(par Berdj Haroutunian)

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  • Les articles résumés proviennent du site
  1. Metals and Cardiovascular Diseases (les métaux et les maladies cardio-vasculaire)
  2. Metals, Psychiatric Disease and mental health (les métaux et les maladies psychiatiques)
  3. Metals and immune system (les métaux et le système immunitaire)
  4. Metals and toxicology (les métaux et la toxicology)
  5. Metals and Skin Diseases (les métaux et les maladies de la peau et des muqueuses)
  6. Metals and Gastrointestinal Diseases ( les métaux et les maladies gastro-intestinales)
  7. Metals and toxicology of endodontic material (les métaux et les produits d’obturations canalaires)
  8. Metals and Oral Diseases (les métaux et les maladies orales)
  9. Metals and the Brain (les métaux, le système nerveux et le cerveau)
  10. Metals and Occupational Exposure (les métaux et les contaminations par le travail)
  11. Diagnostic Procedures in the Determination of Metal Toxicity (procédés de diagnostic pour la determination de la toxicité des métaux)
  12. Release of mercury and metals from dental feelings or from other source (relargage de mercure et métaux à partir d’obturations dentaires ou autres)
  13. Genetic and periodontal disease  (la génétique et la maldie parodontale)
  14. Metals and Alzheiner’s disease , multiple sclerosis, Amyotrophic lateral sclerosis, Parkinson’s disease, Fibromyalgy (maladie d’Alzheimer, le Parkinson, la Fibromyalgie, la sclérose amyotropjique latérale, la sclérose en plaque et les métaux)
  15. Studies on animals ( les études sur les animaux)
  16. Metals, fertility, embryogenesis
  17. Diabete and periodontal disease ( tiré du site
  18. Quelques résumés divers

1. Metals and Cardiovascular Diseases

  1. Use of methyl prednisolone and antioxidants in mercuric cloride-induced experimental vasculitis.
    FJ Quasim, PW Mathieson, S Thiru, DBG Oliveira
    Clin Exp Immunol; 98:66-70
    Then systematic vasculitides are characterized by necrotizing inflammation of blod vessels. Neutrophils are implicated in tissue damage by their presence at the site of injury. They can mediate injury by release of cellular contentincluding proteinases, citokines and reactive oxygen species. Antioxidants such as vitamin E and N-acetyl cysteine (NAC) may therefore be predicted to ameliorate oxidative damages in vivo and could be a cheap and non-toxic form of therapy. We examined the hypothesis in an experimental model of vasculitis which has some similarities to human disease, and in which depletion of neutrophils ameliorates tissue injury. Mercuric chloride (HgCl2) treatment includes an autoimmune syndrome and necrotizing leucocytoclastic vasculitis in the Brown Norway (BN) rat; anti-myeloperoxidase (MPO) anti-glomerular basement (GBM) antibodies are present, and vasculitis is reduced by antimicrobials. Methyl prednisolone given tintravenously was effective in reducing tissue injury, demonstrating that the model was responsive to a treatment used in man.m Vitamin E and NAC were given as daily injections intraperitoneally to BN rats either before, during or after HgCl2 administration. Serial blod samples were taken for anti-MPO and IgE antibodies, which were assayed by ELISA. Necropsies were performed on animals killed at peak disease. At doses of 50-200mg/kg per day vitamin E had no beneficial effect on tissue injury, regardless of timing of treatment. NAC at 100 or 200mg/kg also had no significant positive effect on vasculitis. Autoantibody and IgE levels were not affected by either methyl prednisolone or the antioxidants. The lack of benefits of vitamin E and NAC suggests that oxidative damage, whether generated by neutrophils or other cells, does not play a major role in the pathogenesis of vasculitis, and that antioxidant therapy is unlikely to be of benefit in systematic vasculitis in man.

