Journal of Synchrotron Radiation. 2008 Mar;15
Migration of mercury from dental amalgam through human teeth.
Harris HH, Vogt S, Eastgate H, Legnini DG, Hornberger B, Cai Z, Lai B, Lay PA.
Abstract
Exposure to mercury from dental amalgams, with possible negative health effects, has generally been considered to occur via either erosion or evaporation directly from the surface of fillings, followed by ingestion.
The aim of this study was to determine the relative importance of the direct migration of mercury through the tooth as an alternative exposure pathway. X-ray fluorescence imaging has been used to determine quantitatively the spatial distribution of Hg, Ca, Zn and Cu in sections of human teeth that had been filled with amalgam for more than 20 years. X-ray absorption near-edge spectroscopy (XANES) was also employed to gain chemical information on the mercury present in the teeth. Hg (up to approximately 10 mg g(-1)) and Zn (>100 mg g(-1)) were detected in the teeth several millimetres from the location of the amalgams.
At high resolution, Hg showed higher concentrations in dentinal tubules while Zn was generally evenly distributed. XANES showed that the chemical form of Hg that had migrated into the tooth had been altered from that present in the amalgam. The differing spatial distributions of Hg and Zn suggest distinct transport mechanisms for the two metals, presumably chemical for Zn and initially physical for Hg. Subsequent oxidation of Hg may lead to a loss of mobility or the development of a secondary transport mechanism.
Most importantly the detection of Hg in areas of the tooth that once contained an active bloodstream and in calculus indicates that both exposure pathways should be considered as significant.
PMID: 18296776
Dr. Michael Margolis
presents evidence to the FDA's dental products panel in 2010
that mercury from amalgam fillings is absorbed into the gum and jaw bone.
Introduction
The issue of the toxicity and long-term side effects of dental amalgam fillings remains contentious. The more conservative view, that the benefits of amalgam fillings outweigh possible health concerns, is generally better respected in the scientific literature (Clarkson et al., 2003) and recent comprehensive epidemiological studies suggest that links between the use of dental amalgam and a number of implicated conditions are weak at most (Kingman et al., 2005; Bates et al., 2004).
However, anecdotal evidence for such links is abundant and 'dissident' dentists have developed new techniques for safer removal of amalgam fillings owing to demand from patients.
Meanwhile, in 1997, an estimated 40 metric tons of mercury was used in dental restorations in the USA (Reese Jr, 1997). For perspective, the annual figure for industrially sourced mercury pollution deposited in the USA in 1997 was estimated at 52 metric tons (EPA, 1997).
The fact that the presence of amalgam fillings leads to increased levels of Hg in various organs in the body, such as blood and kidney, as well as in urine is unquestioned (Kingman et al., 1998; Sallsten et al., 1996), but argument continues as to whether these levels are deleterious to human health. With one exception (Hoffmann et al., 2000), studies of amalgam toxicity have assumed that the only significant pathway of exposure to be via ingestion or inhalation of elemental Hg from the surface of fillings. However, exposure via migration of mercury through the tooth and into the active bloodstream of the pulp, and/or by concentration in the calculus, may considerably confound epidemiological results.
We have performed an initial study using X-ray microprobe techniques on extracted amalgam-filled teeth in an effort to determine the significance of these pathways and, owing to the greatly varying toxicity of different chemical forms of mercury the type of mercury entering the bloodstream through the tooth.
DISCUSSION:
It is clear from Fig. 1 that both Zn and Hg migrate from amalgam fillings and filling linings, through the dentine, and into the pulp of the tooth (subsequently replaced by secondary dentine some time after the filling), which has an active bloodstream. The significant drop in the levels of these metals observed in the secondary dentine that replaced the pulp, as compared with the original dentine, presumably indicates that they were efficiently removed from the pulp via the bloodstream before the secondary dentine grew, at which time the Hg was no longer mobile, possibly owing to a change in the chemical state of Hg (see Fig. 2). Localization of Hg in the calculus observed on the edge of the tooth distal to the filling may indicate that Hg is also considerably mobile through the mouth, presumably dissolved by bacterial action in the saliva, or possibly via surface diffusion over the tooth surface, and has a higher affinity for deposition in calculus than in other parts of the surface of the tooth.
