“This analysis suggests that high exposure to ethylmercury from thimerosal-containing vaccines in the first month of life increases the risk of subsequent development of neurologic development impairment, but not of neurologic degenerative or renal impairment. Further confirmatory studies are needed.”
“A group of selected 25 patients with serious intolerance to heavy metals used for dental restoration were examined for HLA antigens. A significant increase for HLA — B37, B47 and DR4 was found. The value of the relative risk is not significant after correction for the number of antigens tested and therefore further studies of more patients are needed.”
“We studied the effect of oxidation of sulfhydryl (SH) residues on the inhibition by Mg(2+) of calcium-induced calcium release (CICR) in triad-enriched sarcoplasmic reticulum vesicles isolated from rabbit skeletal muscle. Vesicles were either passively or actively loaded with calcium before eliciting CICR by dilution at pCa 4.6-4.4 in the presence of 1.2 mM free [ATP] and variable free [Mg(2+)]. Native triads exhibited a significant inhibition of CICR by Mg(2+), with a K(0.5) approximately 50 microM. Partial oxidation of vesicles with thimerosal produced a significant increase of release rate constants and initial release rates at all [Mg(2+)] tested (up to 1 mM), and shifted the K(0.5) value for Mg(2+) inhibition to 101 or 137 microM in triads actively or passively loaded with calcium, respectively. Further oxidation of vesicles with thimerosal completely suppressed the inhibitory effect of [Mg(2+)] on CICR, yielding initial rates of CICR of 2 micromol/(mg x s) in the presence of 1 mM free [Mg(2+)]. These effects of oxidation on CICR were fully reversed by SH reducing agents. We propose that oxidation of calcium release channels, by decreasing markedly the affinity of the channel inhibitory site for Mg(2+), makes CICR possible in skeletal muscle.”
“Dental amalgam fillings are known to release significant levels of mercury (Hg) in saliva which could represent a continuous source of oxidative damage to tissues. The present investigation was aimed at verifying this hypothesis by determining a possible correlation between salivary Hg levels and salivary total antioxidant activity (TAA), used as an index of oxidative stress. Samples of saliva from 34 healthy donors were analyzed for Hg content, through vapor atomic absorption spectrometry, and for TAA, by determining the ferric reducing ability (‘FRAP’ method). A significant correlation between Hg and the number of amalgam restorations or total amalgam surface was evident in both the male and female subjects. A significant negative correlation between TAA and Hg levels or number of amalgam restorations or amalgam surface was evident in females, indicating that small increases in salivary Hg were sufficient to produce a decrease in salivary TAA. On the other hand, no significant correlation was found in the males. The present study provides, for the first time, evidence of a pro-oxidant role of the amalgam Hg chronically released in saliva.”
“OBJECTIVE: To understand mechanism of cochlear outer hair cells (OHCs) intracellular Ca2+ mobilization further.
METHODS:
Intracellular calcium of isolated guinea pig was investigated using thimerosal, a–SH group oxidizing agent, and fura-2 fluorescence ratio imaging microscopy.
RESULTS:
In the presence of thimerosal, intracellular Ca2+ concentrations ([Ca2+]i) of OHCs were elevated in a dose-dependent manner. Even in Ca(2+)-free medium, Ca2+ response was still induced. The effects of thimerosal on [Ca2+]i were completely blocked and reversed by (DTT). Neither 1-100 mumol/L ryanodine nor 5-20 mmol/L caffeine altered the effects of thimerosal. Pretreatment with pertussis toxin (PTX) for 30 min did not affect the thimerosal-induced increase in [Ca2+]i The increase in [Ca2+]i when Ca2+ was added during thimerosal application in Ca(2+)-free medium was almost completely blocked by 500 mol/L LaCl3, while nifedipine did not inhibit further increase in [Ca2+]i caused by thimerosal.
CONCLUSION:
Oxidation of the -SH group of the OHC membrane can induce a Ca2+ release from intracellular Ca2+ stores, which are ryanodine- and caffeine-insensitive, and Ca2+ influx through non-specific Ca2+ channels, but not the nifedipine-sensitive Ca2+ Channels. The possible oxidation of–SH group gated Ca2+ channels in OHCs are worthy of further study.”
“Resin-based composite resins and polyacid-modified resin-based composites (compomers) have become popular for the restoration of primary anterior and posterior teeth. In some European countries, resin-based composites or glass-ionomers are the materials of choice for primary teeth because of the controversy over dental amalgam and its alleged adverse health effects resulting from the release of mercury, although a clear correlation between amalgam restorations and health has not been determined. Another reason for the worldwide increased use of resin-based composites and glass-ionomers in pediatric dentistry could be attributed to the growing demand from parents to provide esthetic restorations to their children. More conservative preparations can be performed maintaining more tooth structure because of the adhesive properties of the composites and compomers. The most conservative treatment planning and meticulous care in the placement of the resin-based composites and compomers would produce long-term satisfactory results. These restorations should be placed in patients with low-to-moderate caries risk, and after placement the restorations should be monitored carefully to avoid complications mainly produced by recurrent caries and wear.”
