Biomedical subjects

John C Wataha

Publications and source records attributed to John C Wataha.

At least 19 recordsLinked to original sources

PubMed2005

Blue light differentially alters cellular redox properties.

Blue light (lambda = 380-500 nm) historically has been used to initiate polymerization of biomaterials and recently has been proposed as a therapeutic agent. New evidence suggests that cell-type-specific responses result from redox changes induced by exposure to blue light. Cultured cells were exposed to defined doses of blue light, equivalent to exposure times of 10 s and 2 min, to achieve energies of 5 J/cm2 and 60 J/cm2, respectively, after which (a) viable cell number, (b) cellular protein profiles, (c) mitochondrial succinate dehydrogenase (SDH) activity, (d) total reactive oxygen species (ROS), and (e) induction of apoptosis were compared to that of nonexposed control cultures. Results showed that blue-light exposure arrested monocyte cell growth and increased levels of peroxiredoxins. SDH activity of normal epidermal keratinocytes (NHEK) was slightly enhanced by blue light, whereas identical treatment of OSC2 oral tumor cells resulted in significant suppression of SDH activity. Blue-light exposure generally induced higher levels of total ROS in OSC2 cells than in NHEK. Finally, only OSC2 cells exhibited signs of apoptosis via Annexin V staining following exposure to blue light. These data support the central hypothesis that blue light induces an oxidative stress response in cultured cells resulting in cell-type-specific survival outcomes. The identification of oxidative stress as a mediator of the effects of blue light is a critical first step in defining its biological risks and therapeutic opportunities.

Apoptosis↗

PubMed2005

Thermal risks from LED- and high-intensity QTH-curing units during polymerization of dental resins.

The aim of this study was to test the ability of an infrared (IR) camera to assess temperature changes and distributions in teeth below restorations when quartz-tungsten-halogen (QTH) and light-emitting diode (LED) curing lights were used to photopolymerize the restorative material. Our hypothesis was that the higher power density and broader spectral distribution of the QTH source would cause greater increases in tooth temperature than the LED source, and that these differences would be best demonstrated with the IR camera. Cavities were prepared on human third molars and restored with a resin composite restorative material. The material was light-cured using three light-curing sources using several exposure times. The external (outside the tooth) and internal (inside the pulp chamber) temperature changes during polymerization of the composite material were recorded over 360 s with thermocouples and an IR camera. Using thermocouples the maximum increase in external temperature (+17.7 degrees C) was reported for the Swiss Master light after 20 s of curing time while the minimum temperature rise (+7.8 degrees C) was reported for the Freelight 2. Whereas a 2.6 degrees C increase in internal temperature was observed after curing 20 s with the Freelight 2, 7.1 degrees C was reported after 60 s of light exposure to Astralis 10. Infrared images showed similar trends in external-internal rises in temperature as the thermocouples, although temperatures measured by the IR were generally higher. These results indicate that the higher power density QTH sources caused greater increases in tooth temperatures than the LED source and that thermocouples may underestimate the heat applied to the tooth.

Composite Resins↗

PubMed2005

Blue light generates reactive oxygen species (ROS) differentially in tumor vs. normal epithelial cells.

OBJECTIVES: Blue light of high intensity is commonly used in dentistry to activate polymerization of resin restorative materials. Other than its effects on the retina, the biological effects of blue light (380-500nm wavelengths) are poorly studied. Limited evidence suggests that blue light acts by forming intracellular reactive oxygen species (ROS) that then affect critical cell functions. If the biological effects of blue light are redox-mediated, antioxidants might be used to mitigate unwanted side effects of blue light during clinical use, or blue light might be used therapeutically to modulate redox-sensitive cell signaling responses. METHODS: Intracellular ROS were estimated using HFLUOR-DA (dihydrofluorescein diacetate), a vital fluorescein-based, redox-sensitive dye. ROS were measured in normal (NHEK) and oral squamous carcinoma (OSC2) epithelial cells, shown previously to respond differentially to blue light irradiation. Two-hour cumulative levels of ROS and approximate ROS lifetimes were measured after irradiation doses of 5-30 J/cm(2). The blue light-induced generation of ROS was further tested by the ability of the antioxidants N-acetylcysteine (NAC) and vitamin E to mitigate intracellular ROS levels. RESULTS: Dose-dependent ROS levels were generated in both NHEK and OSC2 cells, but cumulative levels were higher and persisted longer in the OSC2 cells. Both vitamin E and NAC significantly reduced blue-light-induced levels of ROS, but were more effective in the OSC2 cells. SIGNIFICANCE: The induction of intracellular ROS by blue light implies that redox effects may mediate cellular responses to blue light. This result suggests the opportunity to mitigate any effects of direct or coincident exposure during dental treatment via antioxidants, and the opportunity to exploit differences in redox processing among cells for possible treatment of epithelial cancer or wound healing.

