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PubMed1999

Nickel release from orthodontic arch wires and cellular immune response to various nickel concentrations.

AIMS: Results from two previous clinical studies suggested that exposure to high nickel-containing orthodontic arch wires may induce hypersensitivity in certain individuals. The purpose of this study was to measure the amount of nickel released from three types of nickel-containing arch wires into a synthetic saliva in vitro, and determine if the concentrations were sufficient to elicit either cytotoxic (trypan blue exclusion test) or stimulatory (MTT test) responses in human peripheral blood mononuclear cells (PBMCs) derived from nickel-sensitive and nickel-nonsensitive individuals. PBMCs were exposed to five concentrations of nickel sulfate solutions ranging from 0-29 ppm, and results were compared, particularly at concentrations obtained from nickel release experiments. FINDINGS: The amount of nickel released into synthetic saliva ranged from 0.4-4.1 ppb. Wires subjected to a combination of soaking and cyclic straining released significantly more nickel than those that were soaked only (p </= 0.05), and NiTi wires released significantly more nickel than did stainless steel or nitrogen-implanted NiTi wires (p </= 0.05). For PBMCs, significant increased cell proliferation was not observed for any nickel concentration. PBMC cell death rates were highest at nickel concentrations of 29 ppm when the cells were cultured without a cell growth promoter (p </= 0.05), and MTT test values were significantly reduced at both 2.9 and 29 ppm when a growth promoter was included (p </= 0.05). CONCLUSION: The maximum amount of nickel released from all tested arch wires was 700 times lower than the concentrations necessary to elicit cytotoxic reactions in human PBMCs.

Adult↗
PubMed2001

Relating nickel-induced tissue inflammation to nickel release in vivo.

Nickel has a number of adverse biological effects that have made the use of nickel in biomedical implants controversial. Yet information about the distribution of nickel in tissues around nickel-containing implants is scarce. The purpose of the current study was to use a laser ablation technique, combined with inductively coupled mass spectroscopy, to assess the spatial distribution of nickel around nickel-containing implants in vivo. Polyethylene, pure nickel wire, or a nickel-containing alloy (Ni-Cr) were implanted subcutaneously into rats for 7 days. The tissues were analyzed for Ni content and inflammation at 1-mm intervals up to 5 mm away from the implants. The sham surgery sites and the polyethylene caused mild to moderate inflammation 1-2 mm from the implant site with no detectable nickel in the tissue. The nickel wire caused severe inflammation up to 5 mm away from the implant site with necrosis for 1 mm around the implant. Nickel concentrations reached 48 microg/g near the implants, falling exponentially to undetectable levels at 3-4 mm from the implants. The Ni-Cr wire caused inflammation equivalent to polyethylene, with less than 4 microg/g of nickel present in the tissue for 1-2 mm around the implants. The current study showed that the laser-ablation technique was well suited for the analysis of soft tissues for metal-ion content, and that the nickel distribution in tissues correlated well with overt tissue inflammation.

Alloys↗
PubMed2002

Decrease in nickel sensitization in a Danish schoolgirl population with ears pierced after implementation of a nickel-exposure regulation.

BACKGROUND: To reduce the skin nickel exposure of the population, the Danish Ministry of Environment issued a regulation that was implemented in 1992, and the European Union countries have recently adopted an expanded regulation. OBJECTIVES: The aim of our combined patch testing and questionnaire investigation of girls in public schools and high schools/production schools was to evaluate whether the regulation has had an impact on the prevalence of nickel sensitization. METHODS: To find a group of girls with ears pierced mainly after implementation of the nickel-exposure regulation in Denmark, girls were recruited from the fifth and sixth grade in 12 public schools (the public school group). After the public school level almost all girls from a public school population continue their education in high schools or other schools such as production schools or technical schools. Therefore, to find girls demographically similar to the public school girls but older, and with ears pierced before implementation of the regulation, girls from seven high schools and two production schools were recruited (the high school group). Four hundred and twenty-seven girls in the public school group (mean age 12.4 years, range 10-14) and 534 in the high school group (mean age 18.8 years, range 17-22) participated. All participants filled out a questionnaire concerning ear piercing, use of oral braces and former patch testing for nickel sensitivity. Three hundred and five girls (71.4%) in the public school group and 275 (51.5%) in the high school group were patch tested or had been tested previously and the results of these tests were included in the study. The relation between the frequency of nickel sensitization and the various factors that might influence the prevalence of nickel sensitization was evaluated by multivariate logistic regression analysis. The investigation was conducted from March 1999 to March 2000. RESULTS: The study showed that both increasing age and having ears pierced before 1992 enhanced the prevalence of nickel sensitization. We found that 17.1% of the girls in the high school group demonstrated a positive patch test reaction to nickel. In contrast, the prevalence of nickel sensitization in the public school group was only 3.9%. Comparing girls with and without pierced ears, the prevalence of nickel sensitization was significantly higher in girls with ears pierced before, but not after, 1992 (odds ratio 3.34 and 1.20, respectively). Only in the high school group was there a tendency that wearing oral braces before ear piercing had a protective effect on nickel sensitization, but this did not reach statistical significance. CONCLUSIONS: As we found an effect of ear piercing before but not after 1992, this study strongly suggests that implementation of the nickel-exposure regulation in 1992 in Denmark has had the intended effect of protecting the female population from becoming allergic to nickel.

