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Background The prevalence of dentin hypersensitivity is uncertain, yet appropriate diagnosis and treatment of dentin hypersensitivity require accurate knowledge regarding its prevalence. The authors conducted a study to estimate the prevalence of dentin hypersensitivity in general dental practices and to investigate associated risk factors. Methods The authors conducted a cross-sectional survey of 787 adult patients from 37 general dental practices within Northwest Practice-based Research Collaborative in Evidence-based DENTistry (PRECEDENT). Dentin hypersensitivity was diagnosed by means of participants' responses to a question regarding pain in their teeth and gingivae, and practitioner-investigators conducted a clinical examination to rule out alternative causes of pain. Participants recorded their pain level on a visual analog scale and the Seattle Scales in response to a one-second air blast. The authors used generalized estimating equation log-linear models to estimate the prevalence and the prevalence ratios. Results The prevalence of dentin hypersensitivity was 12.3 percent; patients with hypersensitivity had, on average, 3.5 hypersensitive teeth. The prevalence of dentin hypersensitivity was higher among 18- to 44-year olds than among participants 65 years or older; it also was higher in women than in men, in participants with gingival recession than in those without gingival recession and in participants who underwent at-home tooth whitening than in those who did not. Hypersensitivity was not associated with obvious occlusal trauma, noncarious cervical lesions or aggressive toothbrushing habits. Conclusions One in eight participants from general practices had dentin hypersensitivity, which was a chronic condition causing intermittent, low-level pain. Patients with hypersensitivity were more likely to be younger, to be female and to have a high prevalence of gingival recession and at-home tooth whitening. Practical Implications Given dentin hypersensitivity's prevalence, clinicians should diagnose it only after investigating all other possible sources of pain.

Monosodium titanates (MST) are a relatively novel form of particulate titanium dioxide that have been proposed for biological use as metal sorbents or delivery agents, most recently calcium (II). In these roles, the toxicity of the titanate or its metal complex is crucial to its biological utility. The aim of this study was to determine the cytotoxicity of MST and MST-calcium complexes with MC3T3 osteoblast-like cells; MST-Ca(II) complexes could be useful to promote bone formation in various hard tissue applications. MC3T3 cells were exposed to native MST or MST-Ca(II) complexes for 24–72 h. A CellTiter-Blue® assay was employed to assess the metabolic activity of the cells. The results showed that MST and MST-Ca(II) suppressed MC3T3 metabolic activity significantly in a dose-, time-, and cell-density-dependent fashion. MST-Ca(II) suppressed MC3T3 metabolism in a statistically identical manner as native MST at all concentrations. We concluded that MST and MST-Ca(II) are significantly cytotoxic to MC3T3 cells through a mechanism yet unknown; this is a potential problem to the biological utility of these complexes.

The use of zirconia in medicine and dentistry has rapidly expanded over the past decade, driven by its advantageous physical, biological, esthetic, and corrosion properties. Zirconia orthopedic hip replacements have shown superior wear-resistance over other systems; however, risk of catastrophic fracture remains a concern. In dentistry, zirconia has been widely adopted for endosseous implants, implant abutments, and all-ceramic crowns. Because of an increasing demand for esthetically pleasing dental restorations, zirconia-based ceramic restorations have become one of the dominant restorative choices. Areas covered: This review provides an updated overview of the applications of zirconia in medicine and dentistry with a focus on dental applications. The MEDLINE electronic database (via PubMed) was searched, and relevant original and review articles from 2010 to 2016 were included. Expert commentary: Recent data suggest that zirconia performs favorably in both orthopedic and dental applications, but quality long-term clinical data remain scarce. Concerns about the effects of wear, crystalline degradation, crack propagation, and catastrophic fracture are still debated. The future of zirconia in biomedical applications will depend on the generation of these data to resolve concerns.

Background. Methods used by dental practitioners to diagnose and treat dentin hypersensitivity are not well documented. The authors conducted a survey of dentists in the Northwest Practice-based REsearch Collaborative in Evidence-based DENTistry (PRECEDENT) to ascertain the treatment methods they used. Methods. Via an Internet survey, the authors collected data regarding methods used for diagnosis and treatment of dentin hypersensitivity from 209 Northwest PRECEDENT dentists. Results. The PRECEDENT dentists indicated that they most often used fluoride varnishes and gels, advice regarding toothbrushing and diet, bonding agents, restorative materials and glutaraldehyde/2-hydroxyethyl methacrylate (HEMA) to treat dentin hypersensitivity. They reported that the most successful treatments were fluorides, glutaraldehyde/HEMA, bonding agents, potassium nitrates and restorative treatments; they considered observation, advice regarding toothbrushing and diet and laser therapy to be the least successful. Dentists listed fluorides, calcium phosphates, glutaraldehyde/HEMA and bonding agents as the treatments most desirable for inclusion in a future randomized clinical trial of dental hypersensitivity treatments. Conclusions. Dentists rely on patients to assess the severity of dentin hypersensitivity. Modalities for the diagnosis and treatment of hypersensitivity are diverse. Methods used to diagnose and treat dentin hypersensitivity in practice are challenging to justify. Clinical Implications. Practitioners should be aware of the diversity of methods available for diagnosing and treating dentin hypersensitivity as they manage the care of their patients with this condition.