Antioxidants↗

PubMed2005

Effect of vascular stent alloys on expression of cellular adhesion molecules by endothelial cells.

OBJECTIVE: Nickel and cobalt ions activate ICAM1 expression on endothelial cells and keratinocytes. Furthermore, these ions are released in vitro and in vivo from the types of alloys used for vascular stents, but the full biological consequences of this release is not known. In the current study, we determined if release of elements from vascular stent alloys that contained nickel and cobalt was sufficient to activate expression of key cellular adhesion molecules (CAMs) by endothelial cells. Expression of these CAMs is a critical step in the long-term inflammatory response to stent materials and possibly to in-stent restenonsis. METHODS: Stainless steel, NiTi, CoCrNi, and NiCr alloys were placed in direct contact with primary human microvascular endothelial cells for 72 hours after preparation at three roughnesses (120, 320, and 1200 grit). Expression of three CAMs--ICAM1, VCAM1, and e-selectin--was assessed using a modified ELISA procedure. Cytotoxicity of the alloys was assessed by measuring succinate dehydrogenase (SDH) activity and total protein content of the cells, and nickel release was measured by atomic absorption spectroscopy. RESULTS: None of the alloys suppressed SDH activity or total cellular protein significantly at any surface roughness, indicating little or no cytotoxicity. Ni release was measurable from all alloys, was greatest from the rougher surfaces, and was significantly different for the different alloy types. NiTi alloys exhibited the lowest nickel release. However, none of the alloys activated expression of the CAMs, regardless of surface roughness or nickel release level. Supplemental experiments using nickel ions alone confirmed that ICAM1 was inducible on the endothelial cells by Ni(II) concentrations above 100 microM. CONCLUSIONS: In this in vitro system, nickel or other elemental release from several common types of stent alloys was not sufficient to activate expression of CAMs on endothelial surfaces. Although these results indicate a low risk for direct activation of endothelial cells by ions released from stent alloys, other mechanisms, such as modulation of CAM expression by monocytes or smooth muscle cells, must be considered before ion-mediated influence on CAM expression can be dismissed.

Alloys↗

PubMed2004

Effects of subtoxic concentrations of benzoyl peroxide on cell lipid metabolism.

Benzoyl peroxide (BP), a tumor promoter, has been shown to cause free-radical-induced lipid peroxidation and membrane damage at toxic concentrations. However, its effects on lipid metabolism at concentrations that were not overtly toxic have not been investigated. The purpose of the current study was to examine the effects of BP and its final degradation product, benzoic acid (BA), on lipid metabolism. Two cell lines, hamster cheek pouch (HCP) and human monocytes (THP-1), were used to determine the effects of BP, BA, and BP combined with FeCl2 on cell lipid metabolism. Cells were exposed to BP and 14C acetate for 24 h, or cells with prelabeled lipids were harvested, and the lipids were extracted and separated with the use of thin-layer chromatography. Lipid metabolism of some neutral lipids such as triglycerides was altered for both cell types in response to BP. Also, cholesterol content was reduced in THP-1 cells and a phospholipid, phosphatidylethanolamine (PE), was reduced in HCP cells. The final degradation product of BP, BA, failed to elicit any response in lipid metabolism. Subtoxic concentrations of BP induced changes in neutral lipids such as triglycerides and cholesterol. The metabolism of major phospholipids except PE remained unchanged. The effects were related to BP and its degradation and varied with the cell type.

Animals↗

PubMed2004

Sublethal concentrations of Au (III), Pd (II), and Ni(II) differentially alter inflammatory cytokine secretion from activated monocytes.