Adolescent↗
PubMed2003

Nickel (II) enhances benzo[a]pyrene diol epoxide-induced mutagenesis through inhibition of nucleotide excision repair in human cells: a possible mechanism for nickel (II)-induced carcinogenesis.

Nickel (II), a ubiquitous environmental and industrial contaminant, is a well-known human carcinogen, particularly in human lung cancer. Although by itself it is a weak mutagen, nickel (II) is able to significantly enhance the genotoxicity of other mutagens and carcinogens, such as polycyclic aromatic hydrocarbons (PAHs) and ultraviolet light. Certain human populations, especially cigarette smokers, are frequently exposed to both nickel (II) and PAHs. To understand the interplay of nickel (II) and PAHs in mutagenesis and human carcinogenesis, we used a shuttle vector mutagenicity assay to examine the effect of nickel (II) on (+/-) anti-7beta, 8alpha-dihydroxy-9alpha, 10alpha-epoxy-7,8,9,10-tetrahydroxybenzo[a]pyrene (BPDE)-induced mutagenesis in human cells. BPDE is an activated metabolite of benzo[a]pyrene (BP), a major carcinogen in cigarette smoke. The shuttle vector pSP189 modified with BPDE was transfected into human cells with and without nickel (II) exposure. We found that nickel (II) exposure significantly enhanced BPDE-induced mutation frequency, but did not change BPDE-induced mutational spectrum in the supF gene of pSP189 plasmids replicated in nucleotide excision repair (NER)-proficient human cells. However, the enhancing effect of nickel (II) on BPDE-induced mutation frequency was not observed in NER-deficient human XPA cells. We also found that nickel (II) exposure of human cells did not change the spontaneous mutation frequency of the supF gene in NER-proficient or NER-deficient human cells, indicating that nickel (II) did not affect the replication fidelity in human cells. Using a plasmid containing a luciferase reporter gene and a host cell reactivation assay, we have found that nickel (II) exposure greatly inhibited the repair of BPDE-DNA adducts in NER-proficient but not in NER-deficient cells. Together these results strongly suggest that nickel (II) can greatly enhance the mutagenicity and genotoxicity of PAHs by inhibiting the NER pathway in human cells, and this may constitute an important mechanism for nickel (II)-induced human carcinogenesis.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1989

Alteration of nickel-binding proteins in nickel-resistant cells.

Proteins from wild-type and nickel-resistant cells (Balb/c-3T3 and B200, respectively) were studied by one- or two-dimensional sodium dodecyl sulfate polyacrylamide gel electrophoresis and detected either by standard protein staining or by fluorographic analysis of [63Ni] binding. Wild-type cells contained three major nickel-binding proteins with molecular masses of 68 kDa (p68), 55 kDa (p55), and 48 kDa (p48). The p55 was present in high concentrations in the microsomal fraction, whereas the p68 nickel-binding protein predominated in the cytosolic fraction. We were unable to demonstrate that p48 was localized in any subcellular fraction. Both the p55 and p48 proteins appeared to be present in similar amounts in wild-type and nickel-resistant cell lines, based upon silver staining of two-dimensional gels, yet in the nickel-resistant B200 cells, these proteins could not be visualized by [63Ni] binding. This suggested that if nickel binding to these proteins were important for nickel toxicity, then nickel resistance in the B200 cells would be associated with the observed loss of metal binding to these proteins. In addition to the changes in [63Ni]-binding proteins, the total concentration of a 44 kDa protein was increased in B200 cells, but its ability to bind nickel could not be established due to its rapid degradation. Among the nickel-binding proteins studied, the p55 contained nickel-binding sites that were the most resistant to exchange by excess nickel ions. The microsomal fraction that contained the highest concentration of p55 also had the highest nickel-binding activity when standardized for protein concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Nickel as an occupational allergen. A survey of 368 nickel-sensitive subjects.