2. Metals, Psychiatric Disease, and mental health

    1. Psychometric evidence that mercury from silver dental fillings may be an etiological factor in depression, excessive anger, and anxiety.
      Siblerud RL, Motl J, Kienholz E, Rocky Mountain Research Institute, Inc., Fort Collins, CO 80524
      Psychol Rep 1994 Feb;74(1):67-80
      Scores on the Beck Depression Inventory were compared for 25 women who had silver dental fillings (amalgams) and for 23 women without amalgams. Women with amalgams had significantly higher scores and reported more symptoms of fatigue and insomnia. Anger scores from the State-Trait Anger Expression Inventory showed that the women with amalgams had statistically significantly higher mean scores on expressing anger without provocation and experiencing more intense angry feelings. The women without amalgams scored significantly higher on controlling anger, which suggested they invested more energy in monitoring and preventing the experience and expression of anger. Anxiety scores from the State-Trait Anxiety Inventory showed the women with amalgams scored significantly less pleasant, satisfied, happy, secure, and steady, and had a more difficult time making decisions. They had significantly higher Trait Anxiety scores. The women with amalgams also had significantly higher levels of mercury in the oral cavity before and after chewing gum. The study suggests that amalgam mercury may be an etiological factor in depression, excessive anger, and anxiety because mercury can produce such symptoms perhaps by affecting the neurotransmitters in the brain.
    2. Mercury–a factor in mental disease? Part 1. Canmercury-silver amalgams cause psychiatric symptoms?
      Huggins HA.Oral Health. 1983 Dec;73(12):42-5..PMID: (6584812)
    3. The relationship between mercury from dental amalgam and mental health. Siblerud (1989). Am. J. Psychother. 43:575-587. (2618948)
    4. A comparison of mental health of multiple sclerosis patients with silver/mercury dental fillings and those with fillings removed. Siblerud (1992). Psychol. Rep70:1139-1151.(1496084)


  • Acute and chronic neuropsychological consequences of mercury vapor poisoning in two elderly adolescents. Yeates and Mortensen (1994). J. Clin. Exp. Neuropsychol16:209-222.(8021308)
  • Psychometric evidence that mercury from silver dental fillings may be an etiological factor in depression, excessive anger, and anxiety. Siblerud et al., (1994). Psychol. Rep. 74:67-80. (8153237)
  • Psychological effects of low exposure to mercury vapor: application of a computer-administered neurobehavioral evaluation systerm. Liang et al., (1993). Environ. Res60:320-327.(8472661)
  • An epidemiologic study of the relation between symptomss of fatigue, dental amalgam and other factors. Michel et. al., (1989). Swed. Dent. J13:33-38.(2734698)
  • Impact of heavy metals on hormonal and immunological factors in women with repeated miscarriages. Gerhard et al., (1998). Hum. Reprod. Update 4:301-309. (9741713)




3. Metals and immune system

    1. Does amalgam affect the immune system? A controversial issue. Enestrom and Hultman (1995). Int. Arch. Allergy Immunol106:180-203. (7888781)
    2. Effects of mercury on the immune system. Pollard and Hultman (1997). Met. Ions Biol. Syst. 34:421-440. (9046578)
    3. Activation of the immune system and systemic immune-complex deposits in Brown Norway rats with dental amalgam restorations. Hultman et. al., (1998). J. Dent. Res77:1415-1425.(9649170)
    4. Adverse immunological effects and autoimmunity induced by dental amalgam and alloy in mice. Hultman et al., (1994). FASEB J. 8:1183-1190.(7958626)
    5. Localized cellular inflammatory responses to subcutaneously implanted dental mercury. Nadarajah et. al., (1996). J. Toxicol. Environ. Health 49:113-125.(8874531)
    6. Cellular inflammatory responses to implanted dental materials. Nadarajah et. al., (1996). J. Prosthet. Dent. 75:552-561.(8709023)
    7. In vitro effects of mercuric chloride (HgCl2) on human mononuclear cells. Loftenius et. al., (1997). Clin. Exp. Immunol110:418-422.(9409645)
    8. Cytotoxicity and accumulation of Hg, Ag, Cd, Cu, Pb, and Zn in human peripheral T and B lyphocytes and monocytes in vitro. Steffenson et. al., (1994). Gen. Pharmacol25:1621-1633.(7721038)
    9. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes. I. Suppression of T-cell activation. Shenker et. al., (1992). Immunopharmacol. Immunotoxicol14:539-553.(1517533)


  • Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes. II. Alterations in cell viability. Shenker et. al., (1992). Immunopharmacol. Immunotoxicol14:555-577.(1517534)
  • Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes. III. Alterations in B-cell function. Shenker et. al., (1993). Immunopharmacol. Immunotoxicol15:87-112.(8450183)
  • Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes. IV. Alterations in cellular glutathione content. Shenker et. al., (1993). Immunopharmacol. Immunotoxicol15:273-290.(8349953)
  • Immunotoxicology of cadmium and mercury on B-lymphocytes I. Effects on lymphocyte function. Daum et al., (1993). Int. J. Immunopharmacol. 15:383-394.     (7685007)
  • Effects of mercury on human polymorphonuclear leukocyte function in vitro. Contrino et. al., (1988). Am. J. Pathol. 132:110-118.(3394794)
  • Low levles of mercury inhibit the respiratory burst in human polymorphnuclear leukocytes. Malamud et. al., (1985). Biochem. Biophys. Res. Commun128:1145-1151.(2988529)
  • Parameters of immunity acute phase reaction in men in relation to exposure duration to mercury vapours. Moszczynski et. al., (1991). J. Hyg. Epidemiol. Microbiol. Immunol35:351-360.(1725175)
  • The level of mercury in human dental plaque and interactions in vitro between biofilms of Streptococcus mutans and dental amalgam. Little and Bowden (1993). J. Dent. Res. 72:1320-1324.(8360382)
  • Acute exposure to mercury from amalgam: no short-time effect on the peripheral blood lymphocytes in healthy individuals. Loftenius et al., (1998). J. Toxicol. Environ. Health 54:547-560. (9726779)




4.Metals and toxicology

    1. Toxicity assessment of mercury vapor from dental amalgams. Goering et. al., (1992). Fundam. Appl. Toxicol. 19:319-329.(1360929)
    2. The future of dental amalgam: a review of the literature. Part 6: Posssible harmful effects of mercury from dental amalgam. Eley (1997). Br. Dent. J. 182:455-459.(9231518)
    3. Documented clinical side-effects to dental amalgam. Ziff (1992). Adv. Dent. Res6:131-134.(1292453)
    4. Evaluation of the safety issue of mercury release from dental fillings. Lorscheider and Vimy (1993). FASEB J7:1432-1433.(8262327)
    5. Mercury neurotoxicity: mechanisms of blood-brain barrier transport. Aschner and Aschner (1990). Neurosci. Biobehav. Rev14:169-176.(2190116)
    6. The toxicology of mercury. Clarkson (1997). Crit. Rev. Clin. Lab. Sci34:369-403.(9288445)
    7. Cytotoxicity of amalgams, alloys, and their elements and phases. Kaga et. al., (1991). Dent. Mater. 7:68-72.(2016001)
    8. Cytotoxic effects of restorative materials on early passage cultured cells derived from human gingiva. Yamagata and Oshima (1990). Shika Zairyo Kikai 9:541-554.(2134820)
    9. Cytotoxicity of amalgams. Kaga et. al., (1988). J. Dent. Res67:1221-1224.(3166005)
    10. Correlation of cytotoxicity with element release from mercury- and gallium-based dental alloys in vitro. Wataha et. al., (1994). Dent. Mater. 10:298-303. (7498590)
    11. Cytotoxicity of gallium and indium ions compared with mercuric ion. Chandler et. al., (1994). J. Dent. Res73:1554-1559.(7929991)
    12. Quantitative evaluation by measuring affected area for cytotoxicity of dental materials. Kaga et al., (1990). Shika Zairyo Kikai 9:591-599.(2134824)
    13. The mechanism of Hg2+ toxicity in cultured human oral fibroblasts: the involvement of cellular thiols. Liu et. al., (1992). Chem. Biol. Interact. 85:69-78.(1458551)
    14. Toxic effects of various retrograde root fillings materials on gingival fibroblasts and rat sarcoma cells. Peltola et. al., (1992). Endod. Dent. Traumatol8:120-124.(1289070)
    15. In vitro testing of dental materials by means of macrophage cultures: II. Effects of particulate dental amalgams and their constituent phases on cultured macrophages. Syrjanen et. al., (1986). J. Biomed. Mater. Res20:1125-1138.(3782175)
    16. Cytotoxicity of endodontic materials. Osorio et. al., (1998). J. Endod. 24:91-96.(9641138)
    17. Cytotoxicity of retrofill materials. Bruce et. al., (1993). J. Endod19:288-292. (8228748)
    18. Corrosion products from dental alloys and effects of mercuric and cupric ions on a neuroeffector system. Moberg (1985). Swed. Dent. J. Suppl29:1-51.(3866332)
    19. Development of low- and high-serum culture conditions for use of human oral fibroblasts in toxicity testing of dental materials. Liu et. al., (1991). J. Dent. Res70:1068-1073.(2066489)
    20. A possible case of mercury-related toxicity resulting from the grinding of old amalgam restorations. Taskinen et. al., (1989). Scand. J. Work Environ. Health 15:302-304.(2772585)