Many transition metals have been viewed collectively as nonspecific biological toxins in cells, which has limited investigation into their possible therapeutic effects. In the current study, the effects of Au(III), Ni(II), and Pd(II) on the differential secretion of cytokines from monocytes has been investigated. This is critical to understanding any therapeutic potential of these metals, their allergenicity, or the clinical effects of current metal therapies such as chrysotherapy. Lethal concentrations (defined as > 50% suppression of mitochondrial succinate dehydrogenase (SDH) activity) of metals were determined by dose-response curves with the use of 72 h exposures to human THP-1 monocytes. Then, secretion of TNFalpha, IL1beta, and IL6 were measured after the monocytes were exposed to sublethal concentrations of metals, with or without stimulation by lipopolysaccharide. The concentrations of Au(III), Pd(II), and Ni(II) required to suppress SDH activity by 50% were found to be 255, 270, and 90 microM, respectively. No sublethal concentration of any metal alone caused secretion of the cytokines. However, LPS-induced cytokine secretion was significantly and differentially altered by sublethal concentrations of each metal. Differential responses were highly dependent on metal concentration and involved both suppression and potentiation of the LPS activation. In the case of Ni(II), potentiation of TNFalpha, IL1beta, and IL6 ranged from 200% for TNFalpha to over 1200% for IL6. Metals such as Au(III), Pd(II), and Ni(II) differentially alter cytokine expression from monocytes. These results imply that metals have more specific effects on cell signaling than previously assumed. These results also are important in explaining multiple clinical effects often seen with chrysotherapy, identifying potential new avenues for metal therapy, and understanding the inflammatory effects of metals such as nickel.

Cell Line↗

PubMed2004

Casting alloys.

Although the role of dental casting alloys has changed in recent years with the development of improved all-ceramic materials and resin-based composites, alloys will likely continue to be critical assets in the treatment of missing and severely damaged teeth. Alloy shave physical, chemical, and biologic properties that exceed other classes of materials. The selection of the appropriate dental casting alloy is paramount to the long-term success of dental prostheses,and the selection process has become complex with the development of many new alloys. However, this selection process is manageable if the practitioner focuses on the appropriate physical and biologic properties, such as tensile strength, modulus of elasticity,corrosion, and biocompatibility, and avoids dwelling on the less important properties of alloy color and short-term cost. The appropriate selection of an alloy helps to ensure a longer-lasting restoration and better oral health for the patient.

Biocompatible Materials↗

PubMed2004

Biological effects of blue light from dental curing units.

OBJECTIVES: This study assessed the effects of three common dental photo-curing light sources (quartz-tungsten-halogen (QTH), plasma-arc (PAC), and laser) on the cellular function of fibroblasts in vitro. METHODS: Mouse fibroblasts were exposed to light from dental photo-curing units for clinically relevant durations, with total energy exposures ranging from 1.3 to 60 J/cm(2). The temperature rise of the cell-culture medium was measured to assess any possible effect from temperature increases, and cellular function was assessed by succinic dehydrogenase (SDH) activity of mitochondria. To directly compare the three light sources, additional experiments were done using equivalent total energy exposures from each source by adjusting the exposure durations for each unit. RESULTS: In experiments that used clinically relevant exposure durations for each light, exposures ranging from 5 J/cm(2) (laser) to 15 J/cm(2) (PAC, QTH) irreversibly suppressed SDH activity nearly 100% when compared to no-light controls up to 72 h post-exposure. For the PAC and QTH sources, exposures as low as 3.5 J/cm(2) also irreversibly suppressed SDH activity. When equivalent energies were used from each light source, exposures of 1 J/cm(2) did not suppress SDH activity for the QTH and laser sources, but significantly (50%) suppressed SDH for the PAC source, indicating a difference in the biological effects of the outputs of the different curing units. Equivalent energy exposure experiments also indicated a definite dependence of SDH activity on the total light energy of exposure. Temperature rises ranged from 2 to 9 degrees C, and elevated temperatures lasted for 60-300 s above the base temperature of 37 degrees C, but peak temperature and the duration of temperature elevation were not always related and depended on the light source used. SIGNIFICANCE: Results from the current study indicate that these photo-curing sources pose some risk of disrupting cellular function in vivo. Further study is necessary in other cell types and under more clinically relevant conditions to estimate the in vivo risk of photo-curing to oral tissues.