In the biomedical field, palladium has primarily been used as a component of alloys for dental prostheses. However, recent research has shown the utility of palladium alloys for devices such as vascular stents that do not distort magnetic resonance images. Dental palladium alloys may contain minor or major percentages of palladium. As a minor constituent, palladium hardens, strengthens and increases the melting range of alloys. Alloys that contain palladium as the major component also contain copper, gallium and sometimes tin to produce strong alloys with high stiffness and relatively low corrosion rates. All current evidence suggests that palladium alloys are safe, despite fears about harmful effects of low-level corrosion products during biomedical use. Recent evidence suggests that palladium poses fewer biological risks than other elements, such as nickel or silver. Hypersensitivity to palladium alone is rare, but accompanies nickel hypersensitivity 90-100% of the time. The unstable price of palladium continues to influence the use of palladium alloys in biomedicine.

Amorphous peroxotitantes (APT) are insoluble titanium-based particles that bind a variety of metal compounds with high affinity; these particles could be sequestered locally in a solid phase to deliver metal-based drugs. Previous studies have confirmed the 'biodelivery' of metals from metal-APT complexes to fibroblasts, but not monocytes. Our goal in the current study was to use monocytic cytokine secretion to assess delivery of gold or platinum-based compounds from APT to human THP1 monocytes. Cytokine secretion was not triggered by APT alone or metal-APT complexes. In monocytes activated by lipopolysaccharide (LPS), APT alone enhanced or suppressed IL1beta or IL6 secretion, yet TNFalpha secretion was unaffected. Complexes of APT and Au(III) or cis-platin altered LPS-activated IL6 or IL1beta secretion most, TNFalpha least. Our results suggest that the APT deliver metals to monocytes.

Metal ions are notorious environmental contaminants, some causing toxicity at exquisitely low (ppm-level) concentrations. Yet, the redox properties of metal ions make them attractive candidates for bio-therapeutics. Titanates are insoluble particulate compounds of titanium and oxygen with crystalline surfaces that bind metal ions; these compounds offer a means to scavenge metal ions in environmental contexts or deliver them in therapeutic contexts while limiting systemic exposure and toxicity. In either application, the toxicological properties of titanates are crucial. To date, the accurate measurement of the in vitro toxicity of titanates has been complicated by their particulate nature, which interferes with many assays that are optical density (OD)-dependent, and at present, little to no in vivo titanate toxicity data exist. Compatibility data garnered thus far for native titanates in vitro are inconsistent and lacking in mechanistic understanding. These data suggest that native titanates have little toxicity toward several oral and skin bacteria species, but do suppress mammalian cell metabolism in a cells-pecific manner. Titanate compounds bind several types of metal ions, including some common environmental toxins, and enhance delivery to bacteria or cells. Substantial work remains to address the practical applicability of titanates. Nevertheless, titanates have promise to serve as novel vehicles for metal-based therapeutics or as a new class of metal scavengers for environmental applications.

Nickel is a component of biomedical alloys that is released during corrosion and causes inflammation in tissues by as yet unknown mechanisms. Recent data show that Ni(II) at concentrations of 10-50 microM amplifies lipopolysaccharide-triggered, NFkappaB-mediated cytokine secretion from monocytes. In the current study, we tested the hypothesis that Ni(II) amplifies cytokine secretion by activating the Nrf2 antioxidant pathway rather than by enhancing activity of the NFkappaB signaling pathway. Human THP1 monocytes were exposed to Ni(II) concentrations of 10-30 microM for 6-72 h, then immunoblots of whole-cell lysates or cytosolic and nuclear proteins were used to detect changes in Nrf2 or NFkappaB signaling. Our results show that Ni(II) increased (by 1-2 fold) whole-cell Nrf2 levels and nuclear translocation of Nrf2, and amplified lipopolysaccharide (LPS)-induction of Nrf2 (by 3-5 fold), but had no detectable effect on the initial activation or nuclear translocation of NFkappaB. Because Nrf2 target gene products are known regulators of NFkappaB nuclear activity, our results suggest that Ni(II) may affect cytokine secretion indirectly via modulation of the Nrf2 pathway.