  • In vitro effects of mercuric chloride (HgCl2) on human mononuclear cells. Loftenius et. al., (1997). Clin. Exp. Immunol110:418-422.(9409645)
  • Toxicological assessment of amalgam components released in immersion tests. Weiland and Nossek (1991). Dtsch. Zahnarztl. Z. 46:547-550.(1817927)




5. Metals and Skin Diseases

  1. Ear piercing, and nickel and cobalt sensitization, in 520 young Swedish men doing compulsory military service.
    Meijer C; Bredberg M; Fischer T; Widström L
    Contact Dermatitis, 1995 Mar, 32:3, 147-9
    Piercing the earlobes has increased in popularity among males in recent years. This habit would be expected to increase the incidence of nickel and cobalt sensitization. Patch testing with nickel sulfate and cobalt chloride was performed in 520 young Swedish men doing compulsory military service. The overall frequency of nickel/cobalt positive tests was 4.2%. The prevalence of nickel/cobalt positive tests was significantly higher (p < 0.05) in 152 men with pierced earlobes (7.9%) than in those 368 with unpierced earlobes (2.7%). A history of hand eczema (7/152 = 4.6%) or other types of eczema (22/152 = 14.5%) in individuals with pierced earlobes was no more common than in those with unpierced earlobes: 24/368 = 6.5% and 51/386 = 13.9%, respectively (n.s.). Hand eczema was no more common in sensitized (1/22 = 4.5%) than in nonsensitized individuals (32/498 = 6.4%) (n.s.).
  2. Potential efficacy of low metal diets and dental metal elimination in the management of atopic dermatitis: an open clinical study.
    Adachi A; Horikawa T; Takashima T; Komura T; Komura A; Tani M; Ichihashi M
    J Dermatol, 1997 Jan, 24:1, 12-9
    We performed an open clinical study on the effects of low metal diets and/or dental metal elimination on 27 patients with moderate to severe atopic dermatitis (AD), who showed positive patch tests for metal allergens and/or clinical exacerbation by oral provocation tests with metal salts. All the patients were recommended to ingest low metal diets for 3 months and/or undergo dental metal elimination. Marked or moderate improvement was noted in 18 patients (67%); 7 patients (26%) showed marked improvement and 11 patients (41%), moderate improvement. Nine patients (33%) showed minimal improvement or no change. In the patients who showed marked or moderate improvement, we observed statistically significant decreases (p < 0.05) in both peripheral blood eosinophil counts and serum LDH levels after 3 months of treatment. The present study suggests that restriction of ingested metal allergens to which patients have positive patch tests and/or oral challenge tests may be useful in the management of some patients with AD who have metal sensitivity.
  3. Nickel allergy in adolescents in relation to orthodontic treatment and piercing of ears.
    Kerosuo H; Kullaa A; Kerosuo E; Kanerva L; Hensten Pettersen A
    Am J Orthod Dentofacial Orthop, 1996 Feb, 109:2, 148-54
    The aim of this study was to investigate the frequency of nickel hypersensitivity in adolescents in relation to sex, onset, duration and type of orthodontic treatment, and the age at which ears were pierced. The subjects were 700 Finnish adolescents, from 14 to 18 years of age, of which 476 (68%) had a history of orthodontic treatment with metallic appliances. The study consisted of patch-testing for a nickel allergy and a patient history obtained by a questionnaire and from patient record. The frequency of nickel sensitization in the whole group was 19%. Nickel allergy was significantly more often found in girls (30%) than in boys (3%) and in subjects with pierced ears (31%) than in those with no piercing of ears (2%). Orthodontic treatment did not seem to affect the prevalence of nickel sensitization. None of the girls who were treated with fixed orthodontic appliances before ear piercing showed hypersensitivity to nickel, whereas 35% of the girls who had experienced ear piercing before the onset of orthodontic treatment were sensitized to nickel. The results suggest that orthodontic treatment does not seem to increase the risk for nickel hypersensitivity. Rather, the data suggests that treatment with nickel-containing metallic orthodontic appliances before sensitization to nickel (ear piercing) may have reduced the frequency of nickel hypersensitivity.



