Mercury (Hg) was named after the Greco-Roman god known for swift flight. Also called quicksilver, metallic mercury is in liquid state at room temperature. The symbol Hg was dervied from the Latinized Greek hydrargyrum, meaning “water” and “silver.”
In 2008, Norway banned the use of mercury for amalgam restorations. Four states in the United States have developed In-formed Consent Brochures for amalgam restorations that must be given to their dental patients. The authors describe a patient who had a large cavity in his left lower molar tooth no.18 that had to be removed by an oral surgeon. When the patient went to the oral surgeon, the surgeon told the patient that he would replace the carious tooth with a gold implant. He was not given an Informed Consent Brochure regarding dental restorative materials. The oral surgeon extracted the carious tooth, replacing the tooth with a sup-posed gold crown implant. On his yearly dental examination, his dentist took an x-ray of his dental implant and explained that the x-ray could not distinguish whether the implant contained either gold or mercury. Consequently, the dentist referred him to a dental clinic in which the dental implant could be removed without mer-cury contamination of the patient’s neurologic system during the extraction of the implant from the root canal. During the removal of the dental restoration, the dentist found build up expanding into the root canal that had a black color. The crown and underlying tooth were sent to ALT BioScience for analysis. Elemental analy-sis of the crown and underlying tooth confirmed the presence of mercury in the restoration. The patient should have been given an Informed Consent Brochure by the dentist that described the dental restoration that was used in the dental implant.
OBJECTIVES:
Human blood levels of mercury are commonly 10nM, but may transiently reach 50-75nM after dental amalgam placement or removal. Controversy persists about the use of mercury because the effects of these ‘trace’ levels of mercury are not clear. Concentrations of mercury > or =5000nM unequivocally alter redox balance in blood cells including monocytes. In the current study, we tested a hypothesis that concentrations of mercury <100nM altered levels and activities of key proteins that maintain monocytic redox balance.
METHODS:
Human THP1 monocytes were exposed to 10-75nM of Hg(II) for 6-72h, with or without activation by lipopolysaccharide (LPS). The redox management proteins Nrf2 and thioredoxin-1 (Trx1) were separated by electrophoresis, then quantified by immunoblotting. The activity of the seleno-enzyme thioredoxin reductase (TrxR1), important in maintaining Trx1 redox balance, was measured by cell-free and cell-dependent assays.
RESULTS:
Concentrations of Hg(II) between 10-75nM increased Nrf2 levels (3.5-4.5 fold) and decreased Trx1 levels (2-3 fold), but these changes persisted <24h. Hg(II) potently inhibited (at concentrations of 5-50nM) TrxR1 activity in both cell-free and intracellular assays. Furthermore, Hg(II) transiently amplified LPS-induced Nrf2 levels by 2-3 fold and limited LPS-induced decreases in Trx1. All effects of Hg(II) were mitigated by pre-adding N-acetyl-cysteine (NAC) or sodium selenide (Na2SeO3), supplements of cellular thiols and selenols, respectively.
SIGNIFICANCE:
Our results suggest that nanomolar concentrations of Hg(II) transiently alter cellular redox balance in monocytes that trigger changes in Nrf2 and Trx1 levels. These changes indicate that monocytes have a capacity to adapt to trace concentrations of Hg(II) that are introduced into the bloodstream after dental amalgam procedures or fish consumption. The ability of monocytes to adapt suggests that low levels of mercury exposure from dental amalgam may not overtly compromise monocyte function.
Perfluorinated compounds have been used for more than 50 years as process aids, surfactants, and for surface protection. This study is a comprehensive assessment of consumer exposure to perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) from a variety of environmental and product-related sources. To identify relevant pathways leading to consumer exposure to PFOS and PFOA a scenario-based approach has been applied. Scenarios represent realistic situations where age- and gender-specific exposure occurs in the everyday life of consumers. We find that North American and European consumers are likely to experience ubiquitous and long-term uptake doses of PFOS and PFOA in the range of 3 to 220 ng per kg body weight per day (ng/kg(bw)/day) and 1 to 130 ng/kg(bw)/day, respectively. The greatest portion of the chronic exposure to PFOS and PFOA is likely to result from the intake of contaminated foods, including drinking water. Consumer products cause a minor portion of the consumer exposure to PFOS and PFOA. Of these, it is mainly impregnation sprays, treated carpets in homes, and coated food contact materials that may lead to consumer exposure to PFOS and PFOA. Children tend to experience higher total uptake doses (on a body weight basis) than teenagers and adults because of higher relative uptake via food consumption and hand-to-mouth transfer of chemical from treated carpets and ingestion of dust. The uptake estimates based on scenarios are within the range of values derived from blood serum data by applying a one-compartment pharmacokinetic model.