Thioredoxin reductase (TrxR) reduces thioredoxin (Trx), thereby contributing to cellular redox balance, facilitating the synthesis of deoxy-ribose sugars for DNA synthesis, and regulating redox-sensitive gene expression. Auranofin is a gold compound that potently inhibits TrxR. This inhibition is one suspected mechanism of auranofin’s therapeutic benefit in the treatment of rheumatoid arthritis. The use of other gold compounds to treat cancer or inflammatory disease may rely on their ability to inhibit TrxR. In the current study, we tested the hypothesis that a variety of gold compounds may inhibit TrxR. Methods: We exposed rat-TrxR1 to auranofin, gold sodium thiomalate, sodium aurothiosulfate, triphenyl phosphine gold chloride, or gold acetate, and measured TrxR activity ex vivo. We then compared TrxR1 inhibitory levels of gold compounds to those that inhibited mitochondrial activity of THP1 monocytes and OSC2 epithelial cells, estimated by succinate dehydrogenase activity. Results: All gold compounds inhibited TrxR1 at concentrations ranging from 5 to 4000 nM (50% inhibitory concentration). The oxidation state of gold did not correlate with inhibitory potency, but ligand configuration was important. Au(I)-phosphine compounds (triphenyl phosphine gold chloride and auranofin) were the most potent inhibitors of TrxR. All TrxR1 inhibitory concentrations were sublethal to mitochondrial activity in both THP1 and OSC2 cells. Conclusions: Diverse types of gold compounds may be effective inhibitors of TrxR1 at concentrations that do not suppress cellular mitochondrial function. Inhibition may be optimized to some degree by altering the ligand configuration of the compounds. These results support future study of a variety of Au compounds for therapeutic development as inhibitors of TrxR1.

Highly filled composites, Ormocers (organically modified ceramics) and 'smart' materials have been developed to overcome the polymerization shrinkage problems of conventional composite materials. The purpose of the current study was to investigate the effect of longer-term (up to 8 weeks) ageing of these resin-based dental restorative materials and determine the effect of post-curing on cytotoxicity. Twelve discs of each material (Colombus/IDR, Definite/Degussa, Ariston pHc/Vivadent) were either light-cured (Lc) or light-cured and post-cured (Pc). For cytotoxicity testing, the discs were placed in contact with cell culture medium (DMEM) and incubated at 37 degrees C. Extracts from composite materials were collected after 24 h and weekly over a time period of 8 weeks. Cytotoxicity of the eluates to cultured fibroblasts (Balb/c3T3) were measured by the succinic dehydrogenase (SDH) activity (MTT assay) and the results expressed in percentage of negative controls (Teflon discs). The results showed that ageing significantly influenced the cytotoxicity of the materials. Except for Ariston pHc, materials were less cytotoxic after 8 weeks of ageing than they were in early intervals and post-curing was not generally useful in reducing cytotoxicity. The Ariston pHc was initially moderately toxic, but then become highly cytotoxic for 5 weeks before returning to initial levels. The current study demonstrated the importance of assessing the cytotoxicity of resin composite materials at multiple times.

In dentistry, antibacterial photodynamic therapy (a-PDT) has shown promising results for inactivating bacterial biofilms causing carious, endodontic and periodontal diseases. In the current study, we assessed the ability of eosin Y exposed to 3 irradiation protocols at inactivating Enterococcus faecalis biofilms, in vitro.E. faecalis biofilms formed on hydroxyapatite disks were incubated with eosin Y (10-80μM), then activated with blue light using different irradiation protocols. Biofilms exposed to continuous exposure were incubated for 40min before being light-activated for 960 s. For the intermittent exposure, biofilms were exposed 4 times to the light/photosensitizer combination (960 s total) without renewing the photosensitizer. For repeated a-PDT, the same light dose was delivered in a series of 4 irradiation periods separated by dark periods; fresh photosensitizer was added between each light irradiation. After treatment, bacteria were immediately labeled with LIVE/DEAD BacLight Bacterial Viability kit and viability was assessed by flow cytometry (FCM). Results were statistically analyzed using one-way ANOVA and Tukey multiple comparison intervals (α=0.05).The viability of E. faecalis biofilms exposed to 10μM eosin Y, was significantly reduced compared to controls (light only-eosin Y only). After a second exposure to blue light-activated eosin Y, viability significantly decreased from 58% to 12% whereas 6.5% of the bacterial biofilm remained live after a third exposure (p0.05). Only 3.5% of the bacterial population survived after the fourth exposure.The results of this study indicate that blue light-activated eosin Y can photoinactivate E. faecalis biofilms grown on hydroxyapatite disks. Also, repeated exposures to blue light-activated eosin Y were shown to significantly improve efficacy. Further studies seem warranted to optimize the antibacterial activity of blue light-activated eosin Y on major oral pathogens.

Recent studies suggest that light in the UVA range (320-400 nm) activates signaling pathways that are anti-inflammatory, antioxidative and play a critical role in protection against cancer. These effects have been attributed to NF-E2-related factor (NRF2)-mediated up-regulation of 'phase 2' genes that neutralize oxidative stress and metabolize electrophiles. We had previously shown that small doses of blue light (400-500 nm) had selective toxicity for cultured oral tumor cells and increased levels of peroxiredoxin phase 2 proteins, which led to our hypothesis that blue light activates NRF2 signaling.A431 epidermoid carcinoma cells were treated in culture and as nude mouse xenografts with doses of blue light. Cell lysates and tumor samples were tested for NRF2 activation, and for markers of proliferation and oxidative stress.Blue light activated the phase 2 response in cultured A431 cells and reduced their viability dose dependently. Light treatment of tumors reduced tumor growth, and levels of proliferating cell nuclear antigen (PCNA), and oxidized proteins.Cellular responses to these light energies are worth further study and may provide therapeutic interventions for inflammation and cancer.