3T3 Cells↗

PubMed2004

Cytotoxicity and sealing properties of four classes of endodontic sealers evaluated by succinic dehydrogenase activity and confocal laser scanning microscopy.

The objectives of this study were to evaluate the cytotoxicity and sealing properties of four classes of endodontic sealers (PCS/Kerr, RoekoSeal/Roeko, TopSeal/Dentsply, and EndoREZ/Ultradent). For cytotoxicity testing (MTT method), the materials were either placed immediately in contact with cultured cells or 24 h after setting, then evaluated at three subsequent time points (24 h, 48 h, or 1 wk). For the leakage study, extracted human roots were obturated with acrylic cones and sealers and immersed for 48 h into rhodamine-labeled lipopolysaccharide. The roots were then observed under a confocal laser scanning microscope to estimate (semiquantitatively) the presence of the rhodamine-lipopolysaccharide (LPS) inside the canal. The results showed that cytotoxicity generally increased with time, and that most materials pose significant cytotoxic risks, particularly in the freshly mixed condition. Further, all materials showed significant leakage although there was large variation among teeth. Overall, the silicon-based material (Roeko Seal) was less cytotoxic and more effective in sealing root canals against LPS leakage than other materials.

Analysis of Variance↗

PubMed2003

Toothbrushing causes elemental release from dental casting alloys over extended intervals.

The release of elements from dental alloys has been linked to alloy biocompatibility. Much of the research measuring elemental release has been done in vitro under passive conditions. The current study supplements a previous report that measured elemental release from dental alloys during and after the equivalent of 1 week of toothbrushing. In the current study, toothbrushing times were extended to the equivalent of 2 years, and elemental release was measured during and after brushing, with and without toothpaste. The results showed that for the major classes of dental alloys, brushing alone caused no significant elemental release during the brushing, and only minor increases after brushing. Brushing with toothpaste caused significant increases in elemental release for all elements of all alloys, but the largest increases were for the two nickel-based alloys. Nickel released during brushing with toothpaste reached 600-800 microg/cm(2) of alloy surface. Both beryllium-containing and non-beryllium-containing nickel-based alloys behaved similarly, refuting claims that non-beryllium alloys are superior in this regard. Thus, brushing with toothpaste under these extended in vitro conditions appears to increase the biological liabilities from elemental release for all alloys, but primarily for nickel-based alloys.

Alloys↗

PubMed2003

Effect of subtoxic concentrations of metal ions on NFkappaB activation in THP-1 human monocytes.

THP-1 human monocytes and human peripheral blood monocytes have altered inflammatory cytokine secretion profiles after exposure to a variety of metal ions known to be released from biomaterials. Transcriptional regulation of these cytokines often involves activation of the transcription factor NFkappaB. The present study was designed to determine whether metal ion treatment of monocytes results in changes in levels of activated NFkappaB. THP-1 cells were grown in suspension in the presence of sublethal concentrations of ions of Ag(+), Co(2+), Cu(2+), Hg(2+), Ni(2+), and Pd(2+). After 24 h of exposure to metal ions, the cells were harvested, counted, and the nuclear proteins extracted. Electrophoretic mobility shift assays were performed using a (32)P-ATP end-labeled oligonucleotide consensus sequence for the NFkappaB transcription factor. DNA/protein complexes were quantified by phosphorimage analysis and compared by ANOVA (Tukey, alpha = 0.05). Exposure of THP-1 cells to 100 microM of Pd(2+) caused a significant increase in activated NFkappaB (p < 0.05) whereas treatment with 5 microM of Ag(+) resulted in significantly decreased levels of nuclear NFkappaB (p < 0.05). No other metal ions tested caused a significant change in basal levels of nuclear NFkappaB (Co(2+), Hg(2+), Ni(2+), and Cu(2+)). However, exposure to 50 microM of Cu(2+) resulted in a reproducible, though not significant, increase in nuclear NFkappaB levels. These results indicate that inflammatory responses to some metal ions may be influenced by NFkappaB-mediated transcriptional regulation.