Porphyromonas gingivalis (Pg), a Gram-negative anaerobic black-pigmented rod bacterium, has been recognized as the most potent etiologic bacte-rium in human chronic periodontitis. It possesses a variety of putative virulence factors providing both tissue destruction and host evasion including lipopolysac-charides (LPS), fi mbriae, various proteinases, etc. These factors actively participate in periodontal tissue destruction. However, recent evidence suggests that Pg has also evolved mechanisms to inhibit or confuse host immune systems. Thus, Pg is suggested to behave not only like an “active invader”, but also like a “stealth element” in periodontal lesions. In the present study, repeated exposure of Pg components induced tolerance resulting in selective inhibition of cytokine produc-tion of both monocytes and gingival fi broblasts in a different fashion from that described for LPS in Escherichia coli. It was also revealed that Pg LPS induced a unique dendritic cell subset with a CD14+CD16+ phenotype that exhibited weak maturation. In animal studies, administration of live Pg or its LPS exerted a regula-tory effect on systemic markers such as triglycerides or adiponectin. Taken together, these fi ndings suggest that Pg may be able to adapt to the local immune defense, contributing to the connection between systemic and periodontal disease.
Anthropogenic activities have enriched mercury in the biosphere by at least a factor of three, leading to increases in total mercury (Hg) in the surface ocean. However, the impacts on ocean fish and associated trends in human exposure as a result of such changes are less clear. Here we review our understanding of global mass budgets for both inorganic and methylated Hg species in ocean seawater. We consider external inputs from atmospheric deposition and rivers as well as internal production of monomethylmercury (CH₃Hg) and dimethylmercury ((CH₃)₂Hg). Impacts of large-scale ocean circulation and vertical transport processes on Hg distribution throughout the water column and how this influences bioaccumulation into ocean food chains are also discussed. Our analysis suggests that while atmospheric deposition is the main source of inorganic Hg to open ocean systems, most of the CH₃Hg accumulating in ocean fish is derived from in situ production within the upper waters (<1000 m). An analysis of the available data suggests that concentrations in the various ocean basins are changing at different rates due to differences in atmospheric loading and that the deeper waters of the oceans are responding slowly to changes in atmospheric Hg inputs. Most biological exposures occur in the upper ocean and therefore should respond over years to decades to changes in atmospheric mercury inputs achieved by regulatory control strategies. Migratory pelagic fish such as tuna and swordfish are an important component of CH₃Hg exposure for many human populations and therefore any reduction in anthropogenic releases of Hg and associated deposition to the ocean will result in a decline in human exposure and risk.
This paper reviews the evidence for the interaction of oral disease (more specifically, periodontal infections) with cardiovascular disease. Cardiovascular disease is a major cause of death worldwide, with atherosclerosis as the underlying aetiology in the vast majority of cases. The importance of the role of infection and inflammation in atherosclerosis is now widely accepted, and there has been increasing awareness that immune responses are central to atherogenesis. Chronic inflammatory periodontal diseases are among the most common chronic infections, and a number of studies have shown an association between periodontal disease and an increased risk of stroke and coronary heart disease. Although it is recognised that large-scale intervention studies are required, pathogenic mechanism studies are nevertheless required so as to establish the biological rationale. In this context, a number of hypotheses have been put forward; these include common susceptibility, inflammation via increased circulating cytokines and inflammatory mediators, direct infection of the blood vessels, and the possibility of cross-reactivity or molecular mimicry between bacterial and self-antigens. In this latter hypothesis, the progression of atherosclerosis can be explained in terms of the immune response to bacterial heat shock proteins (HSPs). Because the immune system may not be able to differentiate between self-HSP and bacterial HSP, an immune response generated by the host directed at pathogenic HSP may result in an autoimmune response to similar sequences in the host. Furthermore, endothelial cells express HSPs in atherosclerosis, and cross-reactive T cells exist in the arteries and peripheral blood of patients with atherosclerosis. Each of these hypotheses is reviewed in light of current research. It is concluded that although atherosclerotic cardiovascular disease is almost certainly a multifactorial disease, there is now strong evidence that infection and inflammation are important risk factors. As the oral cavity is one potential source of infection, it is wise to try to ensure that any oral disease is minimised. This may be of significant benefit to cardiovascular health and enables members of the oral health team to contribute to their patients’ general health.