OBJECTIVE: To define the role of nickel as an occupational allergen. DESIGN: Survey using path-test results. SETTING: Contact dermatitis clinic in the university hospital of a large industrial British city. PATIENTS: Three hundred sixty-eight nickel-allergic patients seen during a 5-year period were assessed for the relevance of nickel contact in their workplace. Patients were divided into possible occupational nickel allergy and nonoccupational nickel allergy groups. RESULTS: Nickel was considered an occupational allergen or possible occupational allergen in 84 (22.8%) of 368 patients shown to be nickel sensitive on patch testing. The main workers in whom nickel was a common allergen were hairdressers, retail clerks, caterers, domestic cleaners, and metalworkers. Those for whom occupational exposure was possible had a significantly higher prevalence of hand dermatitis compared with the nonoccupational nickel allergy group. Nickel allergy seemed to function as a secondary occupational influence, often in conjunction with other factors, such as irritants. CONCLUSIONS: Although the overall importance of nickel as an occupational allergen cannot be easily assessed, there is evidence of its importance in some occupations, especially those involving wet work. The possibility that nickel is acting as an occupational allergen needs to be assessed on an individual basis, taking into account personal circumstances and environment, but particularly should be considered in patients with hand dermatitis.

Adolescent↗
PubMed2001

Nickel on the Swedish market before the Nickel Directive.

Nickel allergy is by far the most frequent contact allergy, affecting 10-15% of women in the general population, and causing dermatitis and hand eczema. The EU Nickel Directive, aimed at the prevention of nickel allergy, comes fully into force by July 2001. The Directive covers piercing materials, items in contact with the skin, and requirements on resistance to wear. We carried out a study of the prevalence on the market, before the Nickel Directive, of items that release nickel and of nickel in piercing posts. Nickel release, as shown by a positive dimethylglyoxime (DMG) test, was detected in 25% of 725 items intended for direct and prolonged contact with the skin. Of 15 posts intended for use during epithelialization after piercing, 60% contained more than 0.05% nickel. These products do not comply with the requirements of the EU Nickel Directive. It is suggested that experts in contact dermatitis participate in the prevention of nickel allergy by explaining its effects: the r le of skin exposure and which parts of an item are in contact with the skin, and the crucial question of nickel release versus nickel content.

Dermatitis, Allergic Contact↗
PubMed1999

Corrosion of stainless steel, nickel-titanium, coated nickel-titanium, and titanium orthodontic wires.

Orthodontic wires containing nickel have been implicated in allergic reactions. The potential for orthodontic wires to cause allergic reactions is related to the pattern and mode of corrosion with subsequent release of metal ions, such as nickel, into the oral cavity. The purpose of this study was to determine if there is a significant difference in the corrosive potential of stainless steel, nickel titanium, nitride-coated nickel titanium, epoxy-coated nickel titanium, and titanium orthodontic wires. At least two specimens of each wire were subjected to potentiostatic anodic dissolution in 0.9% NaCl solution with neutral pH at room temperature. Using a Wenking MP 95 potentiostat and an electrochemical corrosion cell, the breakdown potential of each wire was determined. Photographs were taken of the wire speci mens using a scanning electron microscope, and surface changes were qualitatively evaluated. The breakdown potentials of stainless steel, two nickel titanium wires, nitride-coated nickel titanium, epoxy-coated nickel titanium, and titanium were 400 mV, 300 mV, 750 mV, 300 mV, 1800 mV, and >2000 mV, respectively. SEM photographs revealed that some nickel titanium and stainless steel wires were susceptible to pitting and localized corrosion. The results indicate that corrosion occurred readily in stainless steel. Variability in breakdown potential of nickel titanium alloy wires differed across vendors' wires. The nitride coating did not affect the corrosion of the alloy, but epoxy coating decreased corrosion. Titanium wires and epoxy-coated nickel titanium wires exhibited the least corrosive potential. For patients allergic to nickel, the use of titanium or epoxy-coated wires during orthodontic treatment is recommended.

