Biomedical subjects

J C Wataha

Publications and source records attributed to J C Wataha.

At least 19 recordsLinked to original sources

PubMed2007

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.

Animals↗

PubMed2006

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.

Cell Line, Tumor↗

PubMed2006

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.

Adsorption↗

PubMed2005

Dynamics of composite polymerization mediates the development of cuspal strain.

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.

Composite Resins↗

PubMed2005

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.

Cations, Divalent↗

PubMed2005

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.

Buthionine Sulfoximine↗

PubMed2005

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.

Antirheumatic Agents↗

PubMed2004

Cytotoxicity of commercial and novel binary titanium alloys with and without a surface-reaction layer.

Titanium-based alloys form a surface reaction layer when cast. This study investigated the effect of the surface reaction layer on the cytotoxicity of novel Ti-based binary alloys. The cytotoxicities of the novel alloys were compared with commercially pure titanium, Ti-6Al-4V and Ti-6Al-7Nb. Cast discs with or without the reaction layer were first tested for cytotoxicity, then for elemental release into cell-culture medium. The elements released into the extracts were measured by means of an inductively coupled plasma atomic emission spectrometer. The commercial and novel binary Ti-based alloys showed no statistically significant cytotoxicity, although some trends were noted for several alloys. The presence of the reaction layer did not significantly alter the cytotoxicity. These favourable biocompatibility results show that these novel alloys have promise for use in dental restorations.

Alloys↗

PubMed2004

Future directions in bonding resins to the dentine-pulp complex.

Resin-based materials are rapidly becoming the primary restorative material to replace tooth structure and the low percentage of biological problems reported for resin-based restorations is testimony to their relative biocompatibility. Despite considerable advances in the understanding of the mechanisms, which govern the integration of resin composite materials with the dentine-pulp complex, considerable potential for improvement remains. Most of these improvements centre around a better understanding of the biological and microbiological risks of resin materials and will only be possible with improved in vitro and in vivo models. There are also a number of possible future developments in materials, clinical techniques and diagnostic methods that may improve the long-term success and reliability of resin-based restorations. The remainder of this paper describes the most likely avenues for future improvements.

Biocompatible Materials↗

PubMed2004

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.

Animals↗

PubMed2003

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.

Cell Division↗

PubMed2003

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.

HSP72 Heat-Shock Proteins↗

PubMed2003

Effects of enamel matrix protein application on the viability, proliferation, and attachment of human periodontal ligament fibroblasts to diseased root surfaces in vitro.

OBJECTIVES: The purpose of this research was to examine the influence of enamel matrix proteins (EMP) on the viability, proliferation, and attachment of periodontal ligament fibroblasts (PDLF) to diseased root surfaces. MATERIALS AND METHODS: Primary cell cultures of PDFL were obtained from clinically healthy third molars or premolar teeth. Viability and proliferation rates were carried out over a 10-day period. A total of 80,000 cells were plated in 24-well plates followed by EMEM with 10% FBS (positive control) and EMEM plus EMP at 25, 50, 75, and 100 micro g/ml. Cells were harvested on days 1, 3, 5, 7, and 10 and viability was performed utilizing an MTS assay. PDLF proliferation rates were assessed by a CyQUANT GR dye assay. SEM analysis was used to examine the qualitative effects of cellular attachment to diseased root surfaces following EMP compared to nontreated controls. RESULTS: The results indicated that viability was negatively affected for higher doses over time while lower doses displayed viability effects similar to control. Proliferation, however, appeared to be ameliorated following exposure to EMP. The SEM analysis suggests that cellular attachment to diseased dentin was enhanced following EMP application. CONCLUSION: These in vitro studies support the concept that EMP may act as a suitable matrix for PDLF.

Adolescent↗

PubMed2002

Low-dose, long-term exposures of dental material components alter human monocyte metabolism.

