You are here: Home / News / The Ugly Facts on dental Amalgam

The Ugly Facts on dental Amalgam

17 Gennaio 2013 by

by Michael J. Wahl, DDS

“The great tragedy of science: the slaying of a beautiful hypothesis by an ugly fact.” Thomas Henry Huxley

Dental amalgam has been maligned as a filling material, both because of its clinical properties and its alleged effects on systemic health, but reports of its demise have been premature. As of 2008, 57% of dentists were placing amalgam (March 2008 Dental Products Report Survey). A large 2011 survey showed that dentists in the United States placed more dental amalgam than composite for first-time restorations in posterior teeth.1

Still, amalgam use has certainly declined over the last two decades, in part because of improved alternative filling materials and techniques and declining rates of caries in children and young adults. When the automobile replaced the horse and buggy as the primary mode of transportation, there were few if any emotional attacks on horses, and no one called for a ban on horse and buggies – they were simply replaced with automobiles. Similarly, when composite resins were commercially introduced, they fairly quickly replaced silicate cements as the material of choice for anterior fillings. As was the case with automobiles replacing horses, there were few if any emotional attacks on silicate cements, and no one called for a ban on silicate cements – they were simply replaced with better materials.

Compare this to dental amalgam. Never has a material been so vituperatively savaged as dental amalgam. And it’s not just the dental amalgam itself, but also the dentists who place amalgam. Maroon described anyone still using amalgam as “a fool….AMALGAM SUCKS!”2 (Using reasoning like this, there must be a lot of “fools” in our profession since dental amalgam may be the most commonly used restorative for posterior fillings.) Dickerson called amalgam “…a disgusting restoration.”3 He was probably not just referring to the restoration’s color. Harper stated that amalgam is “…an inferior restoration that I would not place in the mouths of my family or friends, much less into patients’ mouths.”4 Lowe stated that direct posterior composites’ “clinical superiority over amalgam in class I situations has been well documented…”5 No documentation was provided. Lutz et al. stated, “Adhesive cavity preparations for Class I, III, IV, and V restorations are achieved, and their clinical superiority over the conventional amalgam restorations is well documented.”6

Dickerson referred to the fact that dental amalgam is the most common restoration as not just unfortunate, but even criminal: “What is even more of a crime is that the most common restoration today is the same as it was 100 years ago. Where is the progress in our profession? What other industry has not had a significant advancement in materials used in the last 100 years?”7

Many dentists proudly assert that they practice “mercury-free” dentistry – they place no amalgam restorations. To dentists who do place amalgam, it would seem ludicrous to assert that there have not been significant advances in dental amalgam materials and techniques in the last 100 years, but “mercury-free” dentists who have not placed any amalgams in many years may be unaware of them. A few of these advances include amalgam bonding, new preparation techniques including slot preparations and the elimination of sharp line angles and point angles, preweighed dosages, encapsulated and self-activating dispensing techniques, and more. I remember using hatchets, hoes, and chisels to help create sharp line and point angles when I went to dental school in the 1980s, but I have never used them since! Regardless, the fact that a material or technique is over 100 years old does not make it a “crime.” Airplanes, aspirin, automatic dishwashers, automobiles, contact lenses, electric light, telephones, toilet paper, trains, mechanical dental chairs, and postage stamps are all over 100 years old and in common use today. Even modern composite resins can be traced to the discovery of acrylic acid over 150 years ago and the discovery of methacrylate esters and their polymers over 100 years ago.8

Cusp Fracture
Amalgam restorations are often criticized because they allegedly contribute to cusp fractures: Erickson has stated, “[T]he cuspal fracture characteristic of amalgam is well-known and observed almost daily in every general dental practice.”9 Referring to the likelihood of cusp fractures, Davis stated that Class II amalgam restorations are “time bombs [that] may threaten not only specific teeth, but possibly an entire dentition.”10 It is understandable (but arguable) to allege that a filling material may play a role in a future cusp fracture of that tooth, but how the “time bomb” would threaten an entire dentition is not explained and no examples of “amalgam-induced edentulousness” are provided. DiTolla asked, “[W]hy would I plant this amalgam ‘crown seed’ and then wait for the tooth to break[?]”11

Dickerson asserted, “Many studies have shown that, after seven years, 50 percent of the teeth filled with amalgam have fractured.”3 Although no studies were cited in the article, Dickerson later cited just two (personal communication, February 3, 2000), both of which were on endodontically-treated teeth with large MOD restorations.12 In the first study, there were only 181 MOD (probably unbonded) amalgam restorations and 40 resins. The teeth with resin had a much lower incidence of cusp fractures, but the author stated that the results of the study “should be cautiously interpreted, especially since the number of resin-restored teeth was rather small.” In two similar but much larger studies published by the same author two years later, there were much different results: in 1584 endodontically-treated teeth with MOD amalgam restorations, 34% (532) had cusp fractures after 20 years13 and in 190 endodontically-treated teeth with MOD composite, 28% had cusp fracture after 10 years.14 The incidence of cusp fracture after 20 years in (presumably unbonded) amalgam-restored teeth was thus about the same as the incidence of cusp fracture in composite resin-restored teeth after only 10 years. From these studies, it is clear that the cusp fracture incidence in endodontically-treated teeth restored with MOD amalgam restorations is more favorable than that of endodontically-treated teeth with resin composite restorations.

The other study cited by Dickerson showed that the incidence of cusp fractures in endodontically-treated teeth with MOD amalgam was much greater after 1979 than before 1975.15 Anti-amalgamists have asserted that the greater incidence of cusp fracture coincided with the introduction of high-copper amalgams around 1975. Another possibility was also cited by the authors, and this explanation seems more likely: the common use of Gates Glidden burs and straight-line access to endodontic apices, along with larger access openings began in 1979, and these lead to weaker teeth.

But enough about cusp fractures in endodontically-treated teeth – those teeth should be restored with crowns or some other type of cuspal coverage anyway.16,17 When evaluating cuspal fractures, it is more appropriate to examine amalgam-restored vital teeth under more common clinical conditions. In a long-term 1989 study of about 600 amalgam-restored teeth, there was less than a 1.5% cusp fracture rate after 5 years.18 In a 1993 study of 1415 class II amalgam-restored teeth, only 1.8% had a fractured cusp after 10 years.19 After 15 years, a 1996 study of 1214 class II amalgam-restored teeth showed only 3.8% failed because of enamel fracture only and only 5.0% failed because of enamel fracture only or a combination of enamel fracture, isthmus fracture, and/or caries.20

Amalgam bonding increases fracture resistance and decreases cuspal deflection21-24 at least as much as composite bonding does25 and can allow for smaller preparations and restorations, which last longer and are less likely to be associated with cusp fracture.26-31 Consider that these studies were before amalgam bonding and conservative preparation techniques were in common use, but the amalgam restorations still had a low incidence of cusp fracture.

Many studies on cusp fracture in amalgam- and composite-restored teeth are also inherently biased against amalgam-restored teeth because they don’t take restoration size into account.32 Dentists have long been advised to use composite only for smaller restorations but amalgam for larger ones.33 Larger restorations generally do not last as long as smaller restorations, and larger restorations are more likely to be associated with cusp fractures.28,29 In spite of restoration size bias, amalgam restorations compare favorably to composite restorations in cusp fracture incidence and longevity. Even tying one hand behind its back, (unbonded, larger) amalgam restorations perform well versus (bonded, smaller) composite restorations.