6. Metals and Gastrointestinal Diseases or related to micro-organism

  1. Methylation of mercury from dental amalgam and mercuric chloride by oral streptococci in vitro. Heintze et. al., (1983). Scand. J. Dent. Res91:150-152.(6222462)
  2. Mercury sensitization induced by environmental exposure. Mori et al., (1998). Nippon Eisenigaku Zasshi 52:661-666.(9528265)
  3. An epidemiological study of factors relating to mercury sensitization. Sato et al., (1995). Arerugi 44:86-92. (7726753)
  4. The dental amalgam mercury controversy-inorganic mercury and the CNS; genetic linkage of mercury and antibiotic resistances in intestinal bacteria. Lorscheider et al., (1995). Toxicology 97:19-22. (7716785)
  5. Mercury released from dental « silver » fillings provokes an increase in mercury- and antibiotic -resistant bacteria in oral and intestinal floras of primates. Summers et. al., (1993). Antimicrob. Agents Chemother.37:825-834.(8280208)
  6. Resistance of the normal human microflora to mercury and antimicrobials after exposure to mercury from dental amalgam fillings. Edlund et. al., (1996). Clin. Infect. Dis22:944-950.(8783691)
  7. The dental amalgam mercury controversy-inorganic mercury and the CNS; genetic linkage of mercury and antibiotic resistances in intestinal bacteria. Lorscheider et al., (1995). Toxicology 97:19-22. (7716785)
  8. Mercury released from dental « silver » fillings provokes an increase in mercury- and antibiotic -resistant bacteria in oral and intestinal floras of primates. Summers et. al., (1993). Antimicrob. Agents Chemother.37:825-834.(8280208)
  9. Resistance of the normal human microflora to mercury and antimicrobials after exposure to mercury from dental amalgam fillings. Edlund et. al., (1996). Clin. Infect. Dis22:944-950.(8783691)
  10. The impact of mercury released from dental « silver » fillings on antibiotic resistances in the primate oral and intestinal bacterial flora. Liebert et. al., (1997). Met. Ions Biol. Syst34:441-460.(9046579)
  11. Dental amalgam and antibiotic resistance-an association? Editorial (1997). Sci. Prog. 80:103-106.(9263508)
  12. Antibiotic resistance mechanisms in bacteria of oral and upper respiratory origin. Roberts (1998). Int. J. Antimicrob. Agents 9:255-267.(9573495)
  13. Cloning of mercury-resistance gene from R-plasmid in Escherichia coli isolated from dental hospital sewage. Arii and Abiko (1989). Gen. Pharmacol20:609-614.(2691324)
  14. Heavy metal resistance in clinical isolates of Pseudomonas aeruginosa. Vasishta et. al., (1989). Folia Microbiol. (Praha.) 34:448-452.(2517120)
  15. Study of the horizontal transfer of mercury resistance genes in natural populations of bacteria using antibodies to mercury reductases. Bogdanova et. al., (1988). Mol. Gen. Mikrobiol. Virusol. 12:16-23.(3150770)



