNA binding. These results suggest that many commonly used metals alter monocyte function at concentrations that are not overtly toxic, and that protein levels controlled in part by NF kappa B also may be altered.

Hg2+ and Ni2+ alter induction of heat shock protein-72 in THP-1 human monocytes.

The biological liabilities that result from the release of metal ions from biomedical alloys, particularly Ni(2+) and Hg(2+), continue to be a concern. Heat-shock proteins (HSP) are a class of molecular chaperones that may be induced under conditions of cellular stress, including oxidative stress. Our hypothesis was that because Hg(2+) and Ni(2+) alter other cellular stress responses such as glutathione levels and cytokine secretion, these metal ions may alter HSP induction in monocytes, which are key cells in the response of tissues to biomedical alloys. THP-1 monocytes were exposed to sublethal concentrations of Hg(2+) or Ni(2+) for 1 h with or without heat stress (43 degrees C), then allowed to recover at 37 degrees C for 2-6 h. HSP72 was measured using immunoblotting with phosphorimage quantification. Hg(2+) exposures of 2-10 micromol/L induced HSP72 without heat stress. With heat stress, HSP72 levels were altered by Hg(2+) versus heat stress alone. The response depended on the concentration of Hg(2+) and the recovery time. Hg(2+) at 10 micromol/L caused uniformly lower HSP72 levels. Ni(2+) exposures of 20-100 micromol/L did not induce HSP72 without heat stress, but significantly altered heat-induced HSP72 expression, with a significant increase in expression over heat alone at 40 and 100 micromol/L. Results from the current study support the hypothesis that these metal ions can, at concentrations relevant to those released from biomedical alloys, modulate HSP expression in human monocytes. The modulation of HSP expression indicates an early sign of cellular stress that may be important to the overall biological response to biomedical alloys containing and releasing these metal ions.

Release of elements from dental casting alloys into cell-culture medium over 10 months.

OBJECTIVE: The release of elements from eight types of commonly used dental casting alloys into cell-culture medium was measured over a 10-month period. The release of elements was determined to provide information about the long-term biological risk these alloys may pose to the oral tissues. The current work extends previous studies of shorter time periods, and is more relevant to the in vivo situation, where dental alloys are present intraorally for years. METHOD: The alloys were Au-, Ag-, Pd-, and Ni-based with nobilities ranging from 0 to 95 at.%. Alloy samples (n = 12) were exposed to cell-culture medium. The medium was changed every 30 days for 10 months. Elemental release into the medium was measured by means of atomic absorption spectrophotometry. Differences in mass release were determined using ANOVA and Tukey multiple comparison intervals (alpha = 0.05). RESULTS: The release of elements continued through 10 months, and it appeared that the release was constant throughout most of the experiment. Higher initial rates were suspected but not verified. Most alloys reached a constant rate after < 100 days of exposure to the medium. Long-term element release was not generally intuitive based on the amount of an element in an alloy or the overall nobility of the alloy. Total mass lost over the 10-month period ranged from < 2 micrograms/cm2 for the Au-Pd alloy to 55 micrograms/cm2 for the Au-Ag-Cu alloy (Tukey interval at alpha = 0.05 was 0.8 microgram/cm2). By comparison, pure Cu lost 4500 micrograms/cm2 during this period. SIGNIFICANCE: Tests which assess biological risk from elemental release must consider longer-term release because elemental release continues for extended periods. Longer-term mass loss from a given alloy is often not intuitive based on its overall composition or noble metal content.

Elemental release from dental casting alloys into biological media with and without protein.

OBJECTIVE: The objective of this study was to determine the role of proteins in affecting elemental release from a variety of clinically available dental casting alloys. An important role for proteins was suspected based on previous reports about the corrosion of stainless steel and the cytotoxicity of alloys after exposure to a saline-protein solution. METHODS: Clinically available alloys with compositions ranging from 0 to 94at.% noble elements were exposed for 1 week to either saline, saline with 3% bovine serum albumin (BSA), or complete cell-culture medium with 3% serum. Atomic absorption spectrophotometry was used to measure the release of elements from the alloys. Elemental release was normalized for the exposed surface area of the alloys. RESULTS: In general, more elemental release occurred into the saline-BSA solution compared to saline alone for all released elements (Ag, Cu, Pd, and Zn) except for Ni. Ni release from the NiCr alloy was lower in the presence of BSA. Each element responded somewhat differently with Pd being the least predictable in its behavior. Elemental release was less in the cell-culture medium than in the saline-BSA solution for most elements. For alloys which released multiple elements, all elements responded similarly but not identically to the presence of protein. A high elemental release during exposure to the saline-BSA solution correlated with a low alloy cytotoxicity post-exposure to the saline-BSA. SIGNIFICANCE: This study demonstrates the importance of defining exactly the composition of biological solutions used to assess in vitro corrosion and biocompatibility of dental casting alloys. Other molecules in addition to proteins appeared to be critical to the corrosion of these alloys in vitro.