Failing implants with loss of alveolar bone are associated with gram-negative bacteria that carry lipopolysaccharide (LPS) in the bacterial cell wall. Bony regeneration around these implants is still an unpredictable procedure due to the many clinical factors involved. One important factor is the presence of contaminants such as LPS on the implant surface. The effect of implant-associated LPS on the attachment of bone cells to the implant surface is unknown. This project investigated the effect of LPS on the attachment of osteoblast-like cells (MC3T3-E1) to titanium and titanium alloy surfaces in vitro. We hypothesized that LPS would inhibit bone cell attachment either through loss of cellular attachment sites or alteration of cellular function. Three experimental approaches were used. First, alloy surfaces were exposed to LPS (100 μg/mL) before the cells were allowed to attach. In the second approach, the cells were exposed to the LPS before they were allowed to attach. Last, the cells were allo...

Certain cells of the periodontium are necessary for the regeneration of tissues that are destroyed as a result of periodontal disease. There has been debate regarding which cells are the primary participants in periodontal regeneration. It is a well-known fact that osteoblasts are essential in new bone formation, but controversy surrounds the role that gingival fibroblasts may play in the regeneration of the hard tissues of the periodontium. If gingival fibroblasts could contribute to the regeneration of these tissues, they might provide an additional source of progenitor cells. The bone morphogenetic proteins are potent stimulators of cell differentiation and have been shown to induce new bone formation in many experimental models. This project investigated the ability of recombinant human bone morphogenetic protein–2 (rhBMP-2) to (1) enhance the production of markers of osteoblastlike cells (osteocalcin and mineralization in culture) in human osteosarcoma cells (MG63) and to (2) induce the expr...

The use of nickel casting alloys for long-term restorations in dentistry has long been controversial. A ‘tug-of-war’ between economic, engineering and biological considerations is central to this controversy; nickel-casting alloys have low costs and favorable physical properties, but are corrosion-prone in the oral environment. Clinicians and researchers have questioned the safety of nickel-containing dental alloys because several nickel compounds are known to cause adverse biological effects in vivo and in vitro in contexts outside of dentistry. The debate revolves around the extent to which corrosion products from oral restorations cause intraoral or systemic biological problems. Current evidence suggests that nickel alloys may be used successfully and safely in dentistry if clinical risks are taken into account. However, these alloys may cause significant clinical problems, primarily allergenic and inflammatory, if the risks are ignored.

An in vitro screening test was used to compare the cytotoxicity and elemental release from mercury- and gallium-based dental restorative materials.The test employed three sequential extractions of the samples into cell-culture medium which were then used to evaluate the cytotoxicity of the samples and the release of elements from the samples. Cytotoxicity was measured by placing the extract in contact with Balb/c mouse fibroblasts for 24 h and measuring the succinic dehydrogenase activity of the cells. The release of elements was measured by means of atomic absorption spectrophotometry.Samples of Tytin (Kerr) showed no cytotoxicity compared to Teflon controls. Dispersalloy (Johnson and Johnson) was severely cytotoxic initially when Zn release was greatest, but was less toxic between 48 and 72 h as Zn release decreased. Gallium Alloy GF (Tokuriki Honten) was moderately cytotoxic after 8 h, and increased in cytotoxicity thereafter, which correlated with a substantial and persistent release of Ga from this material.The results of the current study concurred with in vivo assessments of these materials, and the use of sequential extractions was useful in determining trends in the cytotoxicity and elemental release from these materials.

Cytotoxicity testing of dental restorative materials must be viewed as an assessment of hazards, that is the potential of the material to cause pulpal problems. In this context, composites, glass ionomers, amalgams, zinc-based cements and peroxide bleaching agents are all possible hazards to the pulp. The risks that these materials will cause pulpal toxicity in vivo can be partly estimated by assessing the cytotoxicity of the substances which are released from these materials in vitro and comparing these cytotoxic concentrations with those concentrations that are present in vivo. The resin components of composites, metal ions and hydrogen peroxide, all of which are released from dental restorative materials, have been shown to be cytotoxic in vitro in sufficient concentrations. The potencies of these substances are quite diverse. However, the cytotoxicity of these substances in usage tests, and therefore the risks of pulpal toxicity, depends on their ability to diffuse through the dentine and accumulate in the pulp.

Summary The diffusion through dentine by a number of biological and synthetic molecules, including resins and dyes, is reported. In vitro measurements were derived by experiments with a modified ‘split-chamber device’. Diffusion was found to be indirectly proportional to dentine thickness for all molecules. Permeability of water-soluble molecules and ethanol-soluble molecules was proportional to the molecular weights, except for fluorescein, hydrogen peroxide (H2O2) and urethane dimethacrylate. The resin components tested are not soluble enough in an aqueous medium to diffuse through 0.5 mm dentine at sufficient concentrations to cause cytotoxicity to pulpal cells.

