ArticlePDF Available

Biological detoxification and mercury dental amalgam

Authors:
  • Italian Association for Metals and Biocompatibility Research – A.I.R.M.E.B., Milan, Italy.
http://jdr.sagepub.com/
Journal of Dental Research
http://jdr.sagepub.com/content/87/9/800.1
The online version of this article can be found at:
DOI: 10.1177/154405910808700912
2008 87: 800J DENT RES
Gianpaolo Guzzi and Claudio Minoia
BIOLOGICAL DETOXIFICATION AND MERCURY DENTAL AMALGAM
Published by:
http://www.sagepublications.com
On behalf of:
International and American Associations for Dental Research
can be found at:Journal of Dental ResearchAdditional services and information for
http://jdr.sagepub.com/cgi/alertsEmail Alerts:
http://jdr.sagepub.com/subscriptionsSubscriptions:
http://www.sagepub.com/journalsReprints.navReprints:
http://www.sagepub.com/journalsPermissions.navPermissions:
What is This?
- Sep 1, 2008Version of Record >>
by guest on October 14, 2011 For personal use only. No other uses without permission.jdr.sagepub.comDownloaded from
International and American Associations for Dental Research
Controlled CliniCal trials and PraCtiCe-
based researCh in dentistry
To the Editor:
In his recent editorial (Mjör, 2008), Ivar Mjör extolled the
virtues of practice-based research, but seemed to suggest that
practice-based settings may not be conducive to the conduct
of randomized clinical trials (RCTs). His point depends on
the perception of a RCT as done to demonstrate efficacy in a
very controlled environment by one or two highly trained and
calibrated expert clinicians who are able to devote extraordinary
time and attention to it. However, there is no reason why RCTs
cannot be used in a practice-based setting to demonstrate
effectiveness (the outcome in practice). One would focus on the
intervention as used in practice, with simple clinical outcomes.
Variations of participating dentists in background and skill
would be present, but are part of the background noise. If the
outcome is not significantly greater than the background noise,
then it won’t have any impact on practice.
An example is an upcoming RCT in NW PRECEDENT
in which we will compare mineral trioxide aggregate (MTA)
and calcium hydroxide as pulp-capping materials in member
practices. Each dentist will be randomized to use only one
of the two for all pulp caps needed over a specified period.
Outcomes after two years will be whether the treated tooth
required endodontic treatment or extraction, or if it remains
vital. This addresses the kind of “identified” and ”recurring”
clinical problem Dr. Mjör suggests should be pursued in dental
practice-based research networks, but does so with a RCT
design that should produce the highest-quality evidence of
effectiveness.
— Timothy A. DeRouen
Executive Associate Dean for Research and Academic Affairs, University
of Washington, Seattle, USA
— Jack Ferracane
Chairman, Department of Restorative Dentistry, Oregon Health and Science
University, Portland, USA
Co-Directors, Northwest PRECEDENT Dental Practice Based Research
Network
reFerenCe
Mjör IA (2008). Controlled clinical trials and practice-based research in
dentistry (guest editorial). J Dent Res 87:605.
The author replies:
Thank you for the opportunity to comment on the Letter
to the Editor from Drs. DeRouen and Ferracane at the NW
PRECEDENT practice-based network. I am pleased to note
that we agree that RCTs can be done in practice-based research
(P-BR), as expressed in my Guest Editorial. The network’s
pulp study referred to is an example of a RCT design carried
biologiCal detoxiFiCation and MerCury
dental aMalgaM
To the Editor:
In their randomized controlled trial, Melchart et al. (2008)
addressed the important issue of how to treat health conditions
associated with amalgam.
We wish to raise two points. In the group termed “removal-
plus group”, a “biological detoxification” therapy was used to
treat patients’ symptoms consistent with exposure to amalgam.
Me lchart and co -workers see m u naware that s el enium
selenite—which was chosen in their trial—while an essential
element, is also a toxic compound (Guzzi and La Porta, 2008).
We were surprised that the authors chose to supplement the
“removal-plus group” with inorganic sodium selenite, usually
used in experimental studies (Tandon et al., 1986).
Because of the “biological detoxification”, we would expect
to see organic selenium (selenomethionine, selenocysteine, and
selenium-yeast) instead of sodium selenite in the supplemented
group. Selenium supplementation decreases the excretion of
mercury, and the formation of mercury selenide (Hg-Se) may
become a secondary source of mercury, worsening the retention
toxicity owing to mercury (Tandon et al., 1986; Agarwal and
Behari, 2007). Furthermore, selenium may increase brain levels
of methyl mercury (Tandon et al., 1986), which is present in the
saliva in individuals with amalgam.
Selenium is very far from being safe for persons exposed to
mercury.
In addition, neither intravenous vitamin C (in a clinical
study) (Dirks et al., 1994) nor ascorbate (in an animal model)
(Guzzi and La Porta, 2008) has been shown to be beneficial in
removing mercury from human tissues. We believe that there is
no evidence that biological detoxification may have benefit in
persons with symptoms associated with exposure to amalgam.
