Amalgam - Dental amalgam
Posted by John Doe at Dental Assistant on February 2, 2012.
Categories: Dental Materials
Share
Print
Email-
+11
Vote
13 votes
FACTORS RELATED TO FINISHING AMALGAM RESTORATIONS
When an amalgam restoration has been properly placed, with adequate condensation, and the excess mercury has been removed from the final surface layer of the restoration, it will be sufficiently hardened within a few minutes to permit careful carving. If the restoration is not well condensed, it will not harden promptly, and the carving operation must be delayed. Usually the amalgam is sufficiently well set and hardened that carving with sharp instruments can be started almost immediately after condensation.
Burnishing, or rubbing the newly condensed amalgam with a metal instrument having a broad surface contact, can be employed to smooth the surface, thereby making the amalgam more susceptible to finishing and polishing. Burnishing can produce a tenfold reduction in surface roughness.
If final finishing and polishing are to be done at a second appointment, the restoration should be left undisturbed for a period of at least 24 hours. The patient should be cautioned that the freshly inserted restoration is relatively weak and that heavy biting forces should be avoided for a few hours after the time of insertion. Occlusal contacts must be carefully established. However, current all-spherical high-copper alloys have a much higher early strength than other types and can withstand biting forces sooner than earlier amalgams. One-hour compressive strengths of spherical high-copper alloys are about twice as high as high-copper admixed types and are comparable with those of low-copper alloys at 6 to 7 hours.
High-copper unicompositional amalgams with high early strengths can be finished at the first appointment. After condensation the surface is burnished and carved for clear definition of the margins, and all excess amalgam is removed. A creamy paste of triple-x silex and water is applied gently with an unwebbed rubber cup and a slow-speed handpiece. Light pressure should be applied for no more than 30 seconds per surface, and polishing should be directed from the center toward the margins of the restoration.
This early finishing begins 8 to 10 minutes after the start of trituration, depending on the particular alloy. Results of a 3-year clinical study have shown that restorations polished 8 minutes after trituration and those polished after 24 hours had no difference in longevity. Also, as time in the mouth increased, it became difficult to determine which method had been used to finish the restoration. The 24-hour polishing procedure used in the study was that normally used for polishing amalgam restorations. The procedure used for the 8-minute polish was different; no polishing bur was used, and the amalgam was carved carefully. Because the 24-hour polishing technique requires a second appointment, many restorations go without polishing. The main advantage of the 8-minute polishing technique is the elimination of the second appointment. This technique is limited to those amalgams that have high early-compressive strengths.
A well-finished and well-polished restoration will retain its surface appearance and be easier to keep clean than one that is poorly finished, because a rough surface on the restoration contains microscopic pits in which acids and small food particles from the mouth accumulate. These pits tend to encourage galvanic action on the surface of the restoration, leading to tarnish and perhaps even a corroded appearance.
The final polish at a second appointment is developed through a series of final finishing and polishing steps after a careful carving operation. This final polish is accomplished through a sequence of operations that includes the use of fine stones and abrasive disks or strips. To develop the final polish, a rotating soft brush is used to apply a suitable polishing agent, such as ex-trafine silex, followed by a thin slurry of tin oxide.
During the final polishing operation, the restoration should remain moist to avoid overheating from the use of dry polishing surfaces. Because the amalgam is weak in tension and shear resistance, it should not be drawn over the margin by burnishing or drawing operations that tend to produce extensions that subsequently will be fractured from the amalgam mass. To avoid such overextensions, all recommended operative practices should be followed faithfully.
BONDING OF AMALGAM
Although amalgam has been a highly successful restorative material when used as an intracoronal restoration, it does not restore the strength of the clinical crown to its original strength. Additional features, such as pins, slots, holes and grooves to increase retention of the restoration, must be supplied with the preparations for large amalgam restorations, but they do not reinforce the amalgam or increase its strength.