Medline, CENTRAL, LILACS, TRIP Database, National Guideline Clearinghouse, OPENSigle and a number of other medical / dental databases and websites, as well as reference lists.Randomised controlled trials and controlled clinical trials in any language that compared oxalates with placebo or no treatment were eligible for inclusion.Three reviewers extracted data with two people assessing quality independently using the Cochrane risk of bias domains. Standardized mean differences (SMD) were estimated by random-effects meta-analysis and heterogeneity between studies was quantified with the I2-statistic.12 reports were included. Interventions were diverse and included: monohydrogen-monopotassium oxalate, ferric oxalate, di-potassium oxalate, or oxalate containing pre-polymerized resin, and combinations of monohydrogen-monopotassium and di-potassium oxalate. Follow up intervals varied between immediate to 1 year. Hypersensitivity was elicited by tactile, evaporative or thermal stimuli, and a number of outcomes used to measure pain. Risk of bias was high in a number of studies and statistical heterogeneity high. Based on 187 and 179 units (patients or teeth) in the intervention and placebo groups from seven studies, the summary SMD for 3% monohydrogen-monopotassium oxalate was -0.71 (95% Confidence Interval (CI):-1.48, 0.06), which suggests it may not be beneficial. There was no improvement with the other interventions.The review identified no evidence to indicate benefit from treating dentine hypersensitivity with oxalates beyond a placebo effect.

Compliance measurements, used in the past to measure the viscoelastic properties of dental impression materials, were used to assess these properties in vulcanized cis-polyisoprene orthodontic elastics, and the results were compared with traditional force decay measurements. Both methods were also used to evaluate the effect of repeated stretching on these elastics. Compliance measurements successfully characterized the viscoelastic behavior of the elastics, and the results agreed with force decay measurements. Repeated stretching significantly reduced the force and the compliance of the elastics. There was no statistical difference in the force or compliance measurements after the elastics were stretched more than 200 times. Stretching for 1000 cycles of 400% extension reduced elastic force by approximately 12%.

The kinetics of the release of elements from six dental casting alloys into cell-culture medium was assessed by means of atomic absorption spectroscopy. Alloys were evaluated in the polished and polished-cleaned conditions so that the effects of cleaning could be determined. Auger scanning microscopy was used for analysis of the surfaces of selected alloys before and after exposure to the cell-culture medium. Release patterns for each element were characterized by the shape of the dissolution us. time curve, concentration of the element at 12 h as a percentage of the 72-hour concentration, and the relative slope of the curve from 48 to 72 h. Three patterns of release were observed for elements in these alloys. Type I patterns had logarithmic shapes with relatively large 12-hour concentrations and low 48-72-hour slopes. Type II patterns had logarithmic shapes but with moderate 12-hour concentrations and 48-72-hour slopes. Type III patterns were polynomial in shape, had relatively low 12-hour concentrations, and had large 48-72-hour slopes. Cleaning did not change the pattern of release but did generally significantly decrease the quantities of elements released (p = 0.05). The type of dissolution vs. time curve appeared to be dependent upon the element and the composition of the alloy. When cleaning reduced dissolution, surface analyses showed that the cleaning process increased the abundance of elements such as Au and Pd and reduced the abundance of Ag and Cu. Elements which were released from the alloys were more abundant on the surface than in the bulk in both polished and polished-cleaned conditions. Auger analyses of alloy surfaces after exposure to medium showed the presence of organic films up to 50 nm thick. This study demonstrated the importance of consideration of the cleaning method and kinetic release pattern when in vitro tests which assess the cytotoxicities of these alloys are planned.

The objectives of this study were to determine the cytotoxic concentrations of 11 components of resin composites on monolayers of cultured Balb/c 3T3 fibroblasts, to study the inhibitory effects of these components on DNA synthesis, total protein content, and protein synthesis, and to determine whether effects were reversible when the components were withdrawn from the medium. These data were reported as concentrations which inhibited 10% (ID10) and 50% (ID50) of a particular metabolic process as well as the range of concentrations over which cell metabolism was irreversibly inhibited. For any individual component, the ID50 values for all three metabolic parameters were of the same magnitude. The same was true for the ranges of irreversibility. Ethoxylated Bis-phenol A dimethacrylate (E-BPA) was the most toxic molecule of the group (ID50 being between 1 and 10 μmol/L). The ID50 concentrations for three of the components, including Bis-GMA, UDMA, TEGDMA, and Bis-phenol A, ranged between 10 and 100 μmol/L, while the ID 50 values of three components (N,N dihydroxyethyl-p-toluidine, camphoroquinone, and N,N dimethylaminoethyl methacrylate) were above 100 μmol/L. The concentrations to which the cells and tissues are exposed in uiuo are not known. This study should help to identify the concentrations of organic composite components which pose clinical cytotoxic hazards.