Coated Materials, Biocompatible↗
PubMed2006

Nur, a nickel-responsive regulator of the Fur family, regulates superoxide dismutases and nickel transport in Streptomyces coelicolor.

Nickel serves as a cofactor for various microbial enzymes including superoxide dismutase (SOD) found in Streptomyces spp. In Streptomyces coelicolor, nickel represses and induces production of Fe-containing and Ni-containing SODs, respectively, primarily at the transcriptional level. We identified the nickel-responsive regulator (Nur), a Fur (ferric-uptake regulator) homologue, which binds to the promoter region of the sodF gene encoding FeSOD in the presence of nickel. Disruption of the nur gene caused constitutive expression of FeSOD and no induction of NiSOD in the presence of nickel. The intracellular level of nickel was higher in a Deltanur mutant than in the wild type, suggesting that Nur also regulates nickel uptake in S. coelicolor. A putative nickel-transporter gene cluster (nikABCDE) was identified in the genome database. Its transcription was negatively regulated by Nur in the presence of nickel. Purified Nur protein bound to the nikA promoter region in a nickel-dependent way. These results support the action of Nur as a regulator of nickel homeostasis and antioxidative response in S. coelicolor, and add a novel nickel-responsive member to the list of versatile metal-specific regulators of the Fur family.

ATP-Binding Cassette Transporters↗
PubMed1994

Antagonistic effect of nickel on the fermentative growth of Escherichia coli K-12 and comparison of nickel and cobalt toxicity on the aerobic and anaerobic growth.

The facultative anaerobic enterobacterium Escherichia coli requires the activity of nickel-containing hydrogenase for its anaerobic growth. Deficiency of the specific nickel transport system led to a hydrogenase-minus phenotype and slowed down the fermentative growth in the nik mutant. Addition of 300 microM nickel to the growth medium could restore the hydrogenase activity. This restoration resulted in the recovery of anaerobic growth. A further increase of nickel concentration inhibited growth. Thus nickel shows an antagonistic effect on the anaerobic growth of E. coli. To study the mechanism of nickel toxicity, two classes of nickel-resistant mutants were isolated. The nkr mutant was obtained by selecting colonies grown on nickel-containing minimal plate. It acquired simultaneously the resistance to cobalt. A nonspecific magnesium transport mutant corA was isolated on cobalt-containing plate. The corA mutant was also resistant to nickel. When analyzing the influence of nickel and cobalt on the bacterial growth, we obtained two interesting observations. First, anaerobic growth was less sensitive than aerobic growth to cobalt toxicity. In contrast, nickel toxicity did not vary from the growth conditions. Second, cobalt seems to abolish the growth, while nickel appears to slow down the growth rate under the condition used.

Aerobiosis↗
PubMed1998

Urinary nickel excretion in populations living in the proximity of two russian nickel refineries: a Norwegian-Russian population-based study.

The Russian nickel refineries located in the cities of Nikel and Zapolyarny close to the Norwegian border are responsible for extensive sulfur dioxide and nickel pollution, as well as severe ecological damage in both countries. The aim of our study was to investigate human nickel exposure in the populations living on both sides of the Norwegian-Russian border. The design was a cross-sectional population-based study of adults aged 18-69 years residing in Sor-Varanger municipality, Norway, and Nikel and Zapolyarny, Russia, during 1994 and 1995. Individual exposure to nickel was assessed by measurements of nickel in urine using electrothermal atomic absorption spectrometry. For controls, urine was collected from adults in the Russian cities of Apatity and Umba (Kola Peninsula) and the Norwegian city of Tromso, all of which are locations without nearby point sources of nickel. Altogether 2,233 urine specimens were analysed for nickel. People living in Nikel had the highest concentrations (median 3.4 microg/l), followed by Umba (median 2.7 microg/l), Zapolyarny (median 2.0 microg/l), Apatity (median 1.9 microg/l), Tromso (median 1.2 microg/l), and Sor-Varanger (median 0.6 microg/l). Regardless of geographical location, the Russian study groups all had a higher urinary-nickel average than those in Norway (p<0.001). With the exception of Nikel, neither the Russian nor the Norwegian urinary-nickel levels were associated with residence location near a Russian nickel refinery. We concluded that industrial nickel pollution alone could not explain the observed discrepancy between Norway and Russia; we also discuss other possible nickel exposure sources that may account for the high urinary levels found in Russia.