With the development of adhesive systems for dental composites came the opportunity to attempt to bond amalgams to tooth structure. Adhesive plastics containing 4-META, an acronym for 4-methacryloxyethyl trimellitic anhydride (see Chapter 10), have been the most successful products. Shear bond strengths of amalgam to dentin as high as 10 MPa have been reported using these adhesives. Comparable values for the shear bond strength of microfilled composites to dentin using these same adhesives have been 20 to 22 MPa. The fracture resistance of teeth restored with amalgam-bonded MOD restorations was more than twice that of restorations containing unbonded amalgams. Also, in spite of the lower shear strength of amalgam-bonded-to-dentin test samples compared with composites, the fracture strength of MODs in teeth restored with bonded amalgams was as high as for composites, although neither were as high (45% to 80%) as values for the intact tooth. As expected, amalgam bonded MODs with narrow preparations had higher strengths than those with wide preparations. Other studies showed the retention of amalgam-bonded MODs with proximal boxes was as great as pin-retained amalgams. In addition, amalgam-bonded restorations decreased marginal leakage in Class 5 restorations compared with unbonded amalgams. Finally, the plastic bonding agents for amalgam have not been successful in increasing the amalgam-to-amalgam bond strength in the repair of amalgam restorations. Thus at this stage of development, adhesive bonding of amalgam restorations to tooth structures is an improvement over non-bonded amalgams.
MERCURY AND BIOCOMPATIBIUTY ISSUES
Amalgams have been used for 150 years; about 200 million amalgams are inserted each year in the United States and Europe. In spite of its substantial history, however, periodically concern arises about the biocompatibility of amalgam. Allergic reactions to mercury in amalgam restorations do occur, albeit infrequently. This is not surprising, because there is no material that 100% of the population is immune to 100% of the time. However, such allergic responses usually disappear in a few days or, if not, on removal of the amalgam. Aside from varying reports of mercury accumulation, no other local or systemic effects from mercury contained in dental amalgam have been demonstrated. If amalgam is used correctly, biocompatibility should not be a problem.
Even in their passive condition, metals are not inert. In vitro and in vivo experiments have established that there is a passive dissolution from all metals. The following eight questions are linked to the issues of dissolution, corrosion, and potential allergic response and toxicity:
- Is any material released into the mouth?
- What material is released?
- What is the form of the released material?
- How much material is released?
- In what subsequent reactions do the released products get involved?
- What percentage of the released products is excreted and what percentage is retained?
- Where does the retained percentage accumulate?
- What biological responses will result from the retained fraction?
Therefore any analysis of the literature and discussion of mercury toxicity in amalgams must continually refer to these eight questions, particularly questions 3 and 4, relating to the dosage and form of the mercury to which the body is exposed.
SOURCES OF MERCURY
In addressing these eight questions, the sources of the potential toxins must be evaluated. Exposure to mercury can occur from many different sources, including diet, water, air, and occupational exposure (Table 11-4). The World Health Organization (WHO) has estimated that eating seafood once a week raises urine mercury levels to 5 to 20 (Xg/L, two to eight times the level of exposure from amalgam (1 (J-g/L = 1 mg/m3 = 1 part per billion [ppb]). Thus the amount of mercury vapor released from amalgam is less than that received from eating many common fish. It has been estimated that a patient with 9 amalgam occlusal surfaces will inhale daily only about 1% of the amount the Occupational Safety and Health Administration (OSHA) allows to be inhaled in the workplace. Blood and urine mercury levels are easily influenced by other factors and cannot often be directly linked to amalgam. In general, elemental mercury from amalgam seems to make only a small contribution to the total body burden of mercury. On the basis of epidemiological studies, blood and serum mercury levels correlate highly with occupational exposure and diet, whereas urine mercury relates to amalgam burden. Urine mercury levels relate to methods of condensation and ventilation more than to the amalgam per se.
FORMS OF MERCURY
Mercury has many forms, including organic and inorganic compounds. The most toxic organic compounds are methyl and ethyl mercury, and the next most toxic form is mercury vapor. The least toxic forms of mercury are the inorganic compounds. Liquid mercury reacts with silver to form an inorganic silver-mercury compound via a metallic bond. Reports of people and animals being poisoned by eating food high in mercury are traced to the contamination of these foods by methyl mercury.