Objectives In the current study, we used electronic speckle pattern interferometry (ESPI) to measure tooth deformation in response to polymerization of five resin composites with a range of polymerization shrinkage. Our hypothesis was that composites with higher polymerization shrinkage should cause more cuspal strain as measured by ESPI. Methods Standardized MOD cavities were prepared and placed into the ESPI apparatus before the cavities were filled with composites (n = 10). The ESPI apparatus was constructed to measure the out-of-plane displacement of the lingual cusps of the teeth during the polymerization of the restorative material. A thermocouple was attached to the specimen to monitor thermal changes throughout the polymerization process. Results Experiments with empty preparations demonstrated that the ESPI technique was temporally responsive and sensitive to dimensional changes. However, the correlation between polymerization shrinkage of composite resins and ESPI-measured tooth deformation was not straightforward. In particular, a flowable material did not deform the tooth significantly more that a conventional hybrid. Further, an experimental silorane material (with the lowest axial shrinkage) induced the least tooth deformation. Significance We concluded that ESPI is a viable method for assessing cuspal strain induced by shrinkage of bonded composite restorations, but that polymerization shrinkage data may overestimate shrinkage-induced tooth deformation. The rate of polymerization shrinkage appeared to mediate the development of cuspal strain.

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 (

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.

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.

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 μTBS 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 (α=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 μTBS 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.

The release of elements from dental casting alloys is a continuing concern because of the potentially harmful biological effects the elements may have on local tissues. The surfaces of the alloys appear to be most important in controlling the release of these elements. In the current study, the surfaces of high-, reduced-, and no-gold dental alloys were analysed by X-ray photoelectron spectroscopy before and after they were exposed to a biological medium for up to 96 h. The goal was to relate the release of elements from these alloys to their surface composition, and to determine the depth of the effect of the medium. The depth of the effect of the exposure was determined by argon milling of the alloy surface after exposure to the medium. Elements that were released into the medium were measured by means of atomic absorption spectroscopy. The release of elements from alloys was greater when the atomic ratio of noble to non-noble elements at the surface was less than 1. The depth of the effect of the medium varied with the alloy, but was always less than 100 A. The surface composition was significantly different from layers only 5 A below. It was concluded that the surface concentration of noble elements is important in controlling the release of non-noble elements from these alloys, and the surface composition appeared to be only one or two atomic layers thick. Of the three types of alloys, the high-gold alloy appeared to develop the most stable surface composition which released the lowest levels of elements.

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.

A~ffr Objectives. The choice of cell line for in vitro biological tests which assess the cytotoxicity of dental materials remains controversial, yet this issue is important because these tests are widely used to rate the biocompatibility of new and existing materials, and many different cell lines are commonly used. The purpose of the current study was to quantify the responses of four cell lines (Balb/c 3T3, L929, ROS 17/2.8 and Wl-38) to 14 metal ions which are released from dental materials, and relate these responses to the metabolic activity and population doubling times of these cells. Methods. Succinic dehydrogenase (SDH) activity was used to monitor metabolic activity and cytotoxic response. Results. The cell lines responded differently to most metal ions. In general, the Balb/c 3T3 line was the most sensitive, and the Wl-38 line was the least sensitive. However, there were many exceptions depending on the metal ion. The passage number of the cells also affected the cytotoxic response. It was concluded that the cytotoxicity of materials which release metal ions will be significantly different depending on which cell line is selected and its passage number. Significance. Based on the findings that cell lines ranked the toxicities of the metal ions similarly, it seems reasonable to use these types of in vitro tests to rank the cytotoxicities of materials. However, if these types of tests are used to predict in vivo cytotoxicity, care should be taken to choose conditions and cells which are relevant.

The effects of Ag[sup +1], Au[sup +3], Cd[sup +2], Cu[sup +2]; Ga[sup +3]; In[sup +3], Ni[sup +2], Pd[sup +2], and Zn[sup +2] on DNA synthesis, protein synthesis, succinic dehydrogenase activity, and total cellular protein of mammalian fibroblasts were measured for exposures less than 12 h. The rates at which these cellular functions responded to metal ion exposure were compared and related to the uptake rate of the ions into the cells. These rates of response were significantly different: DNA synthesis decreased the fastest, followed by protein synthesis, succinic dehydrogenase activity, and total protein. This order of response was similar for most metal ions. At 4 h, the rate of uptake of the metal ions correlated most closely with depression of succinic dehydrogenase activity, whereas at 8 h, the uptake correlated most closely with depression of protein synthesis. The similar response of cells to all metal ions may imply that these ions act on cells by similar mechanisms. The rates of uptake of Ag[sup +1], Cu[sup +2], and Zn[sup +2] were sufficiently fast that in vivo exposures of tissues to these metals for periods less than 12 h would be capable of disrupting cellular metabolism.