Adolescent↗
PubMedDate not supplied

Chronic allergic-like dermatopathies in nickel-sensitive patients. Results of dietary restrictions and challenge with nickel salts.

Nickel frequently contaminates foods. In sensitized patients, dietary nickel can cause a relapse of contact eczema and also widespread chronic dermatopathies quite similar to those triggered by authentic food allergy (IgE-mediated), from atopic dermatitis to chronic urticaria with angioedema. The present study was intended to evaluate the the results of an elimination diet and of the oral challenge test with nickel salts in a population of adults suffering from chronic urticaria or angioedema, pruritus or atopic dermatitis, and concomitant contract sensitization to nickel salts. The study involved a population of adult patients (112 subjects, 106 women and 6 men, aged from 16 to 58, mean age 29 +/- 10) with widespread allergic-like dermatopathies and contact sensitization to nickel salts (positive patch test). All of these subjects were prescribed a low nickel diet for four weeks. The patients who recovered or whose clinical manifestations greatly improved underwent an oral double-blind, placebo-controlled challenge: they were administered two successive, noncumulative doses of 10 and 20 mg nickel sulphate hexahydrate, respectively equal to 2.23 and 4.47 mg of elemental nickel. A search for specific IgE and the check on skin reactivity by skin-prick test against nickel were carried out in the patients who had shown particularly severe reactions after the oral challenge. A low nickel diet was effective in controlling the symptoms in 44 patients (39.28%, among whom there was one man). The oral double-blind, placebo-controlled challenge test was positive in all the patients who had favourably responded to the elimination diet, except one. In the patients with anaphylactoid reactions on the oral challenge, skin-prick tests were negative and no serum-specific IgE antibodies against nickel were found. Such findings appear to demonstrate that, in some patients with concomitant contact allergy, intolerance to ingested nickel salts might be the real cause of the onset and perpetuation of widespread, chronic, allergic-type dermatopathies.

Administration, Oral↗
PubMed1979

Urinary and plasma concentrations of nickel as indicators of exposure to nickel in an electroplating shop.

The relationship between atmospheric exposure to nickel and urine and plasma nickel concentrations was studied by following four workers from an electroplating shop for one work week by daily measurements of the nickel concentration in workroom air with personal samplers and nickel concentrations in blood and urine samples collected before and after the work shift. The workroom air concentrations ranged from 0.03 to 0.16 mg/m3. The urinary and plasma nickel concentrations were higher in the samples taken after than before the work shift and a close positive correlation was found between the air nickel concentrations and the urine and plasma nickel concentrations, respectively. There was also a close correlation between urinary and plasma nickel concentrations. A slight accumulation of nickel occurred as judged from the increasing concentrations of nickel in the urine and plasma morning samples during the study week. This study indicates that both plasma and urine nickel concentrations may be used as biological indicators of exposure to soluble nickel compounds.

Adult↗
PubMed1984

Nickel-bound chromatin, nucleic acids, and nuclear proteins from kidney and liver of rats treated with nickel carbonate in vivo.

The in vivo binding of nickel to chromatin, nucleic acids, and nuclear proteins from rat kidney and liver was investigated. Evidence is presented for the direct interaction of nickel with chromatin from rat tissues following i.p. injection of nickel carbonate. A gentle DNA isolation procedure was developed and used to isolate nickel-bound whole chromatin, DNA + histone octamer complex (polynucleosomes), and deproteinized DNA from kidney and liver nuclei. A similar procedure was developed for isolating nickel-bound RNA from the cytoplasm. The level of nickel bound to whole chromatin from kidney was higher than that from liver, and these levels could be related to the nuclear concentration of nickel. Much higher levels of nickel were bound to the DNA + histone octamer complex and purified, deproteinized DNA from kidney as compared to liver. Substantial levels of nickel were bound to nonhistone proteins and/or chromatin-associated RNA from kidney and liver nuclei. Nickel was also associated with histone octamer proteins from kidney; however, little or no nickel was associated with histone octamer proteins from liver. 63Ni binding to nuclear proteins in rats given injections of 63Ni(II) was investigated by using two different gel electrophoretic systems. Electrophoretic conditions in both systems were found to remove protein-bound 63Ni. These results are discussed relative to the molecular mechanism of nickel carcinogenesis.