7. Metals and toxicology of endodontic material

  1. Cytotoxicity of endodontic materials. Osorio et. al., (1998). J. Endod. 24:91-96.(9641138)
  2. Cytotoxicity of retrofill materials. Bruce et. al., (1993). J. Endod19:288-292. (8228748)
  3. Toxic effects of various retrograde root fillings materials on gingival fibroblasts and rat sarcoma cells. Peltola et. al., (1992). Endod. Dent. Traumatol8:120-124.(1289070)
  4. Corrosion products from dental alloys and effects of mercuric and cupric ions on a neuroeffector system. Moberg (1985). Swed. Dent. J. Suppl29:1-51.(3866332)



8. Metals and Oral Diseases

  1. An amalgam tattoo causing local and systemic disease?
    Thomas Weaver, Lieutenant Commander DC) USN, Paul L. Auclair. Commander (DC) USN and George M. Taybos, Captain (DC) USN
    Oral Surg. Oral Med. Oral Pathol. 1987;63:137-40
    Amalgam tattoos are common oral lesions. The case presented here involved a 33-year-old woman who had had an amalgam tattoo for 2 years and complained of localized soreness and occasional swelling as well as systemic symptoms of weight loss, fatigue, sinusitis, and headaches. After excisional biopsy of the lesion, the patient’s complaints ceased dramatically. It is suggested that alterations in healing due to the presence of amalgam particles led to systemic as well as local disease.
  2. Mercury Released from Dental « Silver » Fillings Provokes an Increase in Mercury- and Antibiotic-Resistant Bacteria in Oral and Intestinal Floras of Primates
    Anne O. Summers, Joy Wireman, Murray J. Vimy, Fritz L. Lorescheider,
    Bonnie Marshall, Stuart B. Levy, Sam Bennett and Lynne Billard
    Anti-microbal Agents and Chemotherarp, April 1993, Vol. 37, No. 4, p. 825-834
    In a survey of 640 human subjects, a subgroup of 356 persons without recent exposure to antibiotics demonstrated that those with a high prevalence of Hg resistance in their intestinal tiaras were significantly more likely to also have resistance to two or more antibiotics. This observation led us to consider the possibility that mercury released from amalgam (« silver ») dental restorations might be a selective agent for both mercury-and antibiotic-resistant bacteria in the oral and intestinal floras of primates. Resistances to mercury and to several antibiotics were examined in the oral and intestinal floras of six adult monkeys prior to the installation of amalgam fillings, during the time they were in place, and after replacement of the amalgam fillings with glass lonomer fillings (in four of the monkeys). The monkeys were fed an antibiotic-free diet, and fecal mercury concentrations were monitored. There was a statistically significant increase in the incidence of mercury-resistant bacteria during the 5 weeks following installation of the amalgam fillings and during the 5 weeks immediately following their replacement with glass lonomer fillings. These peaks in incidence of mercury-resistant bacteria correlated with peaks of Hg elimination (as high as 1 mM in the feces) immediately following amalgam placement and immediately after replacement of the amalgam fillings. Representative mercury-resistant isolates of three selected bacterial families (oral streptococci, members of the family Entcrobacteri-aceae, and enterococci) were also resistant to one or more antibiotics, including ampicilhin, tetracycline, streptomycin, kanamycin, and chloramphenicol. While such mercury- and antibiotic-resistant isolates among the staphylococci, the enterococci, and members of the family Enlerobacteriaceac have been described, this is the first report of mercury resistance in the oral streptococci. Many of the enterobacterial strains were able to transfer mercury and antibiotic resistances together to laboratory bacterial recipients, suggesting that the loci for these resistances are genetically linked. Our findings indicate that mercury released from amalgam fillings can cause an enrichment of mercury resistance plasmids in the normal floras of primates. Many of these phasmidis also carry antibiotic resistance, implicating the exposure to mercury from dental amalgams in an increased incidence of multiple antibiotic resistance plasmids in the normal floras of nonmedicated subjects.
  3. The Relationship Between Mercury from Dental Amalgam and Oral Cavity Health
    Robert L. Siblerud, M.S.
    Annals of Dentistry, Number 2, Winter 1990 p. 6-10
    The findings presented here suggest that mercury from dental amalgam may play a role in the etiology of oral cavity health. Comparisons between subjects with arid without amalgam showed signif-icant differences of diseases of the mouth. Subjects who had amalgams removed re-ported that symptoms of diminished oral health were improved or eliminated after removal. The data suggest that inorganic mercury from dental amalgam does affect the oral cavity.
  4. Contact stomatitis to mercury associated with spontaneous mononuclear cell infiltrates in brown Norway (BN) rats with HgC12-induced autoimmunity.
    Warfvinge G; Larsson, Department of Oral Pathology, Lund University, Malmö, Sweden
    Oral Pathol Med, 23(l0):441-5 1994 Nov
    Light microscopy and immnunocytochemistry have been used to study the tissue reaction to non-irritant concentrations of mercury painted onto the oral mucosa of genetically mercury-sensitive BN rats. Low-dose skin injections of HgCl2 in BN rats result in an autoimmune syndrome, including also a spontaneous migration of T lymphocytes into the oral mucosa. Our results show that such infiltrates confer an increased degree of reactivity (contact stomatitis) to HgCJ2 painted onto the BN (Hg) rat oral mucosa. In contrast, results were negative in the LEW rat strain, which is also resistant to development of autoimmunity to skin-injected mercury. The possible involvement of mucosal mercury-loaded macrophages is discussed. The results are also discussed with respect to possible etiologic and pathogenetic mechanisms involved in the development of dental material (amalgam)-associated lichenoid lesions of human oral mucosa.
