Amalgam Fillings and Periodontal Problems
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Periodontal disease produces hydrogen sulfide and methylthiol compounds as evidenced by numerous publications (and breath odor). Hydrogen sulfide (H2S) reacts with mercury vapour to produce mercury sulfide (HgS) which produces the "amalgam tattoo" often seen around infected teeth in the mouths of individuals with amalgams (note HgS is the mineral cinnabar from which Hg is mined, HgS is classified as extremely toxic). More importantly, methylthiol reacts with Hg to form methylthiol-mercury which is extremely cytotoxic, like methyl-mercury and dimethyl mercury. These mercury methylthiol compounds are more lethal than Hg2+.
(from Prof Boyd Haley report.)
There are several published studies linking the presence of amalgam fillings and periodontal problems. Catsakis and Sulica, (108) from the Georgetown University School of Dentistry in Washington D.C. reported a case of persistent periodontitis which did not clear up, despite constant periodontal therapy up to and including periodontal surgery, until all the amalgams were removed. The periodontal problem had persisted for seven years but after the amalgams were removed, the periodontal condition healed quickly and the tissues remained healthy for a period of more than two years up to the time of publication of that report.
Fisher et al. (247) reported a study where 54 amalgams were placed in 43 patients and followed up, for up to four years. Yearly measurements were made between the alveolar crest and the apical margin of the fillings in the experimental group and the cementoenamel junction and the alveolar crest in the control group. They found that in the experimental group the level of alveolar crest resorption was almost twice that of the control group, i.e. 0.8 mm vs 0.45 mm. This study needs to be considered in the light of the work of Freden in 1974.(248) He measured the amount of mercury in tissues in contact with amalgams and found average levels 49 times higher than control tissues from the same mouth. Is it reasonable to postulate, in light of our knowledge of the extreme toxicity of mercury, that some deleterious effect could be expected in tissues that have 49 times more mercury compared with tissues which have no mercury? Is it even more reasonable when one considers research has shown that mercury in a concentration as low as 20 parts per billion (ppb) was sufficient to stop osteoblastic activity. (Personal communication in Oct 1985 regarding preliminary studies at the Department of Biology, University of Colorado, Colorado Springs). Ellender et al (246) reported that nickel needed a concentration of 200 ppb to achieve the same result. Finally, consider the findings of Koivumma & Makila (249) who reported that, of a variety of materials, amalgam, in a human mouth, attracted more plaque than any other material.