There has been recent concern about the inadvertent exposure of dentin with patent tubules as well as gingiva to bleaching systems containing 10-15% carbamide peroxide or 2-10% hydrogen peroxide for more than a few minutes. The aims of the present study were: (1) to determine the cytotoxicity of dilutions of hydrogen peroxide in cell culture; (2) to measure hydrogen peroxide diffusion from bleaching agents through dentin in vitro; and (3) to determine the risk of hydrogen peroxide-induced cytotoxicity from exposure of dentin to these vital bleaching agents. The 50% inhibitory dose (ID50) of hydrogen peroxide to succinyl dehydrogenase activity in cultured cells was found to be 0.58 mmol/L after 1 h. All bleaching materials demonstrated diffusion of hydrogen peroxide through dentin in an "in vitro pulp chamber" device. The one- and six-hour diffusates of all bleaching agents through 0.5-mm dentin exceeded the ID50 in monolayer cultures. Inhibition of succinyl dehydrogenase activity corresponded to the amount of hydrogen peroxide that can rapidly diffuse through dentin in vitro and reach concentrations which are toxic to cultured cells in less than 1 h.

The effect of cell density (number of cells per unit area of a monolayer culture) on the in vitro cytotoxicity of metal ions which are known to be released from dental materials was investigated. The effects of cell density (1) may explain previous discrepancies in in vitro tests, (2) may be important in wound healing where cell density changes over time, and (3) may help clarify the mechanisms of cytotoxicity of metal ions. Balb/c 3T3 fibroblasts were plated at cell densities ranging from 10,000-80,000 cells/cm2 and were exposed to 8 concentrations of 10 different metal ions. After 24 h, the succinic dehydrogenase activity and DNA synthesis were measured to quantify the cytotoxic effect. Higher cell densities markedly reduced the sensitivity of these fibroblasts to all metal ions except Al+3 and Zn+2, but the magnitude of the reduction was metal dependent. In addition, the DNA synthesis was inhibited more than the succinic dehydrogenase activity for all metal ions except Zn+2. The unique effect of cell density on each metal ion supported the hypothesis that the effect was not simply caused by a dilution of the number of metal ions per cell. Given these results, the effect of cell density should be carefully selected in in vitro cytotoxicity tests.

Atomic absorption spectroscopy was used to assess uptake of Ag+1, Au+4, Cd+2, Cu+2, In+3, Ni+2, Pd+2, and Zn+2 by in vitro cultures of Balb/c 3T3 fibroblasts as a function of concentration of the cations in cell-culture medium. Reversibility of this uptake was also measured. Metal cations exhibited a 400-fold difference in their tendency to accumulate in the cells; In+3 tended to accumulate the most, whereas Pd+2 accumulated the least. Uptake of the cations in the cells increased linearly with the concentration of the cation in the medium for all cations up to their 50% toxicity concentrations. Reversal of this uptake was slower than that of the initial uptake for three cations studied in more detail (Cd+2, In+3, and Ni+2). The duration of the initial exposure affected the proportion of the metal cations that were retained by the cells 5 h after the cations were removed from the medium. The proportion of retained Cd+2 did not change when the initial exposure was increased from 2 h to 6 h, whereas the proportion of retained In+3 decreased and Ni+2 increased over the same period. The tendency of the cells to accumulate these cations correlated with their cytotoxic potency (measured previously). © 1993 John Wiley & Sons, Inc.

Effects of duration of exposure of single metal cations (Ag+1, Cd+2, Cu+2, Ga+3, Ni+2, and Zn+2) on 3H-thymidine (3H-Tdr) incorporation and 3-[4,5-dimethyl-thiazol-2yl-]-2,5-diphenyl tetrazolium bromide-formazan (MTT-f) production in cultured murine fibroblasts (Balb/c 3T3) were investigated, and the synergistic and antagonistic effects of two metal cations applied simultaneously to the fibroblasts were assessed. The effects of duration of exposure were quantified using TC50 values (concentration of an element required to cause 50% toxicity compared with controls) measured after 24, 48, or 72 h. Using MTT-f production, Cd+2, Cu+2, Ga+3, and Ni+2 showed significantly lower TC50 values with increasing time of exposure, whereas the TC50 values for Ag+1 and Zn+2 remained constant. The TC50 values using 3H-Tdr incorporation exhibited a similar pattern with time of exposure, but the effects were less pronounced. The TC50 values for 3H-Tdr and MTT-f tended to equalize at 72 h. All combinations of cations tested (Ag-Cu, Ag-Zn, Ag-Ni, Cu-Zn, Cu-Ni, Ga-Ni, and Cu-Cd) exhibited synergistic and antagonistic effects as measured by MTT-f production. Synergistic and antagonistic effects were not necessarily mutually exclusive in the same system.