  5. Contact allergy to dental restorative materials in patients with oral lichenoid lesions.
    Laine J; Kalimo K; Happonen RP
    Contact Dermatitis, 1997 Mar, 36:3, 141-6
    118 patients with oral lichenoid lesions (OLL) topographically related to dental fillings were patch tested (PT) to reveal contact allergy to restorative materials. 80 (67.8%) patients displayed positive PT reactions to metals of dental filling materials: 76 reactions were found to various mercury compounds, 4 to sodium aurothiosulphate, 3 to stannic chloride and 2 to silver nitrate. The positive patch test reactions appeared more commonly in patients with restricted contact lesions (85.1%, type-1 lesions) as compared to patients with lesions exceeding to the adjacent areas (38.6%, type-2 lesions). The replacement of dental fillings was carried out in 62/80 PT-positive and 15/38 PT-negative patients. 28 out of 62 (45.2%) PT-positive and 3/15 (20%) PT-negative patients showed complete healing of OLL after a mean follow-up time of 16 months. Complete healing occurred in 29/54 (54.0%) type-1 and 2/23 (8.7%) type-2 lesions. Topographical relation between the lesion and the filling material (restricted versus exceeding the contact area) indicated association of OLL lesion and the filling material, which could be further confirmed by patch testing in the majority of patients. The patch test series should include mercuric chloride (0.1%), mercury (0.5%) and mercury ammonium chloride (1.0%), each in pet.
  6. Release of elements from some gold alloys and amalgams in corrosion.
    Rolf Lappalainen and Antti Yli-Urpo, Institute of Dentistry, University of Kuopio, Kuopio, Finland
    Scand J Dent Res 1987: 95: 364-8
    Abstract – The release of Au, Ag, Cu and Zn elements from six commercially available gold alloys and three amalgam alloys was studied. The polarizing electropotential system with modified Fusayama solution was used. The cycle process was repeated 500 times between ± 1000 mV during a period of 5 h 22 mm. During the process samples of solution were analyzed in order to follow the release of elements. Results revealed rapid release of Zn from most alloys, release of Ag from most alloys and release of Au from two alloys. Also, rapid release of Cu was found from amalgams but not from gold alloys. Release of Ag from gold alloys showed very good passivation up to 3 h, after which it was released in varying amounts.
  7. Methylation of mercury from dental amalgam and mercuric chloride by oral streptococci in vitro.
    Heintze U; Edwardsson S; Dérand T; Birkhed D
    Scand J Dent Res, 1983 Apr, 91:2, 150-2
    The capacity of the oral bacteria Streptococcus mitior, S. mutans and S. sanguis to methylate mercury was investigated in vitro. Mercuric chloride and pulverized dental amalgam in distilled water, respectively, were used as sources of mercury. Methylmercury was found in the bacterial cells of all three tested strains. The results indicate that organic mercury compounds may be formed in the oral cavity.
  8. Cell-mediated immune response to dog pulp tissue altered by N2 paste within the root canal.
    Block RM; Sheats JB; Lewis RD; Fawley J
    Oral Surg Oral Med Oral Pathol, 1978 Jan, 45:1, 131-42
    After pulpal extirpation of twenty teeth in each of four dogs, these animals were primarily immunized intramuscularly with the dogs’ own pulp (three dogs) altered by N2 paste and saline solution with pulp (one dog). A fifth dog was used as a control for skin tests. Secondary immunizations were accomplished via the root canal every 7 days over a 28-day period. Cell-mediated skin tests reactions demonstrated less of a response to the N2 paste alone than when the dogs’ pulp was altered with this material. In vitro analysis of cell-mediated immune response (lymphocyte proliferation) showed a marked response to the pulp altered by N2 paste as compared to the saline-treated pulp (P less than 0.002). Therefore, dogs’ pulp tissue became antigenically altered by the N2 material, recognized by the host, and a specific cell-mediated lymphocyte proliferation resulted.
  9. Immunocompetent cells in amalgam-associated oral lichenoid contact lesions
    Lame J, Konttinen YT, Beliaev N, Happonen RP
    J Oral Pathol Med 1999 Mar;28(3):117-21
    Inflammatory cells in amalgam-associated, oral lichenoid contact lesions (OLL) were studied in 19 patients by immunocytochemistiy using monoclonal antibodies. Ten of the patients displayed allergic patch test (PT) reactions to several mercury compounds and nine were negative. The immunocytochemical quantification showed a uniform composition of the inflammatory mononuclear cells in the two study groups. The number of HLA-D/DR-positive dendritic cells (P<0.001) and CD1a-positive Langerhans cells (P=0.035) was significantly lower in the PT-negative than PT-positive patients. HLA-D/DR expression on keratinocytes varied from negative to full thickness staining of the epithelium. HLA-D/DR expression in the full thickness of epithelium (3) or through the basal and spinous cell layers (2) was seen in 5 of 8 PT-positive patients, whereas none of the PT-negative patients had this staining pattern (P=0.045). These patients also showed a good clinical response after amalgam removal. Consequently, OLL may represent a true delayed hypersensitivity reaction with a trans-epithelial route of entrance of the metal haptens released from dental restorative materials.