In assailing the cusp fractures associated with amalgam-restored teeth, DiTolla stated, “I thought back over my first 6 years in practice and realized that 99 percent of the teeth that required crowns all had silver fillings.”11 DiTolla’s assertion is a classic case of the logical fallacy of “base rate neglect,” in which he focuses only on the irrelevant (the number of teeth requiring crowns) and ignores the relevant base rate (the incidence of amalgam-restored teeth requiring crowns including both those that required crowns and those that did not).34

In a 2004 study we published in JADA, we examined every posterior tooth with an amalgam or composite resin restoration in 1902 consecutive patients. There were a total of 10,689 posterior teeth with amalgam or composite resin, 10,082 with amalgam and 787 with composite resin. Of these, there was a 1.88% cusp fracture rate in amalgam-filled teeth and 2.29% cusp fractures in composite-filled teeth.35 The cusp fracture rate was actually slightly higher in composite-filled teeth than in amalgam filled teeth although the difference was not statistically significant. So why does it seem like amalgam is more likely to be associated with cusp fracture than composite resin? Our study is probably typical of many dental practices – there were 13 times more amalgam-restored teeth than composite-restored teeth in our “snapshot” of patients’ posterior dentition. It therefore follows that there are far more amalgam-restored teeth with cusp fractures than composite resin-restored teeth even though the incidence of fracture was roughly the same. It is common that posterior teeth requiring crowns have been amalgam-restored because it is common that posterior teeth have been amalgam-restored. Another factor may be that dentists spend very little time examining successful restorations, and tend to focus on examining and restoring failed restorations.36

We are told that the amalgam “filling expands and contracts at a rate greater than that of the tooth and that’s why the patient’s MB cusp broke off or there is a marginal fracture, etc.”11 It is thus alleged that dental amalgam expands and contracts to temperature changes more than composite resin does, and that’s what contributes to tooth fractures in amalgam restored teeth. Actually, the opposite is true: the expansion and contraction to temperature changes are greater with resin composite than with amalgam. The coefficient of thermal expansion of composite is greater than that of amalgam.37-41

Fortunately, expansion and contraction of restorative materials is not an important clinical issue. Extreme temperature changes occur only fleetingly in vivo.42 When cold soda or hot coffee contacts teeth, it is usually only fleetingly. The liquid is usually not held against the teeth for very long (if at all) before it is swallowed so thermal expansion is not clinically important.43 Unlike in the mouth, thermal expansion and contraction is an important issue in a concrete sidewalk or the steel of an automobile, where there may intense heat and cold for hours and days at a time. When it comes to likelihood of cusp fractures, far more important than thermal expansion and contraction are issues like tooth preparation size, diet, and masticatory habits.

As mentioned above, teeth filled with composite resin suffer cusp fractures also: In a 1995 study of 1360 composite resin restorations, almost 9% were replaced due to cusp fracture.44 Many dentists consider gold restorations to be the “holy grail” of dentistry, but in a 1993 study of 745 gold restorations, 36% of 139 cast gold restorations that were replaced were replaced due to tooth fracture.45 There is very little evidence that amalgam restorations are associated with high rates of cusp fracture. There is a breach in the argument that amalgam restorations are associated with high rates of cusp fracture.

Amalgam and Recurrent Caries
Amalgam restorations have been criticized because of the alleged high incidence of recurrent caries associated with them. Van Dyke stated, “Almost every amalgam I remove has decay or structural fractures of the tooth.”46 Dickerson has stated, “Over 40 percent of the amalgams deemed in good clinical shape had caries under them.”3 Although no studies were cited in the article, in a personal communication (February 3, 2000), Dickerson cited two studies of extracted teeth without clinical evidence of caries sectioned and examined microscopically, one on 17 teeth47 and the other on 30 teeth.48 The “caries” in these studies was not clinically detectable, but radiographs were not taken. The caries was detected only after the teeth were extracted, sectioned, and examined microscopically in histologic section – a clinical impossibility! There was no way to detect, locate, or remove the caries clinically. Even then, in the Kidd and O’Hara study,48 the authors noted that “demineralization was slight, no lesion having progressed to cavitation” and hypothesized that the microscopic caries was arrested. Kidd has also noted that many “recurrent” caries are actually residual caries left at the time of preparation, 49 which would have nothing to do with the filling material but would be a factor of the preparation technique.

There were at best only sketchy dental histories provided, and there was no radiographic examination. The studies were published before amalgam bonding came into common use so the amalgams in the studies were probably unbonded. Amalgam bonding decreases microleakage50 as much as bonding does in composites,51 which decreases recurrent caries.52 Finally, there were no nonamalgam controls in these studies. What was not cited by Dickerson was a comparative study on microscopic caries that showed higher rates in composite resin restorations than in amalgam restorations.53

These studies of microscopic caries on 47 histologically-sectioned teeth do not offer good evidence that amalgam restorations are prone to recurrent caries. Instead, let us look at clinical studies to determine the incidence of recurrent caries in amalgam and resin composite restorations.

Recurrent caries has been studied extensively in clinical restorations in thousands and thousands of teeth, and it is true that recurrent caries is the most common cause of amalgam failure.54-60 However, recurrent caries is also the most common cause of resin failure44,55,56,58-60,61-67 and even cast gold restoration failure.45 In fact, recurrent caries is the most common cause of restoration failure in every kind of restoration.54,68

A 1993 study of 1415 class II amalgams showed only 16 (~1.1%) had recurrent caries after 10 years.19 At 10 years, none of 35 class II amalgams had recurrent decay.69 After 14 years, less than 5% had recurrent decay.70 In a 2000 randomized, prospective study of 1748 restorations in children over seven years, the composite restorations had an incidence of recurrent caries 3.5 times greater than that of the amalgam restorations.71 In a 2007 cross-sectional radiographic study of 557 amalgam and 93 resin composite interproximal restorations, there was an 8% rate of secondary caries in the amalgam restorations versus a 43% rate in the resin composite restorations.63 In a 1993 five-year prospective study of small class II restorations of primary caries: composite restorations had a higher incidence of recurrent caries than amalgam.72 Composites have higher levels of cariogenic bacteria at margins than amalgam restorations.73,74 It is clear that there are holes in the argument that amalgam restorations are associated with high levels of recurrent caries.

Amalgam Bonding
Many dentists assert that amalgam cannot be bonded to dentin. Freedman has stated, “Composites are bonded to dentin and enamel, recreating the monobloc of the original undecayed tooth. Amalgam simply fills a cavity, and may act as a wedge during mastication….Teeth are prepared more conservatively for composite restorations…. The preparation for amalgams requires extensions for retention and prevention, implying the loss of healthy tooth structure.”75 Vasserman stated that amalgam “has forced us to extend cavity preparations to accommodate the material rather than have the materials accommodate the preparation.”76

Some more recent comments on the Dentaltown message boards show that many dentists still believe that amalgam cannot be bonded: “amalgam needs significant bulk… it needs 90 degree cavosurface margins… and it needs mechanical undercuts. I agree they can be done conservatively… but those requirements still exist. Resin I can make thin… with any margin I want… and no need for undercuts. Coach DDS …. The preperation [sic] for an amalgam is by my standards today… extreme and excessive. What's the point of the restoration lasting 30 years if it predisposes the tooth to breaking in 2? That's why I'm glad I can do resins well… because I like saving teeth… not destroying half of them out in order to hold an MODL amalgam.” [ Accessed October 6, 2011.] It is possible, indeed probable, that dentists with such beliefs are proudly “amalgam-free” – they place no amalgams. As a result, they may not be aware of many of the latest amalgam techniques and materials, including amalgam bonding.

Although some assert that amalgam cannot be bonded to teeth, scientific evidence belies such assertions. There have even been successful amalgam pit and fissure sealants! (Please note that this author does not advocate using amalgam pit and fissure sealants.) In a pit and fissure sealant study comparing bonded amalgam sealants and resin sealants, there was no difference between the two types of sealants at 6 months, 1 year, 2 years, and 5 years.77 Some amalgam sealants lasted 5 years. If that doesn’t prove to even the most fervent anti-amalgamist that amalgam can be bonded to teeth, then nothing will. The potential benefits of amalgam bonding are similar to the potential benefits of resin composite bonding and include decreased microleakage, decreased incidence of recurrent caries, decreased postoperative sensitivity, increased fracture resistance of the tooth, decreased cuspal deflection, conservation of tooth structure, and increased retention.78 As a result of amalgam bonding, tooth preparation for amalgam restorations can be done exactly the same as for composite resin restorations.

Many comparative studies have shown better bonding and less leakage in amalgam restorations than in composite resin restorations.79 Amalgam bonding is effective and can help ensure minimal cavity preparation techniques.26,80 One study has questioned the efficacy of amalgam bonding,81-83 but this study included amalgam bonding agents other than 4-META HPA. Amalgam restorations bonded with 4-META HPA (Amalgambond) powder adhesive are generally superior to those bonded with other types of bonding materials.84 Amalgam bonding with 4-META HPA has been shown to be equal to pin retention in large complex restorations.85

When comparing longevity of amalgam and composite restorations, it is not clear how important bond strength to dentin is. That is, beyond a certain (but as yet unknown) minimum level, it is unclear how important additional bond strength is.86 But for those who think that amalgam and composite bond strength is important, there have been studies showing amalgam bond strengths as high as 27 MPa87,88 and 33 MPa,89 compared to 23 to 25 MPa typically reported in composite restorations.90 In a 1999 comparative study, the bond strength to dentin was 33.0 MPa in the amalgam versus 26.4 MPa in composite.91 There is obviously a gap in the argument that amalgam cannot be bonded to dentin.