“Recently, it has been recognized that oral infection, especially periodontitis, may affect the course and pathogenesis of a number of systemic diseases, such as cardiovascular disease, bacterial pneumonia, diabetes mellitus, and low birth weight. The purpose of this review is to evaluate the current status of oral infections, especially periodontitis, as a causal factor for systemic diseases. Three mechanisms or pathways linking oral infections to secondary systemic effects have been proposed: (i) metastatic spread of infection from the oral cavity as a result of transient bacteremia, (ii) metastatic injury from the effects of circulating oral microbial toxins, and (iii) metastatic inflammation caused by immunological injury induced by oral microorganisms. Periodontitis as a major oral infection may affect the host’s susceptibility to systemic disease in three ways: by shared risk factors; subgingival biofilms acting as reservoirs of gram-negative bacteria; and the periodontium acting as a reservoir of inflammatory mediators. Proposed evidence and mechanisms of the above odontogenic systemic diseases are given.”
“The aim was to determine the relationship between mercury content of resting and stimulated saliva, and blood and urine. Eighty subjects participated; 40 of them attributed their self-reported complaints to dental amalgam (patients), the others were matched with respect to age, sex and amalgam restorations (controls). Serum, 24-h urine, resting and chewing stimulated saliva were analyzed for mercury using the ASS-technique. Quality, number, surfaces and total area of amalgam fillings were recorded clinically and using study models. Median (range) mercury levels in serum were 0.67 (0.1-1.52) microgram/l for patients and 0.60 (0.1-1.3) for controls. In urine levels were found to be 0.77 (0.11-5.16) and 0.94 (0.17-3.01) microgram/g creatinine respectively. No significant differences were found between the groups. Resting saliva contained 2.97 (0.10-45.46) micrograms/l in patients and 3.69 (0.34-55.41) in controls (not significant). Chewing mobilized an additional amount of 16.78 (-6.97 to 149.78) micrograms/l in patients and 49.49 (-1.36 to 504.63) in controls (P < or = 0.01). Only a weak correlation was found between mobilized mercury in saliva and serum (r = 0.27; P < or = 0.05) or urine (r = 0.47; P < or = 0.001). For resting saliva the respective values were r = 0.45 (P < or = 0.001) and r = 0.60 (P < or = 0.001). Saliva testing is not an appropriate measure for estimating the mercury burden derived from dental amalgam.”
“Oral lichenoid lesions caused by hypersensitivity to mercury in amalgam fillings may mimic oral lichen planus on clinical and histologic examination. A positive patch test reaction to more than one mercurial allergen increases confidence in the diagnosis and justifies the removal and replacement of all amalgam fillings with those made of other materials. A complete remission may be expected about 3 months after the last amalgam filling is removed.”
“The aim of this study was to investigate to which extent noble-metal dental alloys contribute to the total platinum (Pt), palladium (Pd), and gold (Au) body burden of the general population. The urinary Pt, Pd, and Au excretion was determined in three non-occupationally exposed volunteers before and up to 3 months after insertion of a highgold dentalalloy. The in-vitro release of Pt, Pd, and Au from four different types of dental alloys into either artificial saliva or 1% lactic acid solution was additionally investigated. The Pt, Pd, and Au concentrations were determined by sector field inductively coupled plasma mass spectrometry (SF-ICP-MS). Before insertion of the high-gold dental alloy, the Pt excretion of the patients ranged between 1.0 and 7.4 ng l-1 (0.6-3.3 ng g-1 creatinine). In the immediate post-insertion phase the Pt excretion rose to 10.5-59.6 ng l-1 (14.5-33.2 ng g-1 creatinine). This is a mean increase by a factor of 12 compared with the average Pt excretion before insertion. Three months after insertion, the Pt excretion was still elevated by a factor of 7. Contrary to Pt, the Au and Pd excretion in urine was not significantly increased after insertion of this type of high-gold dental alloy. Our in-vitro investigations confirm the assumption that Pt, Pd, and Au are released from noble metal containing dental alloys by corrosion. Under the applied conditions, the release was in the lower ng cm-2 range. It can be concluded that the Pt release from dental alloys can predominantly contribute to the Pt exposure of non-occupationally exposed persons. It can exceed the exposure from all other environmental sources including the Pt release from automobile exhaust catalysts.”