The short-term degradation of dental polymers and alloys in biological environments has been well documented, but recent evidence indicates that oral tissues may be chronically exposed to low levels of these released components. The effect of these chronic exposures on the ability of cells to respond to a subsequent challenge is not known. To investigate this idea, we exposed human THP-1 monocytes to sublethal concentrations of HEMA, TEGDMA, Hg(2+), and Ni(2+) for 2 weeks and then assessed the monocytic response to subsequent 24-h challenge with the same components at higher concentrations. Chronic (2 week) exposures of monocytes to HEMA and both metal ions significantly altered monocyte response to short-term (24 h) secondary exposures, even when overt effects of the chronic exposures were not apparent. However, cellular responses were highly variable depending on the material and its concentrations. For TEGDMA, no effects were seen. These results demonstrate that the chronic effects of materials must be considered even when the chronic exposure has no initial overt effect. The effect on cells may only be apparent if the cell is challenged by a secondary exposure.

Cells, Cultured↗

PubMed2002

Long-term cytotoxicity of resin-based dental restorative materials.

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.

3T3 Cells↗

PubMed2002

Ag, Cu, Hg and Ni ions alter the metabolism of human monocytes during extended low-dose exposures.

The monocyte and macrophage play an important role in the biological response to dental biomaterials. However, the effects of low-level, extended exposures of monocytes to metal ions which are known to be released from dental alloys is not known. Thus, in the current study we characterized the metabolic activity of monocytes in the presence of low doses of Ag, Cu, Hg and Ni ions for up to 4 weeks. THP-1 human monocytes were exposed in vitro to concentrations of metal ions at 1-10% of those known to be lethal during 24 h exposures. Mitochondrial function [succinic dehydrogenase (SDH) activity] and total cellular protein [bicinchoninic acid (BCA) assay] were assessed at weekly intervals during metal exposure. Each metal ion caused a unique pattern of effects from the monocytes. These effects were sometimes delayed until several weeks into the exposure (Cu, Ni). Large increases in total protein or SDH activity per cell were observed (Cu 150%, Hg 40-60%, Ni 50%), but these increases were always transient. The differences between concentrations with minimal effects and those which were lethal (8 versus 12 micromol L(-1) for Ag, 1.0 versus 1.5 micromol L(-1) for Hg) were small. Finally, concentrations which caused total suppression of cellular activity were sometimes preceded by an increased activity (Hg, Ni). We concluded that metal ions alter monocyte metabolic activity during extended exposures in vitro, but that the concentrations required are often near long-term lethal levels. Clinically, these results imply that the levels of metals released from dental alloys may be significant to monocytic function.

Cells, Cultured↗

PubMed2002

Human peripheral blood monocytes versus THP-1 monocytes for in vitro biocompatibility testing of dental material components.

Monocytes play a central role in the response of tissues to biomaterials. Monocytic cell lines such as the THP-1 cell line have been used extensively as models for primary monocytes (directly from blood) in biocompatibility research. However, little information exists about the appropriateness of these cell lines as models. Thus, the current study compared the biological response of both primary peripheral blood monocytes (PBMs) and the THP-1 cell line to four common components of dental materials known to be released into the oral environment: nickel ions, 2-hydroxyethyl methacrylate (HEMA), triethylene glycol dimethacrylate (TEGDMA), and 2,2-bis[4(2-hydroxy-3-methacryloloxy)-phenyl]propane (Bis-GMA). Comparisons were made by constructing dose-response curves for each type of monocyte and the four components. The 50% cytotoxicity values (TC50 values) were then statistically compared. In addition, the response of the monocytes to the materials with and without lipopolysaccharide (LPS) stimulation were assessed by measuring TNF-alpha secretion from the monocytes. The results showed that the PBMs were 5-10 times less sensitive than the THP-1 monocytes to these dental components, but that both cell lines ranked the components identically. TNF-alpha secretion from both types of monocytes often showed similar trends, although some inconsistent results were noted. The current study supports the use of THP-1s as a model for ranking the cytotoxicity of components of dental biomaterials. Furthermore, the secretory activity of PBMs appears to be generally well represented by the THP-1s. However, sufficient differences between these cell types exist to recommend confirmation of any critical results obtained with THP-1s using PBMs.

Analysis of Variance↗

PubMed2002

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.

Analysis of Variance↗