Amalgam Longevity
Dickerson stated, “We can all find amalgam that has lasted a long time, but statistically, that is the exception, not the rule.”92 This assertion is not backed up by scientific studies. In the 1960s, “extension for prevention” was state of the art. Sharp line and point angles were created using hoes and hatchets – and hoes had nothing to do with low women. There was no amalgam bonding. Large-scale studies (published in the 1970s) on amalgams probably placed in the 1950s or 1960s (before amalgam bonding) showed the median life of an amalgam filling to be about 10 years.93,94 Since then, virtually every large study has shown that amalgam longevity is significantly greater than composite resin longevity.55,58,63,71,95-103 It should be noted that as early as 1995104 and 1998,105 some authors had advised dentists to stop using amalgam, yet virtually every large study since then has shown greater longevity for amalgam restorations than for composite restorations.

There are very few studies in which resin composite restorations have shown better longevity than dental amalgam restorations. In two studies by the same authors,61,106 amalgam and composite restorations were placed by the same operator and followed over many years of private practice. The resin composite restorations had a better survival rate than the amalgam restorations. This operator placed virtually all amalgams for posterior teeth in the first decade of his practice from 1983 to 1993. After a two-year transition period, he switched to virtually all posterior composite restorations thereafter. Any restorations placed during the transition period were not included in the study. In other words, virtually all the amalgams were placed by an inexperienced operator (0 to 10 years of private practice) whereas virtually all the composites were placed by (the same) much more experienced operator (13 to 20 years of private practice). These studies do not provide evidence that composite resin restorations last longer than amalgam restorations. Restoration longevity is directly related to operator experience,102 which was significantly greater with the composite resin restorations. In addition, since they were placed between 1983 and 1993, the amalgam restorations were probably unbonded, but the composite resin restorations (which were placed between 1996 and 2003) were bonded. Amalgam bonding has been shown to decrease microleakage, cuspal deflection cusp fracture, recurrent caries, increase retention, and allow for smaller restorations. These could have yielded greater longevity for the amalgam restorations. There are still those who argue that amalgam does not have greater longevity than composite restorations, but this argument is getting old. There is overwhelming evidence that amalgam restorations typically have greater longevity than composite restorations.

Amalgam and Systemic Effects
Mercury occurs in the air, food, and water,107,108 and it is the main ingredient of dental amalgam restorations – about 50% Hg before mixing,109 but less after condensation. Although mercury is tightly bound in set amalgam restorations, tiny amounts of mercury are released. In 1985, Vimy and Lorscheider claimed that patients with amalgam fillings were exposed to an average daily dose of 20 µg Hg and those with 12 surfaces of amalgam as much as 29 µg Hg.110,111 It was later shown that Vimy and Lorscheider grossly overestimated that daily dose of mercury, mostly by misusing the mercury detector in their research, and their studies were widely discredited by several independent researchers.112-114 Using Vimy and Lorscheider’s own data, the independent researchers recalculated average daily doses were 1.7 µg Hg,112 1.7 µg Hg,114 and 1.3 µg Hg.115 Since then, Halbach has calculated an integrated daily dose of 3 µg Hg for an average number of fillings and only 7.4 µg for a patient with a high amalgam load.116 These levels are well below the World Health Organization’s tolerable level for daily mercury intake of 2.0 µg/kg body weight or about 68 µg Hg for a 150 lb adult.117

Vimy and Lorscheider have estimated that as much as 15 µg Hg per day can be released from a single occlusal amalgam filling.105 The average weight of a one-surface amalgam is estimated at 310 mg118 so the mercury content would be about 155 mg. If this restoration actually releases 15 µg Hg per day, then the entire mercury content would be depleted in 28 years. Having lost 27 mg of mercury, or nearly 20% of its main component, the restoration would probably implode within 5 years if 15 µg Hg were lost daily. Even the most rabid anti-amalgamists would admit that amalgam restorations do not typically implode within 5 years, or even within 20 years so it is highly unlikely that 15 µg Hg per day could be released from an occlusal amalgam restoration.

In a 1998 study of 1127 healthy males, Kingman et al. estimated there was only a 1 µg Hg/L increase in urinary Hg for every 10-surface increase in amalgam fillings.119 A similar 2005 study of 1626 women, Dye et al. estimated a 1.8 µg Hg/L increase in urinary Hg for every 10-surface increase in amalgam fillings.120 A 1995 study determined that a single amalgam filling releases only 0.03 µg/day of mercury so a patient would require 2,740 amalgam fillings in order to reach the mercury exposure threshold limit value of 83.30 µg /day considered dangerous for occupational exposure in the United States.121 Obviously, it is impossible for a patient to have anywhere near that many amalgam fillings. The World Health Association has stated that urine mercury levels are raised more from eating seafood once a week than from dental amalgam exposure.122

Mercury from dental amalgam accumulates in body tissues, especially the kidneys and brain,123,124 and there is a correlation between the number of amalgam surfaces and the amount of mercury accumulation in tissues.125 Some imply that this accumulation proves that mercury from dental amalgam causes systemic health effects,126 but the question is not whether mercury from dental amalgam can accumulate in body tissues (it can and does), but rather whether this accumulation can cause systemic health problems. There have been numerous studies attempting to show that dental amalgam causes systemic health problems, but there has never been a credible scientific study showing that mercury from dental amalgam causes systemic health problems in humans, other than occasional reports of allergic reactions.

A 2001 University of Calgary study showed disruption of “the membrane structural integrity of neurites and the growth cones of identified neurons” after exposure to mercury.”127 Anti-amalgamists asserted that this study “should remove all doubt regarding the role that dental mercury from amalgam fillings plays in the development of Alzheimer’s disease.”128 It’s curious that this study would be the one to remove all doubt since it was done on the tissue of dead snails. In fact, partly because there has never been a snail (either dead or alive) diagnosed with Alzheimer’s Disease, it is questionable whether this study has any relevance at all to the issue of amalgam restorations and Alzheimer’s Disease – let alone whether it should “remove all doubt” about the relationship. Another study cited by anti-amalgamists is a 1997 study from the Universities of Calgary and Kentucky purportedly showing that some rats exposed to high levels of mercury showed brain lesions similar to those in patients with Alzheimer’s Disease.129 But the rats were exposed to 100 times the level of mercury that patients with 25 surfaces of amalgam restorations would typically inhale even under stimulated conditions so its relevance is also questionable at best.

Well-controlled human studies have failed to show any relation between mercury exposure from dental amalgam restorations and Alzheimer’s Disease. A relatively homogenous group of Roman Catholic nuns was studied for the performance on a battery of neuropsychological tests, including one from the Consortium to Establish a Registry for Alzheimer’s Disease. There was no correlation with the presence, absence, or number of surfaces of amalgam.130 It is a result of studies like these that the Alzheimer’s Association has concluded, “According to the best available scientific evidence, there is no relationship between silver dental fillings and Alzheimer's.”131

In a 2006 randomized study of more than 500 patients in the Journal of the American Medical Association, there were no differences in neuropsychological or renal effects in children with amalgam versus composite restorations.132 In another 2006 randomized study of more than 500 patients, also published in the Journal of the American Medical Association, there was no difference in neurobehavioral effects in children with amalgam versus composite restorations.133 Clarkson et al., writing in the New England Journal of Medicine, concluded, “Patients who have questions about the potential relation between mercury and degenerative diseases can be assured that the available evidence shows no connection….There is no clear evidence supporting the removal of amalgams [for health reasons].”134

A 2011 study compared subjective health complaints in patients who had all their amalgam restorations replaced with composite versus patients who had no amalgam restorations replaced.135 After 3 years, those who had their amalgam restorations replaced had significant reductions in self-reported health complaints. This study does not provide scientific evidence that amalgam restorations cause health problems or that their removal improves health although it may show a beneficial psychological effect to amalgam removal. The health complaints were subjective and self-reported by the patients without any preoperative or postoperative medical examination (other than preoperative and postoperative mercury levels in the treatment group), and there was no information on the number of surfaces of amalgam restorations and whether there was any matching of the number of surfaces with the control group.