Effect of photoinitiator level on properties of a light-cured and post-cure heated model resin system.

OBJECTIVES: This study evaluated the effect of increased levels of photoinitiator components on biaxial flexural strength, monomer conversion, and dynamic thermal properties of an unfilled model resin system in both the light-cured only state as well as after post-cure heating. METHODS: Unfilled polymer discs were made using 50/50 mole% Bis-GMA and TEGDMA and were rendered photo-curable using a common (normal) concentration of photoinitiators (camphorquinone 0.3 wt% and DMAEMA 0.75 wt%) as well as twice and four-fold this amount. Specimens were light-cured and left unheated or were post-cure heated in a commercial unit. Biaxial flexural strength was obtained at a constant stressing rate (100 MPa/s), monomer conversion was determined using FTIR, and dynamic mechanical thermal properties (E', E", and Tg) were measured with DMA. Data were analyzed using ANOVA and Turkey-Kramer post-hoc test (p < 0.05). RESULTS: Increased levels of photoinitiator above normal significantly increased monomer conversion and Tg values for unheated as well as for post-cure heated specimens. Biaxial flexural strength for light-cured only groups remained unaffected by change in initiator concentration, but was significantly increased by post-cure heating. Increase in initiator concentration did not affect E' values for post-cured specimens, but significantly increased values for the unheated, light-cured only groups. E" values for post-cure heated specimens were significantly lowered by increasing initiator concentration. SIGNIFICANCE: The clinical implications of these results indicate that increasing photoinitiator levels results in post-cure heated restorations with significantly higher Tg and monomer conversion values. Use of elevated initiator concentrations for post-cured resins could result in restorations with enhanced resistance to deformation at elevated oral temperatures as well as significantly lower amounts of leachable components.

The effect of glaze on porcelain strength.

The self-glazing technique provides an esthetic and hygienic surface for crowns and fixed partial dentures that use porcelain veneers. A study of the biaxial flexure strengths of polished vs. glazed specimens is needed to verify that current laboratory methods are appropriate for planned fatigue studies. Four groups of 50 porcelain disk specimens each were subjected to the following polishing and firing procedures: group one was fired, glazed-no hold, and polished; group two was fired, polished, and glazed-no hold; group three was fired, polished and glazed-1 min. hold; group four was fired, polished, and not glazed. The piston-on-three-ball method was used for testing biaxial flexure strengths. Significantly lower differences in biaxial flexure strengths were noted when group two values were compared with values from groups one, three and four. The results show that the Weibull distribution is an appropriate model for our studies. Differences in glaze thickness among the groups were noted in SEM examination; however, bulk (interior) microcrack density differences were absent. The specimens that were fired, polished to a 1 micron surface finish, and not glazed (group four) were significantly higher in flexure strength than groups one and three at the p less than 0.001 level. The hypothesis that glazing of porcelain surfaces improves the biaxial flexure strength of test specimens was rejected.

Effects of HEMA on water evaporation from water-HEMA mixtures.

OBJECTIVES: The aims of this research were: (1) to determine the relative rates of evaporation of water and HEMA, and (2) to determine the effects of increasing concentrations of HEMA on the rate of evaporation of water from water and HEMA mixtures. METHODS: Ten microliters of each solution (100% H2O, 75% H2O-25% HEMA, 50% H2O-50% HEMA, 25% HEMA, 100% HEMA) were placed on the pan of a thermogravimetric analysis instrument held at 37 degrees C. The rate of spontaneous weight loss was measured as a function of time and relative humidity (RH) and compared statistically using ANOVA and Scheffé F test. RESULTS: The rate of evaporation of pure water was 32-fold higher than that of 100% HEMA. Addition of HEMA to water lowered the rate of evaporation of water from the water-HEMA mixtures in a manner that was proportional to its effect on lowering the vapor pressure of water (p < 0.05 comparing 50% HEMA with 75% HEMA). The rate of evaporation of water from water-HEMA mixtures was higher (p < 0.05) when the ambient gas was at 0% RH than when it was at 51% RH. SIGNIFICANCE: The results indicate that as water evaporates from water-HEMA mixtures, the concentration of HEMA rises because it is relatively non-volatile. This rise in HEMA concentration lowers the vapor pressure of water making it more difficult to remove the last amounts of water. This residual water may interfere with polymerization of adhesive monomers, thereby lowering the quality of the hybrid layer.