Animals↗
PubMed1988

Direct and indirect nickel-specific stimulation of T lymphocytes from patients with allergic contact dermatitis to nickel.

Fourteen T lymphocyte clones (TLC) specific for the contact allergen nickel were prepared either from lesional tissue biopsies or from peripheral blood of patients with allergic nickel-contact dermatitis. Two nickel-specific TLC, obtained from lesional tissue, responded to nickel without the participation of antigen-presenting cells (APC). This direct stimulation by nickel was not restricted by major histocompatibility complex-encoded molecules, since antibodies against HLA class I and II molecules did not block nickel-specific proliferation. Proliferation of other nickel-specific TLC was dependent on the presence of APC and was diversely restricted by HLA class II molecules. With one exception, the restriction determinants were present on HLA-DR and HLA-DQ molecules. Four TLC recognized nickel in association with subtypes of these serologically defined molecules. Five TLC seemed to recognize nickel in the context of highly unusual restriction determinants, since their restrictions could not be explained by the function of single polymorphic HLA class II epitopes. The absence of HLA class II restrictions and the occurrence of deviant HLA class II restrictions in part of the nickel-specific TLC are suggested to result from direct interactions of nickel with critical immune response molecules.

Antigen-Presenting Cells↗
PubMed1997

Exposure to soluble nickel in electrolytic nickel refining.

Past and present exposure to nickel was studied in an electrolytic nickel refinery, where an increased incidence of nasal cancer had been reported, using nickel analyses in air, blood and urine. Genotoxic effects were studied using analysis of micronuclei from acridine orange-stained smears from the buccal mucosa of the workers. Workers used respirators or masks in tasks where the exposure was expected to be high. Inside the mask, nickel concentrations were 0.9-2.4 micrograms m-3 in such tasks. In those tasks where masks were not used, nickel concentrations in the breathing zone were 1.3-21 micrograms m-3. Air-borne nickel concentrations (stationary sampling) varied between 230 and 800 micrograms m-3 in 1966-1988 with no systematic change; thereafter lower concentrations (170-460 micrograms m-3) have been observed. After-shift urinary concentrations of nickel were 0.1-2 mumol l-1; they showed no correlation with nickel concentrations in the air. Concentrations of nickel in the urine were still elevated after a 2-4 week vacation. The frequency of micronucleated epithelial cells in the buccal mucosa of nickel refinery workers was not significantly elevated by comparison with referents. No relationship was observed between micronucleus frequencies and levels of nickel in air, urine or blood.

Air Pollutants, Occupational↗
PubMed2003

Release of nickel ions from stainless steel alloys used in dental braces and their patch test reactivity in nickel-sensitive individuals.

Nickel ions leached in sufficient quantities from nickel-containing alloys may induce nickel sensitization or elicit allergic contact dermatitis. Nickel-containing stainless steel alloys are generally considered safe for nickel-sensitive individuals to use. The study summarized in this paper investigated 3 parameters. First, the release of nickel was estimated in artificial saliva and sweat from 4 different stainless steel alloys frequently used in dental braces. Second, in a pilot study, oral mucosa cells harvested from 3 dental patients before and after the attachment of dental braces were analysed for possible nickel content. Third, patch test reactivity of the 4 stainless steel alloys was tested on 31 nickel-sensitive subjects. All 4 stainless steel alloys released small amounts of nickel ions into artificial saliva (<0.13 micro g/cm2/week) and artificial sweat (<0.05 micro g/cm2/week), but no measurable amounts of nickel were found in any of the oral mucosa samples. None of the 31 nickel-sensitive subjects reacted to patch testing with the 4 stainless steel alloys, indicating that these stainless steel alloys would be safe to use in direct and prolonged contact with the skin.

Dental Alloys↗