A 2011 study of 587 mother-child pairs concluded, “This study's results provide no support for the hypothesis that prenatal Hg(0) exposure arising from maternal dental amalgam restorations results in neurobehavioral consequences in the child.”136 In a 2008 randomized, prospective study of 507 children, those restored with amalgam restorations were compared with those restored with composite restorations.137 Children restored with amalgam restorations had a relatively high average of between 8 and 12 surfaces of amalgam, but there were no significant differences in neurological findings in the amalgam versus the composite group. The National Multiple Sclerosis Society states, “There is no scientific evidence to connect the development or worsening of MS with dental fillings containing mercury, and therefore no reason to have those fillings removed.”138

The Food and Drug Administration (FDA) “considers dental amalgam fillings safe for adults and children ages 6 and above….FDA concludes that the existing data support a finding that infants are not at risk for adverse health effects from the breast milk of women exposed to mercury vapor from dental amalgam. The estimated daily dose of mercury vapor in children under age 6 with dental amalgams is also expected to be at or below levels that the EPA and the Centers for Disease Control and Prevention (CDC) consider safe.”139

Extensive reviews on dental amalgam restorations have failed to show any credible evidence of systemic health effects (other than rare cases of allergy) from dental amalgam.122,140,141 The Life Sciences Research Office (LSRO), composed of representatives from the National Institutes of Dental and Craniofacial Research (NIDCR) of the National Institutes of Health, the Centers for Devices and Radiological Health of the U.S. Food and Drug Administration, the Centers for Disease Control and Prevention, and the Office of the Chief Dental Officer of the Public Health Service, conducted an extensive review of the literature on dental amalgam’s health effects in 2004 and concluded, “The current data are insufficient to support an association between mercury release from dental amalgam and the various complaints that have been attributed to this restoration material.”142,143 The American Dental Association has concluded that amalgam remains a safe and effective filling material.144

There are many dentists who assert that dental amalgam should not be used because its main ingredient mercury is “toxic” or “poisonous.” Mosby’s Medical Dictionary defines toxic as “pertaining to a poison.”145 Poison is defined as “any substance that impairs health or destroys life when ingested, inhaled, or absorbed by the body in relatively small amounts. Some toxicologists suggest that, depending on the dose, all substances are poisons.”146

Composite Resin and Toxicity
Many dentists advertise themselves as “mercury-free,” implying that while mercury is toxic, other dental materials like composite resins are non-toxic. It is true that mercury is toxic – it can impair health depending on its dose. But the same is true with any material, including composite resin.147 There are between 14 and 22 potentially hazardous compounds released from composite resin restorations, including 14 to 22 separate potentially hazardous compounds, including DL-camphorquinone; 4-dimethylaminobenzoic acid ethyl ester (DMABEE), drometrizole; 1,7,7-trimethylbicyclo[2,2,1]heptane, 2,2-dimethoxy[1,2] diphenyletanone (DMBZ); ethyleneglycol dimethacrylate (EGDMA); and triethyleneglycol dimethacrylate (TEGDMA).148 Geurtsen et al. identified 35 dental resin composite monomers/additives of commercial composite resins of which 9 were shown to be severely or moderately cytotoxic components.149 Various composite restorative materials implanted into animals have been shown to cause inflammatory responses, including an increase in lymphocytic infiltration as well as fibroblasts and epithelioid cells.150 Some composite resin components are cytotoxic (causing damage or destruction of cells).151-154

Dentin bonding agents and their components are mutagenic (causing mutations in new generations).155-159 Resin composite components “are hazardous in that they all cause significant toxicity in direct contact with fibroblasts.”160 They have been shown to cause immunosuppression or immunostimulation,161 to inhibit DNA162 or RNA163 synthesis, and to suppress the mitochondrial activity of macrophages.164 Composite resin restorative material has been shown to be more cytotoxic than amalgam in a comparative in vitro study.165 The blue light used to cure composite resin restorations may cause retinal damage.166-168

There is no “nontoxic” material for filling teeth. Mackert stated, “A frequent claim by the anti-amalgamists is that ‘no research has shown that dental amalgam is safe,’ yet the same charge can be leveled against composites and other dental materials. No material can ever be judged ‘safe’ with any kind of finality, because new biological evaluation techniques are always being developed, and previously unanticipated adverse effects are continually being discovered for all materials.”169

There have been many cases of allergy to composite resins and their ingredients.170-174 Resin composite effects include hand eczema and skin symptoms in dentists,175 Vinyl, latex, and modified latex gloves are permeable to composite ingredients.176 Resin monomers can encourage the growth of cariogenic microorganisms.177

Even water can be fatal in certain doses. According to the Centers for Disease Control, there were nearly 4,000 fatal drownings in the United States in 2007.178 There have been many cases of fatal water intoxication reported in the medical literature.179,180 It is doubtful that any “mercury-free” dentists eschew water in their practices, even though water is toxic. Those who describe composite resins, glass ionomers, and sealants to patients as “mercury-free” would be intellectually honest if at the same time, they described amalgam restorations as “triethyleneglycol dimethacrylate-free” or “formaldehyde-free” since composite resins, glass ionomers, and sealants have been shown to release formaldehyde, a possible carcinogen.181-185 Water is toxic in high doses, but necessary for life in lower doses. Similarly, warfarin sodium, fluoride, and yes mercury in dental amalgam, are among substances that are toxic in high doses but necessary for health in lower doses in some patients. The argument that mercury from dental amalgam causes systemic health effects is downright poisonous!

Components of composite resin:149

  • BEA Benzyl alcohol
  • BEMA Benzyl methacrylate
  • BHT 2,6-Di-t-butyl-4-methyl phenol
  • Bis-EMA Ethoxylated bisphenol-A-di-methacrylate
  • Bis-GMA Bowen monomer, isopropyliden-bis (2-hydroxy-3-(4-phenoxy)-propylmethacrylate
  • Bis-MA Bisphenol-A-dimethacrylate
  • BL Benzil
  • BME Benzoic-acid-methylester
  • BPE Benzoic-acid-phenylester
  • CA Camphoric acid anhydride
  • CQ CamphoroquinoneDBPA Dibenzoyl-peroxide
  • DCHA Dicyclo-hexylamine
  • DCHP Dicyclo-hexyl-phthalate
  • DDMA 1,10-Decane-diol-dimethacrylate
  • DEAE Diethyl-amino-ethanol
  • DEGDMA Diethyleneglycol-di-methacrylate
  • DHEPT Dihydroxy-ethyl-p-toluidine
  • DICH 1,6-Diisocyanato-hexane
  • DIPA 2,6-Diisopropyl-aniline
  • DMABEE 4-Dimethylaminobenzoic acid ethyl ester
  • DMAPE 2-(4-Dimethyl-aminophenyl)ethanol
  • DMBZ Dimethoxybenzoine
  • DMDDA Dimethyl-dodecane-amine
  • DMPT Dimethyl-p-toluidine
  • DMTDA N,N-Dimethyltetradecylamine
  • EGDMA Ethyleneglycol-di-methacrylate
  • HEMA 2-Hydroxy-ethyl-methacrylate
  • HMBP 2-Hydroxy-4methoxy-benzophenone
  • TEG Triethylenglycol
  • TEGDMA Triethylenglycol-di-methacrylate
  • THA Trihexylamine
  • TPP Triphenylphosphine
  • TPSb Triphenylstibane
  • UDMA Urethane-di-methacrylate

 

Conclusion
Dentists sometimes look for solutions to problems without realizing that the problems weren’t what they seemed or that the solution was right in front of them the whole time. Such is the case with dental amalgam. Thomas Henry Huxley could have been speaking about the “crucifixion” of dental amalgam when he said, “The great tragedy of science: the slaying of a beautiful hypothesis by an ugly fact.”

Dental amalgam certainly has a big drawback – it’s ugly, but according to exhaustive research published in the medical and dental literature, the other “problems” with amalgam are not what they seem. Dental amalgam restorations are associated with excellent longevity and low rates of cusp fractures and recurrent caries, and dental amalgam restorations have not been linked to systemic health problems other than rare reports of allergic reactions. While composite resin restorations are more esthetic and are certainly an acceptable alternative, they generally do not compare favorably in other respects. The “solution” may not necessarily be to switch to composite resins but rather to continue using dental amalgam, not composite resin. It is a wonderful time to practice dentistry and to have so many choices for restorations, including both amalgam and composites. Pardon the pun, but for clinical efficacy and safety, dental amalgam is still the “gold standard” – or the “silver/mercury standard” – to which other direct filling materials including composite resin should be compared.