Mercury vapor is released, in minute quantities, during all procedures involving amalgam, including mixing, setting, polishing, and removal. Mercury vapor has also been reported to be released during mastication and drinking of hot beverages. The amount of mercury on amalgam surfaces has correlated with the quantity of mercury used during trituration. However, measuring the flow and flow rate is difficult and not precise, especially when working with a small area such as the mouth. Furthermore, ambient mercury must be considered, especially if such readings are taken in a dentist's office. With good ventilation, mercury levels return to background levels 10 to 20 minutes after placing an amalgam, and a charcoal filter system decreases levels 25% during the operative procedure. Fresh amalgams release more mercury than 2-year-old amalgams even with a Streptococcus mutatis biofilm, and it has been shown that most oral organisms can grow in dental plaque containing 2 |LLg of mercury. Under normal conditions amalgam is covered by saliva, tending to reduce vapor pressure. Amalgams can also be constrained with a sealant resin for the first several days after insertion. Adding indium (8% to 14%) also decreases the vapor pressure.
CONCENTRATIONS OF MERCURY
OSHA has set a Threshold Limit Value (TLV) of 0.05 mg/m3 as the maximum amount of mercury vapor allowed in the workplace. Nearly all dental offices worldwide comply with this standard. As an example of the factor of safety in this boundary, the fetuses of pregnant rats exposed to atmospheres with mercury concentrations of 2 mg/m3 showed no ill effects. Fetuses exposed to mercury concentrations of 5 mg/m3, or 40 times the allowable concentration, were stillborn. The lowest dose of mercury that illicits a toxic reaction is 3 to 7 M-g/kg body weight.
Paresthesia (tingling of extremities) occurs at about 500 ug/kg of body weight, followed by ataxia at 1000 |Xg/kg of body weight, joint pain at 2000 (J-g/kg of body weight, and hearing loss and death at 4000 M-g/kg of body weight. Therefore these values are much greater in magnitude than the exposure to mercury from amalgam or from a normal diet.
Mercury in Urine The body cannot retain metallic mercury, but passes it through the urine. By using radioactive mercury in amalgams, it is possible to monitor the mercury levels in urine caused only by dental amalgams. One study showed that urine mercury levels peak at 2.54 |0,g/L 4 days after placing amalgams and, after 7 days return to zero. On removal of amalgam, urine mercury levels reach a maximum value of 4 |0.g/L and return to zero after a week. Although mercury is readily cleared in both cases, peak urine levels of mercury are nearly twice as great when amalgam is removed rather than inserted. The same is true for mercury vapor, with higher levels recorded on removal of an amalgam than on insertion. Other studies, using more sensitive techniques such as atomic absorption spectroscopy, show conflicting findings. There are reports demonstrating no increase in urine mercury levels and reports showing higher levels. Even in those cases in which urine mercury is elevated, the concentrations are still less than 1 (ig/L.
As a comparison, consider the WHO estimate that eating seafood once a week will raise urine mercury to 5 to 20 |J.g/L, or two to eight times the level of exposure from amalgam determined in the study just cited. Neurological changes are not detected until urine mercury levels exceed 500 ug/L, nearly 170 times the peak levels found on insertion of an amalgam.
Mercury in Blood The maximum allowable level of mercury in the blood is 3 (J-g/L. Several studies have shown that freshly placed amalgam restorations elevate blood mercury levels to 1 to 2 |ig/L. Removal of amalgam decreases blood mercury levels, with a half time of approximately 1 to 2 months for elimination of mercury.
However, as with urine mercury levels, there is first an increase of around 1.5 M-g/L, which decreases in about 3 days. One study monitored blood mercury levels for a year and showed that patients with amalgams had a lower than average blood mercury level (0.6 (ig/L) than patients without amalgams (0.8 (J-g/L). Presumably the blood mercury level is easily influenced by other factors and therefore cannot be explicitly related to amalgam. Evidently, a relationship exists between plasma and urine mercury levels.
