Amalgam has been used in dentistry in Europe for at least 100 years. Amalgam consists of about 50% mercury, 30-40% silver and 10-15% tin. Some brands contain copper and zinc (1). Hypersensitivity reactions to amalgam have been reported many times (2,3,4). Mercury binds strongly to SH-groups of proteins and has probably an antigenic action similar to nickel (5). Amalgam is an unstable alloy with several phases, the most corrosible one is the tin-mercury phase (2). In the presence of an electrolyte such as saliva, corrosion will occur. Corrosion is one of the major causes of failure of amalgam restoration (6). Amalgam has a very complicated structure and mercury can freely migrate in the alloy (6). Gold-amalgam (a two-component system, has 14 phases and at least 5 at physiological temperatures, several of them of unknown composition).
During the corrosion process, metallic mercury is set free. Some of the liberated mercury migrates into the other phases and causes them to swell, to become oversaturated and brittle. Mercury migrates rapidly in amalgam (6). If the mercury can bind to macro- molecules, especially those containing SH groups, it will be ionised (5).
If the amalgam is in a cavity in a tooth, local galvanic cells and mercury release will occur at the surfaces with the lowest oxygen tension, ie, towards the walls of the cavity (6). The liberated mercury will migrate through dental tissue and into underlying structures. Values of 125.pg/gram tissue one day after restoration and 50 pg/g after one week have been reported (7). Even after more than three years, high contents of mercury can be detected in gingival tissue adjacent to amalgam (19-380 pg/g) (8). The mercury is transported away from the site of release (7,8). Also, silver is released, which indicates that the mercury-rich silver-amalgam phase is also attacked (8).
In contact with gold the rate of corrosion is considerably increased (4,6,9,10,11). Since 1941, the use of amalgam and gold in contact has been warned against (13) and since 1952 for serious pathological conditions in the mouth and hypersensitivity reactions caused by released metallic ions (4).
The accelerated corrosion is caused by the creation of a gold-amalgam galvanic cell (9-12).In vitro under undisturbed conditions and in the absence of macro-molecules, corrosion can induce the formation of numerous small droplets of mercury on the amalgam surface (6). In a simple salt solution very little mercury will ionise.
In vivo currents less than 1 mA to over 100 mA have been recorded between different parts of single amalgam restorations or between different restorations in metallic contact (14). Currents of this magnitude have also been recorded in vitro between gold and amalgam (10-12). It is not possible to record in vivo the currents between gold-plated brass screws and amalgam in endodontically treated teeth (filled in the roots) or between gold-crowns and underlying amalgam . Nobody has calculated the amount of liberated mercury in gold- amalgam galvanic cells. A current of 100 mA will liberate approximately 5 mg of mercury/day. This amount will give a certain mercury poisoning. The value is calculated on the basis of a 1:1 Hg-Sn ratio in the 2 phase. Tin is the first metal to become ionised and the bound mercury will be liberated. Initially the 2 phase is richer in Sn than in Hg but since the Hg-rich Ag-Hg phase will also be attacked, the ratio chosen seems to be a reasonable approximation. Ag at about half the concentration of Hg can be measured in gingival tissues adjacent to amalgam fillings (8). In contact with gold, no amalgam phase is stable and mercury will be released fast until the gold-amalgam contact is broken or reduced and slower thereafter. The calculated amounts of released mercury might be less by a factor of 3-4 because of the uncertain composition of amalgam but also higher because of simultaneous local galvanic cells. The mercury is mainly released towards the tooth and underlying structures where the oxygen tension is low and very little probably escapes into the saliva. From the pulp chamber there are direct connections to the brain.
Mercury accumulates in the intestinal tissues, skin, hair, all types of glands, liver, pancreas, thyroid, kidneys, testicles, placenta and brain irrespective of route of administration (5). The transport of substances over the blood-brain barrier is impaired and increased permeability induced even by minute amounts of Hg in the blood (in experimental animals). In the brain certain areas accumulate more mercury than others. Inorganic mercury in ionised form enters the brain slowly and leaves it even more slowly. In contrast, mercury vapour and methyl-mercury quickly goes into the brain. Methyl-mercury is more evenly distributed in the brain than inorganic forms and has also a special affinity for dorsal ganglia (5,15).