References

  1. Makhija SK, Gordan VV, Gilbert GH, et al. Practitioner, patient and carious lesion characteristics associated with type of restorative material: findings from The Dental Practice-Based Research Network. JADA 2011;142(6):622-32. Available: http://jada.ada.org/content/ 142/6/622.full.pdf+html Accessed March 21, 2012.
  2. Makhija SK, Gordan VV, Gilbert GH, et al. Practitioner, patient and carious lesion characteristics associated with type of restorative material: findings from The Dental Practice-Based Research Network. JADA 2011;142(6):622-32. Available: http://jada.ada.org/content/142/6/622.full.pdf+html Accessed March 21, 2012.
  3. Maroon M. The fab five. Dental Leader, March, 1998:2-3.
  4. Dickerson WG. Integrating cosmetic dentistry into a busy practice. Dent Econ 1997;87(1):30-6.
  5. Harper W. Amalgam is inferior. [Letter.] Dental Econ 1999;89(8):18.
  6. Lowe E. Restoring form, function, and aesthetics in Class II direct composite restorations. Dentistry Today 1998;17(4):72-7.
  7. Lutz FU, Krejci I, Oddera M. Advanced adhesive restorations: the post-amalgam age. Pract Perio & Aesth Dent 1996;8:385-94.
  8. Dickerson WG. Why is esthetic dentistry grouped with the outlaws? Dental Econ 1998;88(12):42-6,105.
  9. Bowen RL, Barton JA, Mullineaux AL. Composite restorative materials. National Bureau of Standards Special Publication 354. Dental Materials Research. Proceedings of the 50th Anniversary Symposium, Held Oct. 6-8, 1969, Gaithersburg, Md. (Issued June 1972.)
  10. Erickson RH. Controversy continues. [Letter.] Dent Econ 1998;88(7):16-7.
  11. Davis MW, Nesbitt WE. The wedge effect: structural design weakness of Class II amalgam. AACD J 1997;13(3)62-8.
  12. Di Tolla MC. Giving patients freedom of choice. Dent Econ 1998;88(2):10-12,87.
  13. Hansen EK. In vivo cusp fracture of endodontically treated premolars restored with MOD amalgam or MOD resin fillings. Dent Mater 1988;5:169-73.
  14. Hansen EK, Asmussen E, Christiansen NC. In vivo fractures of endodontically treated posterior teeth restored with amalgam. Endod Dent Traumatol 1990;6:49-55.
  15. Hansen EK, Asmussen E. In vivo fractures of endodontically treated posterior teeth restored with enamel-bonded resin. Endod Dent Traumatol 1990;6:218-25.
  16. Hansen EK, Asmussen E. Cusp fracture of endontically treated posterior teeth restored with amalgam. Teeth restored in Denmark before 1975 versus after 1979. Acta Odontol Scand 1993;51(2):73-7.
  17. Summitt JB, Robbins JW, Hilton TJ, Schwartz RS. Fundamentals of Operative Dentistry: A Contemporary Approach. Third Edition. Chicago: Quintessence Publishing Co. Inc., 2006, p. 587.
  18. Roberson TM, Heymann HO, Swift EJ Jr. Sturdevant’s Art and Science of Operative Dentistry. Fifth Edition. St. Louis, MO: Mosby Elsevier, 2006, pp. 847, 883.
  19. Roberson TM, Bayne SC, Taylor DF, et al. Long term clinical failure of dental amalgam. J Dent Res 1989;68(Spec Issue): 208[Abstract 216].
  20. Akerboom HBM, Advokaat JGA, Van Amerongen WE, Borgmeijer PJ. Long-term evaluation and rerestoration of amalgam restorations. Comm Dent Oral Epidemiol 1993;21:45-8.
  21. Gruythuysen RJM, Kreulen CM, Tobi H, et al. 15-year evaluation of Class II amalgam restorations. Comm Dent Oral Epidemiol 1996;24:207-10.
  22. Oliveira JP, Cochran MA, Moore BK. Influence of bonded amalgam restorations on the fracture strength of teeth. Oper Dent 1996;21:110-5.
  23. Eakle WS, Staninec M, Lacy AM. Effect of bonded amalgam on the fracture resistance of teeth J Prosth Dent 1992;68:257-60.
  24. Bailey R, Boyer D. Influence of bonding on fracture resistance of Class I amalgam restorations. J Dent Res 1997;76(Spec; Issue): 67[Abstract 430].
  25. El-Badrawy WA. Cuspal deflection of maxillary premolars restored with bonded amalgam. Oper Dent 1999;24:337-43.
  26. Boyer DB, Roth L. Fracture resistance of teeth with bonded amalgams. Am J Dent 1994;7:91-4.
  27. Parolia A, Kundabala M, Gupta V, et al. Microleakage of bonded amalgam restorations using different adhesive agenets with dye under vacuum. An in vitro study. Ind J Dent Res 2011;22(2):252-5.
  28. Zidan O, Abdel-Keriem U. The effect of amalgam bonding on the stiffness of teeth weakened by cavity preparation. Dent Mater 2003;19:680-5.
  29. Berry TG, Laswell HR, Osborne JW, Gale EN. Width of isthmus and marginal failure of restorations of amalgam. Oper Dent 1981;6:55-8.
  30. Blaser PK, Lund MR, Cochran MA, Potter RH. Effect of designs of Class 2 preparations on resistance of teeth to fracture. Oper Dent 1983;8:6-10.
  31. Osborne JW, Gale EN. Relationship of restoration width, tooth position, and alloy to fracture at the margins of 13- to 14-year old amalgams. J Dent Res 1990;69:1599-1601.
  32. Osborne JW, Summitt JB. Extension for prevention: is it relevant today? Am J Dent 1998;11:189-96.
  33. Wahl MJ. Amalgam – resurrection and redemption. Part 1: the clinical and legal mythology of anti-amalgam. Quintessence Int 2001;32:525-35.
  34. ADA Council on Scientific Affairs, ADA Council on Dental Benefit Programs. Statement on posterior resin-based composites. JADA 1998;129:1627-8.
  35. Hattori M, Nishida Y. Why does the base rate appear to be ignored? The equiprobability hypothesis. Psychon Bull Rev 2009;16(6):1065-70.
  36. Wahl MJ, Schmitt MM, Overton DA, Gordon MK. Prevalence of cusp fractures in teeth restored with amalgam and with resin-based composite. Journal of the American Dental Association 2004;135:1127-32.
  37. Brown LJ, Lazar V. Dental procedure fees 1975 through 1995: how much have they changed? JADA 1998;1296:1291-5.
  38. Versluis A, Douglas WH, Sakaguchi RL. Thermal expansion coefficient of dental composites measured with strain gauges. Dent Mater 1996;12:290-4.
  39. Powers JM, Hostetler RW, Dennison JB. Thermal expansion of composite resins & sealants. J Dent Res 1979;58:584-7.
  40. Dennison JB, Craig RG. Physical properties and finished surface texture of composite restorative resins. JADA 1972;85:101-8.
  41. Optical, thermal, and electrical properties. In: Craig RG, Ward ML, eds. Restorative Dental Materials, 10th ed. St. Louis: Mosby 1997;30-55.
  42. Craig RG (ed). Restorative Dental Materials, ed 9. St. Louis:Mosby 1993.
  43. Youngson CC, Glyn Jones JC, Smith IS, Fox K. In vivo temperature changes during a standardised thermal challenge. J Dent Res 1998;77(Spec Issue):955 [Abstract 247].
  44. Barclay CW. Thermocycling: an unrealistic technique for simulating clinical conditions? J Dent Res 1998;77 (special issue):901 [Abstract 2155].
  45. Browning WD, Dennison JB. Composite resins restorations: factors affecting placement and replacement. J Dent Res 1995;74 (Spec Issue): 42[Abstract 247].
  46. Mjör IA, Medina JE. Reasons for placement, replacement, and age of gold restorations in selected practices. Oper Dent 1993;18:82-7.
  47. Van Dyke BN. No more amalgams! [Letter.] Dent Econ 1999;89(7):18.
  48. Boston DW, Cotmore JM, Sperrazza L. Caries diagnosis with dye-staining at amalgam restoration margins. Am J Dent 1995;8:280-2.
  49. Kidd EAM, O’Hara JW. The caries status of occlusal amalgam restorations with marginal defects. J Dent Res 1990;69:1275-77.
  50. Kidd EA, Joyston-Bechal S, Smith MM. Staining of residual caries under freshly-packed amalgam restorations exposed to tea/chlorhexideine in vitro. Int Dent J 1990;40:219-24.
  51. Al-Jazairy Y, Louka AN. Effect of bonded amalgam restorations on microleakage. Oper Dent 1999;24:203-9.