The management of mercury body burden due to amalgam
remains complete removal of dental amalgam fillings.
— Gianpaolo Guzzi1 & Claudio Minoia2
1Italian Association for Metals and Biocompatibility Research, (AIRMEB),
Via F. Sforza, 15, 20122 Milan, Italy, gianpaolo_guzzi@fastwebnet.it
2Laboratory of Environmental, and Toxicology Testing “S. Maugeri”-
IRCCS, Pavia, Italy
reFerenCes
Agarwal R, Behari JR (2007). Role of selenium in mercury intoxication in
mice. Ind Health 45:388-395.
Dirks MJ, Davis DR, Cheraskin E, Jackson JA (1994). Mercury excretion
and intravenous ascorbic acid. Arch Environ Health 49:49-52.
Guzzi G, La Porta CA (2008). Molecular mechanisms triggered by mercury.
Toxicology 244:1-12.
Melchart D, Vogt S, Kohler W, Streng A, Weidenhammer W, Kremers L,
et al. (2008). Treatment of health complaints attributed to amalgam. J
Dent Res 87:349-353.
Tandon SK, Magos L, Webb M (1986). The stimulation and inhibition of
the exhalation of volatile selenium. Biochem Pharmacol 35:2763-2766.
J Dent Res 87(9):800-801, 2008
letters to the editor
800 by guest on October 14, 2011 For personal use only. No other uses without permission.jdr.sagepub.comDownloaded from
International and American Associations for Dental Research
J Dent Res 87(9) 2008 Letters to the Editor 801
out in practice.
However, there is more to P-BR than training clinicians
to do RCTs in their practices, and that is to identify recurring
problems encountered in practice. Many examples can be
quoted. I will mention two. When resin-based materials came
into common use 30-40 years ago, marginal staining was a
major problem. As the problem was identified, it was solved by
introducing acid etching as part of the restorative procedure.
The clinical diagnosis of secondary (recurrent) caries is a
frequent reason for replacement of restorations. It dates back
a century, when G.V. Black identified it as a major problem
associated with amalgam restorations. Since P-BR has shown
this diagnosis to be the most common reason for replacement
of all types of restorations, it calls for research to solve the
recurring problem. Progress has been made, and more needs to
be done.
I maintain that a recurring clinical problem must be
identified or it will not be resolved. It is unlikely that P-BR will
solve the problem per se, but it will allow the dental research
community to focus on problems relevant to dental practice.
— Ivar A. Mjör, Professor Emeritus
Academy 100 Eminent Scholar, College of Dentistry, University of Florida,
PO Box 100415, Gainesville, FL 32610, USA
note to readers:
In future issues, Letters to the Editor will
appear only in the online Journal of Dental
Research. The JDR can be found online at
http://jdr.iadrjournals.org
by guest on October 14, 2011 For personal use only. No other uses without permission.jdr.sagepub.comDownloaded from
International and American Associations for Dental Research
... First, the authors diagnosed chronic mercury (Hg 0 ) poisoning and prescribed chelation therapy (succimer) and selenoenzymes along with selenoenzymes. 1 The evidence in the literature strongly suggests that the use of selenium (Se) supplementation may decrease mercury excretion 9 and worsen retention kinetic as well as the toxicity of the neurotoxic metal in patients with mercury overexposure. 9 In our view, the clinical usefulness of oral selenium supplementation remains unproved. ...
... First, the authors diagnosed chronic mercury (Hg 0 ) poisoning and prescribed chelation therapy (succimer) and selenoenzymes along with selenoenzymes. 1 The evidence in the literature strongly suggests that the use of selenium (Se) supplementation may decrease mercury excretion 9 and worsen retention kinetic as well as the toxicity of the neurotoxic metal in patients with mercury overexposure. 9 In our view, the clinical usefulness of oral selenium supplementation remains unproved. 9 Therefore, with regard to the use of selenium as nonspecific supportive treatment, 10 as indicated in the management section of the case, 1 it seems much too premature to recommend such therapy. ...
... 9 In our view, the clinical usefulness of oral selenium supplementation remains unproved. 9 Therefore, with regard to the use of selenium as nonspecific supportive treatment, 10 as indicated in the management section of the case, 1 it seems much too premature to recommend such therapy. ...
Article
The clinical manifestations of methylmercury toxicity do not differ greatly according to the acute and/or chronic methylmercury overexposure.