Inorganic mercury poisoning gives headache, weakness, fatigue, anorexia, loss of weight, gastrointestinal disturbances, tremor, increased salivation or dry mouth, inflammatory changes of the gums, skin reactions, heart trouble, behavioural and personality changes, increased excitability, irritability, vertigo, vision disturbances, loss of memory, insomnia, depression, agony, suicide thoughts and several other systems. The kidneys are the critical organs (5,15,16). The limit in Sweden for total daily intake of Hg is 0.4 mg/kg body weight and day – 30 mg/day for an adult. The FAO/WHO limit is 5 pg/kg a week – 50mg/day. Methyl-mercury is the best studied Hg-compound and is, if ingested in food, absorbed to 95% due to its lipid solubility. Symptoms of poisoning can appear at a daily intake of a few hundred micrograms. Inorganic Hg-salts are absorbed to 5-15% in the intestine (5,16). The toxic dose is not well known (5). The dose-response relationship for mercury poisoning due to inhalation of vapours is better known. Concentrations in air over 100 pg/m3 will give symptoms in the majority of exposed persons. Breathing at rest and at 80 % absorption gives during 8 h a dose of about 300 pg. The figure might be doubled because of increased ventilation during work (most cases are from industry). The value is not far from that of methyl-mercury and little is known about individual variability. Mercury can also probably be both methylated and demethylated in the tissues. If the inorganic mercury is liberated inside a tooth it is very likely that most of it will be absorbed and distributed in the body. The toxic dose will then be similar to that of methyl-mercury.
Allergy to amalgam (mainly skin reactions) has been reported many times (3,4) and mercury behaves in respect like a nickel. Due to the binding to SH-groups in proteins and its wide distribution in the body, some of the described effects of chronic mercury poisoning might be of this type. Many diseases are suspected to be of an auto-immune character. The release of mercury from amalgam might therefore be a common factor in the aetiology of several severe diseases. Examples are: multiple sclerosis, arthritis, skin diseases and maybe atheriosclerosis. It is possible that the immune system can wither react to the native protein, only to Hg-containing proteins or both after sensitisation. Human immune reactions to tissue proteins other than from the skin, treated with Hg-salt has, to the best of my knowledge, never been investigated.
There is evidence for these suggestions. The connection between tissue necrosis below the teeth and MS (and also other disorders of the CNS) has been observed in the Clinic by Stortbecker (17). His observations led him to the conclusion that toxins produced by micro-organisms in inflammatory areas were transported to the CNS in nerves and vessels. Mercury in high concentrations causes tissue destruction and inflammation-like changes and it is clear from published papers that extensive dental restorations were present in most cases. Retrograde axonal transport of bacterial toxins might be an additional factor (18). Many cases of especially MS, but also epilepsia, vertigo, headache and optic neuritis were successfully treated by extraction of affected teeth.
The case of mercury as a factor in the etiology of arthritis is also suggestive. Victims of mercury poisoning often have joint pains. Pencillamine is used to treat arthritis, but has the serious side effect of causing kidney damage. The reason for either effect has not been explained (19). Penicillamine or preferably acetyl-penicillamine is used to detoxify after mercury poisoning. It is recommended to use it in combination with haemodialysis to prevent kidney damage (5,16).
Atheriosclerosis might also have a relation to mercury. Increased tissue deposition of cholesterol caused by amalgam was reported several times during the 1930’s (for ref. see extensive list of older publications in 4). Increased serum levels of cholesterol after mercury inhalation have been reported (2). Mercury is probably mutagenic. Cancer in the mouth and intestine was also reported in connection with amalgam (4). A relation between tissue destruction at the roots of diseased (and repaired) teeth and glioblastomas has been suggested (20). All forms of mercury are teratogenic but to different degrees (16).
Because of its almost universal toxic effects and the slow onset of symptoms, mercury can probably be considered one of the worst poisons imaginable. In 2 grams of amalgam there is more than 30,000 times the maximum permissible daily intake of mercury (Swedish values). To keep below the limit (other sources unrecognised), this amount of amalgam must not release its mercury faster than in 82 years. Self-corrosion goes much faster than this. In contact with gold it goes very much faster. These facts were not considered when mercury in the environment was intensely studied. Very few references refer to dentistry and these few are mainly concerned with release of mercury into the environment from dental clinics.
The adverse effects of gold over amalgam was partially recognised as early as 1911 by Hunter (21) but amalgam is probably one of the very few factors which has never been systematically investigated for connections with a large number of common and severe diseases. In view of the large doses of mercury which can be released from dental fillings, the possible connections merit a rapid investigation. Much suffering and large costs might be saved.
Department of Zoophysiology,
University of Lund Helgonavagen 3B
S-223 62 Lund, Sweden