  52. Ölmez A, Cula S, Ulusu T. Clinical evaluation and marginal leakage of Amalgambond Plus: three-year results. Quintessence Int 1997;28:651-56.
  53. Torii Y, Staninec M, Kawakami M, et al. Inhibition in vitro of caries around amalgam restorations by bonding amalgam to tooth structure. Oper Dent 1989;14:142-8.
  54. Hattab FN, Mok NYC, Agnew EC. Artificially formed carieslike lesions around restorative materials. JADA 1989;118:193-7.
  55. Mjör IA, Shen C, Eliasson ST, Richter S. Placement and replacement of restorations in general dental practice in Iceland. Oper Dent 2002;27(2):117-23.
  56. Mjör IA, Moorhead JE. Selection of restorative materials, reasons for replacement, and longevity of restorations in Florida. J Am Coll Dent 1998;65(3):27-33.
  57. Qvist V, Thylstrup A, Mjör IA. Restorative treatment pattern and longevity of amalgam restorations in Denmark. Acta Odontol Scand 1986;44:343-9.
  58. Qvist J, Qvist V, Mjör IA. Placement and longevity of amalgam restorations in Denmark. Acta Odontol Scand 1990;48:297-303.
  59. Burke FJT, Cheung SW, Mjör IA, Wilson NH. Restoration longevity and analysis of reasons for the placement and replacement of restorations provided by vocational dental practitioners and their trainers in the United Kingdom. Quintessence Int 1999;30:234-42.
  60. MacInnis WA, Ismail A, Brogan H. Placement and replacement of restorations in a military population. J Can Dent Assoc 1991;57:227-31.
  61. Al-Negrish AR. Reasons for placement and replacement of amalgam restorations in Jordan. Int Dent J 2001;51(2):109-15.
  62. Opdam NJ, Bronkhorst EM, Roeters JM, Loomans BA. A retrospective clinical study on longevity of posterior composite and amalgam restorations. Dent Mater 2007;23(1):2-8.
  63. Demarco FF, Corrêa MB, Cenci MS, et al. Longevity of posterior composite restorations: Not only a matter of materials. Dent Mater 2012 Jan;28(1):87-101.
  64. Levin L, Coval M, Geiger SB. Cross-sectional radiographic survey of amalgam and resin-based composite posterior restorations. Quintessence Int 2007;38(6):511-4.
  65. Mjör IA. The reasons for replacement and the age of failed restorations in general dental practice. Acta Odontol Scand 1997;55:58-63.
  66. Rasmusson C-G, Lundin S-A. Class II restorations in six different posterior composite resins: five-year results. Swed Dent J 1995;19:173-82.
  67. Friedl KH, Hiller KA, Schmalz G. Placement and replacement of composite restorations in Germany. Oper Dent 1995;20:34-8.
  68. Deligeorgi V, Mjör IA, Wilson NH. An overview of reasons for the placement and replacement of restorations. Prim Dent Care 2001;8(1):5-11.
  69. Forss H, Widström E. Reasons for restorative therapy and the longevity of restorations in adults. Acta Odontol Scand 2004;62(2):82-6.
  70. Mair LH. Ten-year clinical assessment of three posterior resin composites and two amalgams. Quintessence Int 1998;29:483-90.
  71. Osborne JW, Norman RD, Gale EN. A 14-year clinical assessment of 12 amalgam alloys. Quintessence Int 1991;22:857-64.
  72. Bernardo M, Luis H, Martin MD, et al. Survival and reasons for failure of amalgam versus composite posterior restorations placed in a randomized clinical trial. JADA 2007;138(6):775-83.
  73. Mjör IA, Jokstad A. Five-year study of Class II restorations in permanent teeth using amalgam, glass polyalkenoate (ionomer) cermet and resin-based composite materials. J Dent 1993;21:333-43.
  74. Svanberg M, Mjör IA, Ørstavik. Mutans streptococci in plaque from margins of amalgam, composite, and glass-ionomer restorations. J Dent Res 1990;69:861-4.
  75. Paolantonio M, D’Ercole S, Perinetti G et al. Clinical and microbiological effects of different restorative materials on the periodontal tissues adjacent to subgingival class V restorations. J Clin Periodontol 2004;31(3):200-7.
  76. Freedman G. Fifth-generation bonding systems: predictable posterior composite restorations. Dent Today 1996;15(11):68-75.
  77. Vasserman A. It’s time to bury our amalgamators! Dent Econ 2000;90(3):16,171.
  78. Staninec M, Artiga N, Gansky SA, et al. Bonded amalgam sealants and adhesive resin sealants: five-year clinical results. Quintessence Int 2004;35(5):351-7.
  79. Bonsor SJ. Bonded amalgams and their use in clinical practice. Dent Update 2011;38:222-30.
  80. Alptekin T, Ozer F, Unlu N et al. In vivo and in vitro evaluations of microleakage around Class I amalgam and composite restorations. Oper Dent 2010;35(6):641-8.
  81. Gupta I, Gupta S, Kothari A. Revisiting Amalgam: A Comparative Study between Bonded Amalgam Restoration and Amalgam Retained with Undercuts. J Contemp Dent Pract 2011;12(3):164-170.
  82. Bonsor SJ, Chadwick RG. Longevity of conventional and bonded (sealed) amalgam restorations in a private general dental practice. Br Dent J 2009 Jan 24;206(2):E3.
  83. Fedorowicz Z, Nasser M, Wilson N. Adhesively bonded versus non-bonded amalgam restorations for dental caries. Cochrane Database Syst Rev 2009 Oct 7;(4):CD007517.
  84. Murad M. No available evidence to assess the effectiveness of bonded amalgams. Evid Based Dent 2009;10(4):106.
  85. Imbery TA, Coudron J, Moon PC. Fracture resistance of extensive amalgam restorations retained by pins, amalgapins and amalgam bonding agents. Oper Dent 2008;33(6):666-74.
  86. Summitt JB, Burgess JO, Berry TG et al. Six-year clinical evaluation of bonded and pin-retained complex amalgam restorations. Oper Dent 2004;29(3):261-8.
  87. Rocha Gomes Torres C. How much bond strength do we need? J Contemp Dent Pract 2011;12(4):i.
  88. Summitt JB, Miller B, Buikema DJ, Chan DCN. Shear bond strength of Amalgambond Plus cold and at room temperature. J Dent Res 1998;77(Spec Issue A):274 [abstract 1345].
  89. Miller B, Chan DCN, Cardenas HL, Summitt JB. Powder additive affect on shear bond strengths of bonded amalgam. J Dent Res 1998;77 (Spec Issue):274 [Abstract 1346].
  90. Evans DB, Neme AL, Kohn DH. Bondstrength of amalgam and composite adhesive systems. J Dent Res 1997;76 (Spec Issue):67 [Abstract 432].
  91. Swift EJ, Bayne SC. Shear bond strength of a new one-bottle dentin adhesive. Am J Dent 1997;10:184-8.
  92. Evans DB, Neme A-ML. Shear bond strength of composite resin and amalgam adhesive systems to dentin. Am J Dent 1999;12:19-25.
  93. Dickerson WG. The great white hype, or the no silver image? Round #9. Dent Econ 1999;89(6):30.
  94. Robinson AD. The life of a filling. Brit Dent J 1971;130:206-8.
  95. Lavelle CLB. A cross-sectional longitudinal survey into the durability of amalgam restorations. J Dent 1976;4:139-43.
  96. Van Nieuwenhuysen JP et al. Long-term evaluation of extensive restorations in permanent teeth. J Dent 2003;31:395-405.
  97. Soncini JA, Maserejian NN, Trachtenberg F et al. The longevity of amalgam versus compomer/composite restorations in posterior primary and permanent teeth: findings from the New England Children's Amalgam Trial. JADA 2007;138(6):763-72.
  98. Simecek JW, Diefenderfer KE, Cohen ME. An evaluation of replacement rates for posterior resin-based composite and amalgam restorations in U.S. Navy and marine corps recruits. JADA 2009;140(2):200-9.
  99. Mjör IA, Dahl JE, Moorhead JE. Age of restorations at replacement in permanent teeth in general dental practice. Acta Odontol Scand 2000;58:97-101.
  100. Forss H, Widström. From amalgam to composite: selection of restorative materials and restoration longevity in Finland. Acta Odontol Scand 2001;59:57-62.