Previous studies have utilized in vitro alloy cytotoxicity tests to evaluate dental casting alloys. The purposes of this study were to: (1) evaluate the precision of the optical density and visual tests previously used, (2) evaluate a new test measuring absorbance of solubilized formazan dyes, and (3) test the correlation between these tests for cytotoxicity. Balb/c 3T3 cells were plated in 24-well culture trays at 25,000 cells/cm2 around ten types of dental casting alloys (six samples/alloy) and incubated for 72 h. Cells were histochemically stained with MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide)/succinate for 2 h, then fixed, washed, and dried. Toxicity was measured by optical densitometer (OD) scanning, visual assessment, and 560-nm absorbance of DMSO-solubilized dyes. Measurements of rings of inhibition were not used, because they did not provide precise data, and correlated poorly with the other methods. The results were analyzed by ANOVA, Tukey intervals, and coefficients of variation (CV's). MTT required shorter incubation times for adequate staining, allowed for solubilization of the monolayers, and was less expensive than NBT (2,2'-di-p-nitro-phenyl-5,5'-diphenyl-3,3'-dimethoxy-[3,3'-dimethoxy-4,4 '-biphenylene] ditetrazolium chloride). Results showed that all three methods ranked alloy toxicities similarly (p = 0.05). The solubilization method was most discriminating due to lower CV's. Correlation between densitometer and solubilization methods was excellent (R2 = 0.96). Between-experiment CV's were generally less than 20%, and often less than 10%. Between-sample CV's were generally less than 20%.(ABSTRACT TRUNCATED AT 250 WORDS)

The in vitro cytotoxicity of nine metal cations common in dental casting alloys was evaluated using Balb/c 3T3 fibroblasts and four toxicity parameters: total protein production, 3H-leucine incorporation, 3H-thymidine incorporation, and MTT-formazan production. Concentrations causing 50% toxicity compared to controls (TC50's) and reversibility of these effects were determined. The range of potency of the metal cations was 2-3 orders of magnitude, with Cd2+ showing the greatest potency and In3+ showing the least. Potency did not correlate with atomic weight for these metals. For each metal cation, the TC50's of the various toxicity parameters were similar in most cases. However, several cations (Cu2+, Ga3+) showed greater potency with 3H-thymidine incorporation. Reversibility of the toxic effects was observed for all cations; the effects generally became irreversible at concentrations in the range of the TC50 value for each cation. Several stimulatory effects were seen. Small but statistically significant stimulations were observed after 24 h of metal exposure for Ag1+, Au4+, Cu2+, Ga3+, and Ni2+. Residual stimulations 24 h after removal of the metal cations were observed for Au4+, Cd2+, Ni2+, and Zn2+. Stimulations always occurred at concentrations below the TC50 concentrations. This study should be useful in evaluating the potential cytotoxic effects of metal cations released from dental alloys.

Ten dental casting alloys were tested for alloy-element release into cell-culture medium, and this release was related to alloy composition, alloy microstructure, and alloy cytotoxicity (previously determined). Cell-culture medium was analyzed for alloy elements by flame atomic absorption. Concentrations of elements in the medium were normalized by dividing them by their atomic abundance in the alloy, giving element medium-alloy ratios (EMA ratios). Results showed that Au, In, and Pd generally did not dissolve into the medium, but that Ag, Cd, Cu, Ga, Ni, and Zn frequently dissolved. Comparison of EMA ratios for Ag, Cu, and Zn showed that each element retained a behavioral identity in diverse metallurgical environments, but that these environments influenced the release behavior to some degree. Some EMA ratios in multiphase alloys were greater than those in solid solutions, and EMA ratios showed great diversity within all the alloys. Nominal composition seemed to be of little value in the prediction of metal release unless the composition supported multiple-phase formation. In addition, release of alloy elements did not, in itself, completely predict alloy cytotoxicity measured previously. However, cytotoxicity was associated with metal release in each case. The commercial alloys used in this study exhibited more complex and less predictable release behavior than did the simpler ternary alloy systems used by previous investigators. It is believed that the use of commercial preparations is necessary for their in vivo behavior to be modeled.

Increasing concerns over the effects of environmental estrogens on wildlife and humans have highlighted the need for screening systems to assess potentially estrogenic effects of test compounds. As a result, in vitro screening methods such as cell proliferation assays using the estrogen-responsive human breast cancer cell line, MCF-7, have been developed. The present study describes an alternative in vitro approach for the assessment of such xenoestrogens, based on estrogenic rescue of MCF-7 cells from antiestrogen-induced cytotoxicity. This method measures the ability of various estrogenic compounds to compete with a known estrogen-receptor-mediated antihormonal drug, 4-hydroxytamoxifen, using the 1-[4,5-dimethylthiazol-2-yl]-3,5-diphenylformazan (MTT) assay to assess mitochondrial activity. Because 4-hydroxytamoxifen treatment of cells results in a dramatic decrease in mitochondrial dehydrogenase activity which is directly related to their estrogen-receptor content, inhibition of this effect with estrogenic compounds represents an estrogen-receptor interaction, or estrogenic rescue. The estrogenic compounds tested include a weak xenoestrogen, bisphenol A (BPA), and two biological estrogens, 17alpha- and 17beta-estradiol. Competitive inhibition of 4-hydroxytamoxifen-induced cytotoxicity by BPA was compared to that of the biological estrogens. The results indicate that the biological estrogens can successfully compete with the antiestrogen in a dose-dependent manner. In addition, the assay is sensitive enough to detect estrogenic rescue by even the very weak xenoestrogen, BPA, albeit at high BPA concentrations. This simple in vitro method could be used as an alternative or second-line screen for potential xenoestrogens.