The relationship between oral and general health has been increasingly recognised during the past two decades. Several epidemiological studies have linked poor oral health with cardiovascular disease, poor glycaemic control in diabetics, low birth-weight pre-term babies, and a number of other conditions, including rheumatoid arthritis and osteoporosis. Oral infections are also recognised as a problem for individuals suffering from a range of chronic conditions, including cancer and infection with human immunodeficiency virus, as well as patients with ventilator-associated pneumonia. This review considers the systemic consequences of odontogenic infections and the possible mechanisms by which oral infection and inflammation can contribute to cardiovascular disease, as well as the oral conditions associated with medically compromised patients. A large number of clinical studies have established the clinical efficacy of topical antimicrobial agents, e.g., chlorhexidine and triclosan, in the prevention and control of oral disease, especially gingivitis and dental plaque. The possible risks of antimicrobial resistance are a concern, and the benefits of long-term use of triclosan require further evaluation. Oral infections have become an increasingly common risk-factor for systemic disease, which clinicians should take into account. Clinicians should increase their knowledge of oral diseases, and dentists must strengthen their understanding of general medicine, in order to avoid unnecessary risks for infection that originate in the mouth.
This study aimed to investigate a possible connection between removal of dental amalgam restorations supported by antioxidant therapy and indicative changes of clinical chemistry parameters. A group of 24 patients, referred for complaints related to amalgam restorations, underwent a removal of their amalgams. All patients were treated with antioxidants (vitamin B-complex, vitamin C, vitamin E, and sodium selenite). An age- and sex-matched control group of 22 individuals was also included. The mercury (Hg) and selenium (Se) concentration in plasma, Hg concentration in erythrocytes, and 17 clinical chemistry variables were examined in three groups: patients before amalgam removal (Before), patients after amalgam removal (After), and control individuals (Control). The Hg and Se values decreased (p < 0.05) in plasma, and the Hg concentration decreased (p < 0.05) in erythrocytes after amalgam removal. The variables serum lactate dehydrogenase (serum LDH) and serum sodium differed significantly both when comparing Control with Before (p < 0.01) and Before with After (p < 0.01). The variables white blood cell count (WBC), blood neutrophil count, blood eosinophil count, blood basophil count, blood lymphocyte count, blood monocyte count, serum potassium, and serum creatinine differed in the Before/After test (p < 0.05). Multivariate statistics (discriminant function analysis) could separate the groups Before and After with only one misclassification.
OBJECTIVE:
Dental amalgam restorations are subjected to abrasion during selective prophylaxis that can damage or remove the protective oxide and result in increased rates of corrosion and chemical dissolution of mercury. It was the objective of this research to study the corrosion potential change of dental amalgam restorations to obtain an indication of the time required for in vivo repassivation following prophylaxis.
METHODS:
The corrosion potentials of 27 Class I and Class II amalgam restorations were measured pre- and post-prophylaxis using a high impedance voltmeter and a Ag/AgCl micro-reference electrode. Prophylaxis was performed for approximately 2s on each amalgam surface using a slow-speed handpiece with a rubber-cup and commercial abrasive paste. Subjects thoroughly rinsed before the post-prophylaxis corrosion potentials were measured. The data were analyzed using a confidence interval, a t-test and correlation analysis.
RESULTS:
The pre- and post-prophylaxis mean corrosion potentials were, respectively, -132 (27)mV and -126 (27)mV. The mean of the differences between the pre- and post-prophylaxis corrosion potentials was 6.1 (28)mV, with an associated 95% confidence interval of (-4.8, 17)mV. A t-test showed the mean absolute difference in corrosion potential was less than 50 mV (p<0.0001).
SIGNIFICANCE:
The results of this study show that the post-prophylaxis recovery of the corrosion potential of amalgam restorations occurred by at most 10-44 min, indicating that the period of elevated corrosion rate and elevated chemical dissolution rate of mercury, due to oxide damage or removal, may be short-lived.