Another study showed that patients with and without amalgams do not differ in the mean number or percentage of lymphocytes. Some studies have shown the blood mercury levels of dentists to be normal, whereas others report an increase. For those studies that indicate higher blood mercury levels in dentists, results have varied regarding any correlation between mercury concentration and number of amalgams placed. Elevated blood mercury levels may relate to mercury spills in the office, a factor that can easily be controlled. Both blood and serum mercury levels seem to correlate best with occupational exposure and not with the number of amalgams or length of time with amalgams in place.
Release of Corrosion Products Mercury release into various media, including water, saline, buffered citric and phosphoric acid, and synthetic saliva, has been measured by a number of techniques, such as atomic emission spectros-copy and atomic absorption spectroscopy. Ion release tends to be greatest in the first 1 to 24 hours after trituration. Once the amalgam is fully set, ionic dissolution is very low. This reduction in ion flux with time probably results from a combination of the chemical reaction progressing further and the formation of a passive surface film. In general, low-copper alloys release more ions than high-copper alloys, because of their inferior corrosion resistance. Greater amounts of mercury and silver are released from unpolished specimens than from polished specimens.
The effect of electrolytic concentration on corrosion has been compared for conventional and high-copper admixed alloys following storage for 4 months. The main corrosion products were tin compounds at the surface of the amalgams. Low-copper amalgam showed surface corrosion only, whereas subsurface corrosion occurred with high-copper amalgam, especially following immersion in an NaCl solution without phosphate. For low-copper amalgam, the release of elements decreased with time, possibly indicating passivation. For high-copper amalgam, the release of elements increased with time, except for copper and tin in a solution with a high concentration of phosphate, indicating that phosphate inhibits corrosion of the copper-tin phases. Other studies have revealed a tendency for tin and copper to be preferentially released from amalgam. Presumably, tin release originates from surface corrosion, whereas copper release results from subsurface corrosion. Stronger galvanic influences enhance copper release and, to a lesser extent, zinc release. Tin tends to provide a passive layer and to suppress the dissolution of mercury. It is suspected that indium functions similarly. In zinc-free alloys, the tin oxide is mercury depleted.
Another recent study has shown that following 1 week of aging in 0.9% NaCl solution at 37° C, the amount of mercury released from y1 was 14 to 60 times that released from amalgam and 5 times that released from (31. The y2 phase released the least amount of mercury.
ALLERGIC REACTIONS AND DISEASE
Allergic reactions to mercury in amalgam restorations are rare, although there are case reports of allergic contact dermatitis, gingivitis, stomatitis, and remote cutaneous reactions. Such responses usually disappear on removal of the amalgam. Other local or systemic effects from mercury contained in dental amalgam have not been demonstrated. No well-conducted scientific study has conclusively shown that dental amalgam produces any ill effects.
Random reports of various diseases, such as multiple sclerosis, cannot unequivocally link the diseases to amalgams and therefore must be interpreted with caution. Reports of multiple sclerosis patients being instantly cured when amalgam is removed cannot be upheld scientifically. Because a week must pass for all mercury to be cleared by the body, an instantaneous recovery after removing the potential source of the mercury is unlikely.
Local Reactions In patients with oral lesions near amalgam sites, positive patch tests have been reported. However, the appropriate patch test has still not been determined, and many of the materials used for patch testing contain excessive concentrations of mercury. There are also reports of inflammatory reactions of the dentin and pulp, similar to the reactions to many other restorative materials. Mercury has been found in the lysosomes of macrophages and iibroblasts in some patients with lesions. Inflammation can usually be alleviated with a cavity liner. With the increased use of more corrosion-resistant amalgams, the volume of corrosion products and subsequent reactions are reduced.
Macrophages play an important role in the removal of foreign particulate matter from tissue. A number of cell culture studies have assessed the potential cytotoxicity of amalgam and its constituents. Unreacted mercury or copper leaching out from high-copper alloys has usually been the constituent leading to adverse responses. An in vitro study of the effects of particulate amalgams and their individual phases on macrophages showed that all particles except the y2 are effectively phagocytized by macrophages. Cell damage was seen in treated cultures exposed to particulate yv
Systemic Reactions Implantation studies have shown that amalgam is reasonably well tolerated by soft and hard tissue. In a rabbit muscle implantation model, biological reactions to amalgams were found to depend on the time of implantation. All amalgams were strongly toxic 1 hour after setting. After 7 days, only high-copper amalgam showed any reaction.