Autoradiography↗

PubMed2003

In vitro cytotoxicity of traditional versus contemporary dental ceramics.

STATEMENT OF PROBLEM: The biocompatibility of new dental ceramics has not been assessed with the same scrutiny as has been applied to alloys and composites. Yet, the biocompatibility of ceramics is critical to the long-term success of dental prostheses because ceramics are in close contact with oral tissues for extended periods. MATERIAL AND METHODS: Five dental ceramics (2 traditional feldspathic veneer porcelains [Vita Omega and Duceragold], 2 lithium disilicate pressable materials [Stylepress and Empress-2], and a pressable leucite-based material [Empress-1]) were tested for their ability to alter cellular mitochondrial dehydrogenase activity after fabrication using a tetrazolium assay, after aging for 2 weeks in a biologic solution and after post-aging polishing with either a fine diamond or diamond polishing paste. Cellular responses were compared with polytetrafluoroethylene controls (analysis of variance, Tukey pairwise post-hoc comparison, alpha=.05). RESULTS: The feldspathic porcelains caused only mild (<25% of controls) mitochondrial suppression regardless of aging or polishing. The pressable leucite-based material initially caused a 5% stimulation (not significant) of mitochondrial activity, which decreased significantly (P<.05) by 30% with aging to levels comparable to the feldspathic porcelains, and did not change with polishing. Both lithium disilicate materials caused an initial suppression of mitochondrial activity that decreased significantly with aging, but Empress-2 was severely cytotoxic initially (<20% of controls, P<.01), and became more cytotoxic again after polishing. Stylepress was less cytotoxic initially (85% of controls, not significant) and did not become cytotoxic again after polishing. CONCLUSIONS: Dental ceramics are not equivalent in their in vitro biologic effects, even within the same class of material, and biologic safety should not be assumed. Most ceramics caused only mild in vitro suppression of cell function to levels that would be acceptable on the basis of standards used to evaluate alloys and composites. However, 1 Li-disilicate material (Empress-2) exhibited cytotoxicity that would not be deemed biologically acceptable on the basis of prevailing empirical standards for dental alloys and composites.

Aluminum Silicates↗

PubMed2003

In vitro biological response to core and flowable dental restorative materials.

OBJECTIVES: In vitro cytotoxicities of commercially available core and flowable dental restorative materials were assessed and compared to traditional resin composites. Our hypothesis was that the increased resin diluents added to achieve higher flow in flowables would increase cytotoxicities, whereas the higher filler content of core materials would decrease cytotoxicities relative to traditional resin composites. METHODS: Specimens were made under aseptic conditions, then extracted into an artificial saliva solution for 0-4 weeks, to assess the effect of aging on cytotoxicity. After extraction, specimens were tested for cytotoxicity in vitro using Balb/c fibroblasts in direct contact format. Cells were exposed to the materials for 48h, after which the mitochondrial activity of the cells was measured (MTT method). Cellular activity was normalized to Teflon negative controls. RESULTS: Core materials were uniformly and severely (<50% of Teflon cellular activity) cytotoxic initially, but several materials (Corepaste, Definite core) improved somewhat with aging in artificial saliva. Flowable materials were uniformly and severely cytotoxic with no trend toward improvement with aging. The Definite-flow was the least cytotoxic of the flowable materials, but it too was severely cytotoxic. SIGNIFICANCE: Commercially available core and flowable restorative materials showed severe in vitro cytotoxicities that are worse than some traditional composites and most dental casting alloys and amalgams used today. Of particular note was the persistent cytotoxicity of these materials after 4 weeks of extraction with artificial saliva. These cytotoxicities indicate a continuing release of mass from these materials at levels that have biological relevance in vitro. In vivo relevance of these cytotoxicities is less clear, but these results indicate a higher biological risk for these materials compared to traditional materials that exhibit less initial toxicity and improve with aging time.

3T3 Cells↗

PubMed2003

Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes.