  101. Collins CJ, Bryant RW, Hodge K-LV. A clinical evaluation of posterior composite resin restorations: 8-year findings. J Dent 1998;26:311-7.
  102. Antony K, Genser D, Hiebinger C, Windisch F. Longevity of dental amalgam in comparison to composite materials. GMS Health Technol Assess 2008;4:Doc12. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3011298/?tool=pubmed Accessed December 4, 2011.
  103. Sunnegårdh-Grönberg K, van Dijken JW, Funegård U et al. Selection of dental materials and longevity of replaced restorations in Public Dental Health clinics in northern Sweden. J Dent 2009;37(9):673-8.
  104. Roumanas ED. The frequency of replacement of dental restorations may vary based on a number of variables, including type of material, size of the restoration, and caries risk of the patient. J Evid Based Dent Pract 2010;10(1):23-4.
  105. Simonsen RJ. Move over amalgam – at last. Quintessence Int 1995;26:157.
  106. Lorscheider FL, Vimy MJ, Summers AO. Mercury exposure from “silver” tooth fillings: emerging evidence questions a traditional paradigm. FASEB J 1995;9:504-8. Available: http://www.fasebj.org/content/9/7/504.long Accessed January 21, 2012.
  107. Opdam NJ, Bronkhorst EM, Loomans BA, Huysmans MC. 12-year survival of composite vs. amalgam restorations. J Dent Res 2010;89(10):1063-7.
  108. Eneström S, Hultman P. Does amalgam affect the immune system? A controversial issue. Int Arch Allergy Immunol 1995;106:180-203.
  109. Osborne JW. Dental amalgam and mercury vapor release. Adv Dent Res 1992;6:135-8.
  110. Berry TG, Summitt JB, Chung AKH, Osborne JW. Amalgam at the new millenium. JADA 1998;129:1547-53.
  111. Vimy MJ, Lorscheider FL. Intra-oral air mercury released from dental amalgam. J Dent Res 1985;64:1069-71.
  112. Vimy MJ, Lorscheider FL. Serial measurements of intra-oral air mercury estimation of daily dose from dental amalgam. J Dent Res 1985;64:1072-5.
  113. Mackert JR. Factors affecting estimation of dental amalgam mercury exposure from measurements of mercury vapor levels in intra-oral and expired air. J Dent Res 1987;66:1775-80.
  114. Olsson S, Bergman M. Letter to the Editor. J Dent Res 1987;66:1288-9.
  115. Berglund A, Pohl L, Olsson S, Bergman M. Determination of the rate of release of intra-oral mercury vapor from amalgam. J Dent Res 1988;67:1235-42.
  116. Olsson S, Bergman M. Daily dose calculations from measurements of intra-oral mercury vapor. J Dent Res 1992;71:414-23.
  117. Halbach S, Vogt S, Köhler W, et al. Blood and urine mercury levels in adult amalgam patients of a randomized controlled trial: interaction of Hg species in erythrocytes.
  118. World Health Organization. Concise International Chemical Assessment Document 50 Elemental mercury and inorganic mercury compounds: Human health aspects. World Health Organization;2003:Geneva. Available: http://www.who.int/ipcs/publications/cicad/en/cicad50.pdf Accessed January 22, 2012.
  119. Adegbembo AO, Watson PA, Rokni S. Estimating the weight of dental amalgam restorations. J Can Dent Assoc 2004;70(1):30-30e. Available: http://www.cda-adc.ca/jcda/vol-70/issue-1/30.pdf Accessed: January 21, 2012.
  120. Kingman A, Albertini T, Brown LJ. Mercury concentrations in urine and whole blood associated with amalgam exposure in a US military population. J Dent Res 1998;77:461-71.
  121. Dye BA, Schober SE, Dilon CF, et al. Urinary mercury concentrations associated with dental restorations in adult women aged 16-49 years: United States, 1999-2000. Occup Environ Med 2005;62(6):368-75. Available: http://oem.bmj.com/content/62/6/368.long Accessed January 18, 2012.
  122. Berdouses E, Vaidyanathan TK, Dastane A, et al. Mercury release from dental amalgams: an in vitro study under controlled chewing and brushing in an artificial mouth. J Dent Res 1995;74:1185-93.
  123. Uçar Y, Brantley WA. Biocompatibility of dental amalgams. Int J Dent 2011;2011:981595. Available: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3227436/?tool=pubmed Accessed March 21, 2012.
  124. Nylander M, Friberg L, Lind B. Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings. Swed Dent J 1987;11:179-87.
  125. Nylander M, Friberg L, Eggleston D, Björkman L. Mercury accumulation in tissues from dental staff and controls in relation to exposure. Swed Dent J 1989;13:235-43.
  126. Eggleston DW, Nylander M. Correlation of dental amalgam with mercury in brain tissue. J Prosth Dent 1987;58:704-7.
  127. Mutter J. Is dental amalgam safe for humans? The opinion of the scientific committee of the European Commission. J Occup Med Toxicol 2011;6:2. Available: http://www.citt.nu/files/mutter-j-2011-are-hg-fillings-safe-opinion-sci-committee-european-commision-j-ocp-med-tox.pdf Accessed January 22, 2012.
  128. Leong CCW, Syed NI, Lorscheider FL. Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury. Neuroreport 2001;12:733-7. Available: http://migrated.ifokus.se/uploads/8f7/8f72fba0858b215d1244180a40e12b66/leong-et-al.pdf Accessed January 25, 2012.
  129. Bio-Probe News. Scientists connect Alzheimer’s disease to mercury [online]. Available: http://www.bioprobe.com/ReadNews.asp?article-31. Accessed March 31, 2001. Available: http://www.robertgammal.com/PDFs/HgAlzheimers.pdf Accessed January 25, 2012.
  130. Pendergrass JC, Haley BE, Vimy MJ, Winfield SA, Lorscheider FL. Merucry vapor inhalation inhibits binding of GTP to tubulin in rat brain: similarity to a molecular lesion in Alzheimer diseased brain. NeuroToxicology 1997;18:315-24.
  131. Saxe SR, Snowdon DA, Wekstein MW, et al. Dental amalgam and cognitive function in older women: findings from the nun study. JADA 1995;126:1495-1501.
  132. Myth 7: Silver dental fillings increase risk of Alzheimer's disease. Alzheimer’s Association. http://www.alz.org/alzheimers_disease_myths_about_alzheimers.asp Accessed January 14, 2012.
  133. DeRouen TA et al. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. JAMA;2006:295(15):1784-92. http://jama.ama-assn.org/content/295/15/1784.full Accessed January 14, 2012.
  134. Bellinger DC et al. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. JAMA;2006:295(15):1775-83. http://jama.ama-assn.org/content/295/15/1775.full Accessed January 14, 2012.
  135. Clarkson TW, Magos L, Myers G. The toxicology of mercury – current exposures and clinical manifestations. New Engl J Med 2003;349:1731-7. http://sitemaker.umich.edu/m4-assignment/files/nejm_mercurypoisoning_.pdf Accessed January 14, 2012.
  136. Sjursen TT, Lygre GB, Dalen K, et al. Changes in health complaints after removal of amalgam fillings. J Oral Reabil 2011;38(11):835-48. Available: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3229679/?tool=pubmed Accessed January 18, 2012.
  137. Watson GE, Lynch M, Myers GJ, et al. Prenatal exposure to dental amalgam: Evidence from the Seychelles Child Development Study main cohort. JADA 2011;142(11):1283-94.
  138. Lauterbach M, Martins IP, Castro-Cadas A, et al. Neurological outcomes in children with and without amalgam-related mercury exposure: seven years of longitudinal observations in a randomized trial. JADA 2008;139(2):138-45.
  139. Some complementary approaches to avoid. National Multiple Sclerosis Society. Available: http://www.nationalmssociety.org/about-multiple-sclerosis/what-we-know-about-ms/treatments/complementary–alternative-medicine/index.aspx Accessed January 15, 2012.
  140. What should I know before getting a dental amalgam filling? US Food and Drug Administration. Available: http://www.fda.gov/MedicalDevices/ProductsandMedicalProcedures/DentalProducts/DentalAmalgam/ucm171094.htm#2 Accessed March 21, 2012.