Article
Full-text available
Studies were conducted to examine the effect of pre and post-treatment of selenium in mercury intoxication (20 micromole/ kg b.w. each given intraperitoneally) in mice in terms of lipid peroxidation (LPO), glutathione (GSH) content, activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and mercury concentration in liver, kidney and brain. No significant alteration was observed in all the organs examined after mercury or selenium treatment in LPO and GSH but administration of selenium (pre and post) resulted in an increase in the level of LPO and GSH. The activity of SOD was depleted in liver and kidney while that of GPx was lowered in liver of mercury exposed animals. Selenium administration resulted in restoration of the depletion of these enzymatic activities. The activity of CAT in liver and brain was enhanced both in mercury and selenium treated animals. Administration of selenium significantly arrested enhanced CAT activity. Kidney showed the highest mercury concentration among the organs examined. Administration of selenium resulted in further enhancement of mercury concentration in the tissues. An increase in selenium level in liver was observed after mercury treatment, which was also restored by mercury selenium co-administration. Our results indicate that the prooxidant effect of selenium was greater by its pretreatment.
Article
Full-text available
The aim of the present study was to compare the reduction of subjective complaints by 3 treatment strategies in 90 "amalgam patients" whose complaints could not be explained by a medical or psychological disorder. The individuals were randomly assigned either to removal of dental amalgam only (removal group), or removal in combination with a "biological detoxification" therapy with high doses of vitamins and trace elements (removal-plus group), or participation in a health promotion program without removal of dental amalgam (no-removal group). Between baseline and month 12, the sum score of main complaints decreased by 3.5 (SD=2.2) points on average in the removal group as well as in the removal-plus group, and by 2.5 (SD=2.4) points in the no-removal group (p=0.152). Both removal groups showed a significant decrease in steady-state levels of inorganic mercury compared with the no-removal group. Thus, all 3 interventions were associated with clinically relevant improvements.
Article
Administration of methylmercury (1.5-24 mumol kg-1; s.c.) to female rats simultaneously with Na2 75SO3 (0.25 or 24 mumol kg-1; s.c.) causes a dose-dependent increase in the exhalation of dimethylselenide. At the low selenite dose level, exhalation of 75Se over a 24 hr period is about fourfold greater after treatment with 24 mumol kg-1 methylmercury than that (approximately 0.75% of the dose) in the controls, but excretion by other routes (urine, faeces) and the liver and kidney contents of 75Se are not affected significantly. At the higher selenite dose level (24 mumol kg-1) exhalation of 75Se is correlated with the log dose of methylmercury. The faecal and urinary excretion remains essentially unaffected, and in rats treated with 24 mumol kg-1 methylmercury the 75Se contents of the liver, kidneys and blood are reduced by 78%, 86% and 18% respectively. The effects of the alkylmercurial are not specific since, at this selenite dose level, ethylmercury increases the exhalation and decreases the liver and kidney contents of 75Se approximately to the same extent as an equimolar dose of methylmercury. In methylmercury-treated and control animals dosed with 24 mumol kg-1 Na 75SeO3 the exhalation of 75Se is inhibited to the same extent by periodate-oxidized adenosine (PAD; 15 mumol kg-1, i.p.) in the first 6 hr. Later inhibition is less pronounced in methylmercury-treated rats. Under these conditions PAD has little effect on the renal content, but increases the hepatic content of 75Se. It seems, therefore, that the methylation of selenite occurs mainly in the liver and in both control and methylmercury-treated animals, S-adenosylmethionine is the major methyl donor. It is possible that methylmercury does not affect directly the methylation enzyme system but, by competition for protein sulphydryl groups, increases the availability of the intermediary selenide anion.
Article
We tested the hypothesis that intravenous ascorbic acid increases urinary excretion of mercury in subjects with low mercury levels from dental amalgam, food, and other sources. From 89 adult volunteers we selected 28 subjects with the highest mercury excretions (2 to 14 micrograms/24 h). We administered intravenous infusions of 500 ml lactated Ringer's solution with and without addition of 750 mg of ascorbic acid/kg body weight, up to 60 g ascorbic acid. Average mercury excretion during the 24 h after infusion of ascorbic acid was 4.0 +/- 0.5 micrograms (mean +/- SEM), which was not significantly more than after infusion of Ringer's solution alone (3.7 +/- 0.5 micrograms). Lead excretion was similarly unaffected. If ascorbic acid administered intravenously benefits some persons with suspected adverse reactions to mercury, the benefit in subjects similar to ours appears unrelated to short-term enhanced excretion of mercury or lead.
Article
Mercury is an ubiquitous environmental toxin that causes a wide range of adverse health effects in humans. Three forms of mercury exist: elemental, inorganic and organic. Each of them has its own profile of toxicity. Exposure to mercury typically occurs by inhalation or ingestion. Mercury can be an indoor air pollutant, however industry emission remains the most important source of inhaled mercury. Furthermore, fresh water and ocean fish may contain large amounts of mercury and dental amalgam can be another important source of inorganic and mercury vapor. The present review discusses the current information on mercury toxicity and the distinct toxicologic profile of the three forms of mercury. The existing therapeutics, new therapeutics development or agents for treating mercury poisoning will also discussed. Since in general low levels of mercurial are tolerable, herein, we also discuss the defensive mechanisms developed by the cell to protect itself against mercury injury. This aspect may be useful to provide a biological protection against toxic effects exerted by mercury or by specific forms of mercury in view of a medicinal purposes.