OBJECTIVES: The aim of this study was to investigate the hypothesis that dental material components alter cytokine secretion from monocytes if applied for several weeks at sublethal doses. The current study significantly extended exposure times of monocytes to the components over times published in previous studies. These exposure times approached the estimated average life span of monocytes in the bloodstream. METHODS: Human THP-1 monocytes were exposed to 2-hydroxyethylmethacrylate (HEMA, 0-1.2mmol/l), triethyleneglycoldimethacrylate (TEGDMA, 0-0.75mmol/l), Hg(2+) (0-2 micromol/l), or Ni(2+) (0-20 micromol/l) for 2 weeks. The cells were then collected and additionally incubated for 24h, with or without bacterial lipopolysaccharide (LPS), a common component of dental plaque. TNF-alpha secretion from THP-1 was determined using by enzyme-linked immunosorbent assay. RESULTS: None of the dental material components induced TNF-alpha from THP-1 by themselves, but LPS alone strongly induced TNF-alpha secretion as expected. HEMA and TEGDMA significantly suppressed (40-70%) TNF-alpha secretion from cells stimulated with LPS. Hg(2+) at 2.0 micromol/l doubled TNF-alpha secretion from THP-1s stimulated with LPS over LPS alone. Ni(2+) did not significantly affect TNF-alpha secretion, with or without LPS exposure. Significance. The results in this study suggest that sublethal, 2-week exposures of some dental material components may alter TNF-alpha secretion from THP-1 monocytes when the cells are challenged. These alterations may influence the biological response of tissues to materials in an inflammatory intraoral environment.

Analysis of Variance↗

PubMed2003

Microtensile bond strength between adhesive cements and root canal dentin.

OBJECTIVES: The hypotheses tested were that the bond strength of adhesive cements to root canal dentin (1) would be reduced as a function of configuration factor, polymerization process and type of luting material and (2) would be lowered near the apex of the tooth. METHODS: Human canines and premolars were prepared for post cementation using Single Bond/Rely X ARC, ED Primer/Panavia F, C and B Metabond, and Fuji Plus. The specimens were divided into two groups. For intact roots, the posts were luted using standard clinical procedures. For flat roots, the posts were applied directly into flat ground canals. All roots were sectioned into 0.6 mm thick slices, trimmed mesio-distally and stressed to failure at 1 mm/min. The muTBS of each slab was calculated as the force at failure divided by the bonded cross-sectional surface area. The results were compared using a one-way ANOVA and Tukey multiple comparison intervals (alpha=0.05). Least squares linear regression analysis was used to assess the effect of dentin location on bond strength. RESULTS: All cements showed significantly (p</=0.05) lower bond strengths in intact vs. flat roots. The muTBS of posts to intact roots were not significantly different for Single Bond/Rely X ARC and Panavia F, but both were significantly lower (p</=0.05) than the bonds produced by C and B Metabond and Fuji Plus cements. For Single Bond/Rely X ARC and Fuji Plus a significant decrease in bond strength was observed in dentin closer to the apex of the root. SIGNIFICANCE: Stresses from polymerization shrinkage and problems with adequate access to the root canal complicate the formation of high-strength bonds when cementing endodontic posts with resin cements.

Analysis of Variance↗

PubMed2003

Effect of hydrolyzed surface layer on the cytotoxicity and chemical resistance of a low fusing porcelain.

OBJECTIVE: The objectives of this study were to verify the formation of a hydrolyzed surface layer on Duceram LFC and to determine its effect on the cytotoxicity of the porcelain as measured by cellular activity and concentrations of leached ionic species. METHODS: Specimens were fabricated from dentin porcelain by a vibration blotting technique. Half of the specimens underwent accelerated aging by subjecting them to the standard test for hydrolytic resistance (ISO 6872). Fibroblast cell cultures were placed in direct contact with specimens. Cell viability was assessed using succinic dehydrogenase activity. Chemical resistance was determined by leaching specimens with a continuous flow of deionized water and measuring the concentrations of soluble ions in the leachates. Porcelain surface topography was examined using atomic force microscopy, and Fourier transform infrared spectroscopy was used to detect the composition of the surface layer. RESULTS: Hydrolyzation treatment created a smooth texture on the porcelain surfaces but did not result in a hydrolyzed surface layer with increased hydroxyl content. There was a decreased alkali ion content in the surface layer of hydrolyzed specimens. Mean cellular SDH activities for non-hydrolyzed and hydrolyzed porcelain were 75+/-7 and 80+/-5% of Teflon controls, respectively. Only sodium ions were present in significant concentrations in collected leachates. The sodium concentration decreased over the initial 4.5h of leaching. SIGNIFICANCE: The changes in surface layer texture and composition as the result of the aging treatment had little effect on the cytotoxicity and chemical resistance of Duceram LFC. The results suggest that Duceram LFC would pose no biocompatibility risk even after extended exposure to the oral environment. These data also provide baseline material properties to be used in future studies of the effects of porcelain additives.