  141. Ahlbom A, Bridges J, De Jong W, et al. Scientific Committee on Emerging and Newly Identified Health Risks SCENIHR. The safety of dental amalgam and alternative dental restoration materials for patients and users May 6, 2008. Available: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3227436/pdf/IJD2011-981595.pdf Accessed: March 21, 2012.
  142. Wahl MJ. Amalgam – resurrection and redemption. Part 2: the medical mythology of anti-amalgam. Quintessence 2001;32:696-710.
  143. Life Sciences Research Organization. Review and analysis of the literature on the health effects of dental amalgam. Available: http://www.lsro.org/presentation_files/amalgam/amalgam_execsum.pdf Accessed January 15, 2012.
  144. Brownawell AM, Berent S, Brent RL, et al. The potential adverse health effects of dental amalgam. Toxicol Rev. 2005;24(1):1-10.
  145. ADA Council of Scientific Affairs. Statement on dental amalgam. Revised: August 2009. Available: http://www.ada.org/1741.aspx Accessed January 15, 2012.
  146. Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier. http://medical-dictionary.thefreedictionary.com/_/dict.aspx?word=toxic Accessed December 4, 2011.
  147. Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier. http://medical-dictionary.thefreedictionary.com/_/dict.aspx?word=poison Accessed December 4, 2011.
  148. Mackert JR, Wahl MJ. Are there acceptable alternatives to amalgam? J Calif Dent Assoc 2004;32:601-10. Available: http://www.cda.org/Library/cda_member/pubs/journal/jour0704/mackert.pdf Accessed January 25, 2012.
  149. Lygre H, Høl PJ, Solheim E, Moe G. Organic leachables from polymer-based dental filling materials. Eur J Oral Sci 1999;107:378-83.
  150. Geurtsen W, Lehmann F, Spahl W, Leyhausen G. Cytotoxicity of 35 dental resin composite monomoers/additives in permanent 3T3 and three human primary fibroblast cultures. J Biomend Mater Res 1998;41:474-480.
  151. Hansasuta C, Neiders ME, Aguirre A, Cohen RE. Cellular inflammatory responses to direct restorative composite resins. J Prosthet Dent 1993;69:611-6.
  152. Leyhausen G, Lehmann F, Geurtsen. Cytocompatibility of 38 composite monomers/additives in human oral primary cell cultures. J Dent Res 1997;76 (Spec Issue):382 [Abstract 2945].
  153. Arenholt-Bindslev D, Ebbehöj, Hörsted-Bindslev. Cytotoxicity of conditioners and bonding agents. J Dent Res 1994;73 (Spec Issue):952 [Abstract 111].
  154. Bouillaguet S, Wataha JC, Hanks CT, et al. In vitro cytotoxicity and dentin permeabililty of HEMA. J Endodon 1996;22:244-8.
  155. Schweikl H, Spagnuolo G, Schmalz G. Genetic and cellular toxicology of dental resin monomers. J Dent Res. 2006;85(10):870-7.
  156. Schweikl H, Schmalz G. Glutaraldehyde-containing dentin bonding agents are mutagens in mammalian cells in vitro. J Biomed Mater Res 1997;36:284-88.
  157. Schweikl H, Schmalz G, Göttke C. Mutagenic activity of various dentine bonding agents. Biomater 1996;17:1451-6.
  158. Schweikl H, Schmalz G, Bey B. Mutagenicity of dentin bonding agents. J Biomed Mater Res 1994;28:1061-7.
  159. Schweikl H, Schmalz G, Rackebrandt. Mutagenic activity of resin components in mammalian cells. J Dent Res 1997;76 (Spec Issue):382 [Abstract 2946].
  160. Schweikl H, Hiller KA, Bolay C, et al. Cytotoxic and mutagenic effects of dental composite materials. Biomaterials. 2005;26(14):1713-9.
  161. Wataha JC, Hanks CT, Strawn SE, Fat JC. Cytotoxicity of components of resins and other dental resotrative materials. J Oral Rehabil 1994;21:453-62.
  162. Jontell M, Hanks CT, Bratel J, Bergenholtz G. Effects of unpolymerized resin components on the function of accessory cells derived from the rat incisor pulp. J Dent Res 1995;74:1162-7.
  163. Hanks CT, Strawn SE, Wataha JC, Craig RG. Cytotoxic effects of resin components on cultured mammalian fibroblasts. J Dent Res 1991;70:1450-5.
  164. Caughman WF, Caughman GB, Dominy WT, Schuster GS. Glass ionomer and composite resin cements: effects on oral cells. J Prosth Dent 1990;63:513-21.
  165. Rakich DR, Wataha JC, Lefebvre CA, Weller RN. Effects of dentin bonding agents on macrophage mitochondrial activity. J Endodon 1998;24:528-33.
  166. Al-Nazhan S, Sapounas G, Spångberg L. In vitro study of the toxicity of a composite resin, silver amalgam, and cavit. J Endodon 1988;14:236-8.
  167. Wataha JC, Lewis JB, Lockwood PE, et al. Blue light differentially modulates cell survival and growth. J Dent Res 2004;83(2):104-8.
  168. Rotenberg S, Lewis JB, Lockwood PE, et al. Extracellular environment as one mediator of blue light-induced mitochondrial suppression. Dent Mater 2006;22(8):759-64.
  169. Wataha JC, Lockwood PE, Lewis JB, et al. Biological effects of blue light from dental curing units. Dent Mater 2004;20(2):150-7.
  170. Mackert JR. Dental amalgam and mercury. JADA 1991;122(8):54-61.
  171. Blomgren J, Axéll T, Sandahl O, Jontell M. Adverse reactions in the oral mucosa associated with anterior composite restorations. J Oral Pathol Med 1996;25:311-13.
  172. Lind PO. Oral lichenoid reactions related to composite restorations: Preliminary report. Acta Odontol Scand 1988;46:63-5.
  173. Nathanson D, Lockhart P. Delayed extraoral hypersensitivity to composite material. Oral Surg Oral Med Oral Pathol 1979;47:329-33.
  174. Carmichael AJ, Gibson JJ, Walls WG. Allergic contact dermatitis to bisphenol-A-glycidyldimethacrylate (BIS-GMA) dental resin associated with sensitivity to epoxy resin. Br Dent J 1997;183:297-8.
  175. Hensten-Pettersen A. Replacement of restorations based on material allergies. In: Anusavice KJ, ed. Quality evaluation of dental restorations: criteria for placement and replacement. Chicago: Quintessence;1987:357-71.
  176. Örtengren U, Andreasson H, Karlsson S, et al. Prevalence of self-reported hand eczema and skin symptoms associated with dental materials among Swedish dentists. Eur J Oral Sci 1999;107:496-505.
  177. Munksgaard EC. Permeability of protective gloves to (di)methacrylates in resinous dental materials. Scand J Dent Res 1992;100:189-92.
  178. Hansel C, Leyhausen G, Mai UEH, Geurtsen W. Effects of various resin composite (co)monomers and extracts on two caries-associated microorganisms in vitro. J Dent Res 1998;77:60-7.
  179. Unintentional drowning: fact sheet. Centers for Disease Control and Prevention. Available: http://www.cdc.gov/homeandrecreationalsafety/water-safety/waterinjuries-factsheet.html Accessed December 4, 2011.
  180. Gardner JW. Death by water intoxication. Mil Med. 2002 May;167(5):432-4.
  181. Arieff AI, Kronlund BA. Fatal child abuse by forced water intoxication. Pediatrics. 1999 Jun;103(6 Pt 1):1292-5.
  182. Øysæd H, Ruyter IE, Sjøvik Kleven IJ. Release of formaldehyde from dental composites. J Dent Res 1988;67:1289-94.
  183. Hansel C, Leyhausen G, Mai UEH, Geurtsen W. Effects of various resin composite (co)monomers and extracts on two caries-associated microorganisms in vitro. J Dent Res 1998;77:60-7.
  184. Koch MJ, Alves da Rocha M, Stein G, et al. Formaldehyde release from sealant materials. J Dent Res 1994;73 (Spec Issue):293 [Abstract 1533].
  185. Ruyter IE, Sjøvik Kleven I. Formaldehyde release from light-cured glass ionomer restorative materials. J Dent Res 1994;73 (Spec Issue):293 [Abstract 1534].
  186. Larsson KS. Potential teratogenic and carcinogenic effects of dental materials. Int Dent J 1991;41:206-11.
Filed Under: News Tagged With: , ,