The high concentration of Hg detected in the calculus indicates that particular care should be taken to avoid ingestion of loosened calculus by the patient. The seemingly anomalous abundant presence of Zn in the dentine considering its low abundance in amalgam is easily explained by the likely use of Zn(II)-based filling lining materials in these teeth.
The fact that the concentrations of Zn and Hg in the dentine differ by as much as two orders of magnitude, and that the elemental maps do not follow the same distributions, show that at least part of the mechanisms for the transportation of the two metals through the tooth are quite different. Examination of the elemental distribution maps presented in Fig. 3 provides feasible mechanisms for their transport. The similarity of the Zn and Ca maps, the presence of Zn in the divalent state in the lining, and the smaller ionic radius of Zn(II) (74 pm) versus Ca(II) (100 pm) (Shannon, 1976), indicate that chemical replacement of Zn for Ca in the hydroxyapatite structure is the most likely transport mechanism for Zn. Whilst Hg(II) also has ionic radii very similar to Ca(II) of 102 pm (Shannon, 1976), it is initially present only in the elemental state in amalgam. Fig. 3 shows that Hg migrates preferentially through tubules in the dentine along with Cu, suggesting a physically based transport mechanism of malleable Hg-rich amalgam, most likely at the time of restoration. However, analysis of the XANES of Hg in tubules suggests some oxidation of elemental Hg to the divalent state, indicating that a secondary transport mechanism of Hg(II) similar to that for Zn may become important with time. Subsequent association of Hg(II) with sulfides present in the organic contents of the tubules would presumably lead to a reduction in mobility for Hg, and the formation of metal sulfides may also account for the brown staining observed in the optical micrographs. The cause of the observed inconsistency in the migration of metals across the amalgam/dentine boundary remains uncertain.
It is feasible that there is simply inconsistent physical contact over the entire boundary surface; however, the possibility that variation in the exact carious histology (Ten Cate, 1998) on the exposed dentine surface of the cavity affects the migration should also be considered. Unfortunately we were unable to identify distinct histological zones in the dentine of the teeth shown herein. We attribute the presence of the Hg hotspot in Fig. 4 to the physical transport of Hg-rich viscous amalgam at the time of filling installation into a thin filament of pulp that extended into the region of the filling. Such structures are well known in molars (Berkovitz et al., 1992). Dental amalgam is set in place by incrementally packing a Hg-rich plastic phase into the excavated cavity, with excess viscous Hg removed using a dental vacuum. The physical transport mechanism is supported in this case by the presence of Cu and Ag peaks in the fluorescence spectrum of the hotspot (Fig. 4), as these metals are present in the amalgam. In contrast, a chemical transport process would presumably lead to markedly different distributions of these metals. We believe that the process that we have suggested for the source of the hotspot in Fig. 4 may also lead in particular cases to the direct injection of viscous Hg into the pulp, through a range of structures in the tooth including fractures and larger tubules known to exist between the pulp and crown (Berkovitz et al., 1992).
We are unable at present, with only long-term filled teeth available, to determine any time-dependent data on the migration of these metals through teeth.
As such, we are unable to suggest how much Hg may enter the bloodstream on a daily basis but, based on the evidence presented herein, it seems likely that significant amounts do reach the bloodstream, as both elemental Hg and as some form of divalent Hg, via at least two different mechanisms of migration through the tooth, as well as ingestion of Hg-rich calculus.
For years I've read news stories about dental mercury amalgam fillings that failed to ask vital follow up questions for one to form a better understanding of the true risks involved with exposure to mercury fillings. Rarely was a toxicologist, neurologist or bio-chemist interviewed. Instead, the stories would always give dentists such prominence when promoting the safety of a substance of which they knew nothing about, all while never acknowleding the much lower levels of mercury at which our government has removed other products from the market. So now I'm doing what I can to help raise awareness of the many dangerous aspects of dental mercury fillings.