3T3 Cells↗

PubMed2003

Viscoelastic properties of demineralized dentin matrix.

OBJECTIVES: To evaluate the viscoelastic properties of demineralized dentin matrix. Stress-relaxation studies were done on matrices in tension and strain elongation or creep studies were done in both tension and compression. METHODS: Mid-coronal dentin disks were prepared from extracted unerupted human third molars. Disks were 0.5 mm thick for stress-relaxation or tensile creep experiments and 0.2-0.3 mm thick for compressive creep studies. 'I' beam specimens were prepared from dentin disks and the middle region was demineralized in 0.5 M EDTA (pH 7) for 4 days. The specimens were held in miniature friction grips in water and pulled at 100 micro m s(-1) to strains of 5, 10, 15 or 20% and then held for 10 min to follow the decay of stress over time. Creep was determined on demineralized dentin immersed in water in tension and in compression. Compressive creep was measured using an LVDT contact probe with loads of 0.02-0.5 N. Strain data were converted to compliance-time curves (strain/stress) and expressed as total compliance (J(t)), instantaneous elastic compliance (J(o)), retarded elastic compliance (J(R)) and viscous response (t/eta) or creep. RESULTS: The dentin matrix exhibits both stress-relaxation and creep behavior. Stress-relaxation and tensile creep were independent of strain but compressive creep rates were inversely related to compressive strain. Creep values were about 10% at low compressive strains, but fell progressively to 1% at high strains. Compliance-time curves fell with stress and came closer together. However, tensile creep was about 3% regardless of the strain. SIGNIFICANCE: The dentin matrix exhibits viscoelastic properties, but is not linearly viscoelastic. The relatively high creep rates of the matrix under low compressive loads may cause viscous deformations in poorly infiltrated hybrid layers in resin-bonded teeth under function.

Analysis of Variance↗

PubMed2002

Effect of toothbrushing on the toxicity of casting alloys.

STATEMENT OF PROBLEM: The biological properties of casting alloys have been assessed largely under passive conditions. The effect of common intraoral stresses such as brushing, toothpastes, and low pH on alloy toxicity are not known. PURPOSE: This study assessed the toxicity of 5 types of casting alloys commonly used in prosthodontics after toothbrushing, brushing in an acidic environment, or brushing with toothpaste. These toxicities were compared with those observed without any brushing. MATERIAL AND METHODS: Au-Pt, Au-Pd, Pd-Cu-Ga, Ni-Cr-Be, and Ni-Cr (no Be) alloys were brushed for 48 hours in a toothbrushing machine at 90 strokes/minute and 200g force. Alloys were brushed with either saline at pH 7, saline at pH 4 (acidified with sodium lactate), or saline with 1:7 (wt/wt) toothpaste. After the brushing regimen, the cytotoxicity of the alloys was assessed in a standard in vitro test. Cytotoxicities of the alloys after different brushing treatments were compared with unbrushed (control) specimens. Analysis of variance (ANOVA) and Tukey multiple comparison intervals (alpha=.05) were used to identify significant differences among brushing conditions. RESULTS: Brushing at pH 7 significantly increased the toxicity of the Pd-Cu-Ga alloy (15% to 20% over unbrushed specimens). Brushing at pH 4 increased the toxicity of the Au-Pt and Au-Pd alloys by 30% and the Pd-Cu-Ga alloy by >40%. The Ni-based alloys were not affected by acid. After being brushed with toothpaste, both Ni-based alloys were significantly more toxic, but Ni-Cr-Be was the worst, increasing more than 60% in toxicity over the controls. The toxicity of the Au-Pd alloy also increased significantly (15%). CONCLUSION: Brushing dental casting alloys may increase their cytotoxicity in vitro, but the increase depends heavily on the alloy type and brushing condition.

3T3 Cells↗