In another series of studies, low- and high-copper amalgam powders and various phases of amalgam were implanted subcutaneously in guinea pigs. The result was a mild, early inflammatory response, in which particles were taken up by macrophages and giant cells. After 1.5 to 3 months, chronic granulomas developed. With low-copper amalgam, early changes occurred in the intracellular material, associated with the rapid degradation of the y2 phase. Later, intracellular particles from both low- and high-copper amalgam underwent progressive degradation, producing fine secondary particles containing silver and tin, which were distributed throughout the lesions and gave rise to macroscopic tattooing of the skin. Secondary material and small, degrading, primary particles from both types of amalgam were detected in the submandibular lymph nodes.
Elevated mercury levels were detected in the blood, bile, kidneys, liver, spleen, and lungs, with the highest concentrations found in the renal cortex. Mercury was excreted in the urine and feces. Mercury levels in the blood, liver, renal cortex, and feces were lower with the high-copper amalgam.
Black, refractile particulate deposits approximately 1 to 3 urn in diameter were found in the cytoplasm and nuclei of kidney cells. The ratio of nuclear to cytoplasmic deposits was higher in animals receiving high-copper amalgam. The cytoplasmic deposits consisted of collections of fine particles within lysosomes. Both lysosomal and nuclear deposits contained mercury and selenium, which were present in the animals' diet at low levels. Neither this study nor others have demonstrated any changes in biochemical function of any of the laden organs.
Subcutaneous implantation of only the powdered y2 phase led to a limited initial release of mercury from extracellular material. Thereafter, chronic granulomas developed around the implants, and particles degraded slowly in macrophages and giant cells. Fine secondary particles containing tin were produced. Subcutaneous implantation of only the powdered ya phase induced a severe initial tissue response, and the majority of the material was extruded from the healing wounds. This process was accompanied by the release of significant amounts of mercury, which appeared in the body organs and excreta. The small numbers of particles remaining in the tissues underwent a slow degradation in macro-phages and giant cells in chronic granulomas. Minute secondary particles containing silver and sulfur were deposited in the tissues and gave rise to macroscopic tattooing of the skin above the implants.
In another study, primates received occlusal amalgam fillings or maxillary bone implants of amalgam for 1 year. Amalgam fillings caused deposition of mercury in the spinal ganglia, anterior pituitary, adrenal, medulla, liver, kidneys, lungs, and intestinal lymph glands. Maxillary amalgam implants released mercury into the same organs, except for the liver, lungs, and intestinal lymph glands. Organs from control animals were devoid of precipitate.
Note that studies on powders probably overestimate the amount of breakdown products, and therefore biological response, because the surface area of powders can be 5 to 10 times the surface area of a solid component. It must also be emphasized that any reaction to amalgam, whether in cell culture, local tissue response, or systemic response, does not necessarily imply a reaction to mercury. Such reactions could be in response to some other constituent of the amalgam or corrosion product. For example, in vitro cell culture testing that measured fibroblasts affected by various elements and phases of amalgams has shown that pure copper and zinc show greater cytotoxicity than pure silver and mercury. Pure tin has not been shown to be cytotoxic (Fig. 11-14). The ya phase is moderately cytotoxic. Cytotoxicity is decreased by the addition of 1.5% and 5% tin (Fig. 11-15). However, the addition of 1.5% zinc to Yj containing 1.5% tin increases cytotoxicity to the same level as that of pure zinc. Whenever zinc is present, higher cytotoxicity is revealed. High-copper amalgams show the same cytotoxicity as a zinc-free, low-copper amalgam. The addition of selenium does not reduce amalgam cytotoxicity, and excessive additions of selenium increase cytotoxicity. The cytotoxicity of amalgams decreases after 24 hours, possibly from the combined effects of surface oxidation and further amalgamation. The results of this study suggest that the major contributor to the cytotoxicity of amalgam alloy powders is probably copper, whereas that for amalgam is zinc.
Other articles
Both comments and pings are currently closed.