9. Metals and the Brain

    1. Immunological and Brain MRI Changes in Patients with Suspected Metal Intoxication
      Tibbling L; Thuomas KA; Lenkei R; Stejskal VD;
      International Journal of Occupational Medicine and Toxicology, Vol. 4, No. 2, 1995
      Thirty-four patients with central nervous system (CNS) and systemic symptoms suggestive of intoxication from dental amalgam were examined with magnetic resonance imaging (MRI) of the brain (n=32) and with a Memory Lymphocyte Immuno Stimulation Assay (MELISA®) (n=17). Lymphocyte phenotype was analyzed with flow cytometry (FC) in 22 of the patients. One hundred twenty age-matched patients without CNS symptoms served as controls for the MRI study, seventy-seven healthy subjects with dental amalgam fillings served as controls for the MELISA® test, and seventy-five clinically healthy subjects were controls for the lymphocyte phenotype determination. Pathological MRI findings were present in 81% of the patients, most of them with signs of degeneration in the basal ganglia, but none in the controls. The lymphocyte phenotype determination was pathological in 58%. The MELISA® showed pathological findings in 88%, of which 60% showed an immune reaction to mercuric chloride, 62% of the patients had some kind of atopic disease, and 35% suffered from levothyroxine-treated hypothyreosis. A high rate of immunopathologies and objective signs of immunological reactions in the majority of the patients with MRI changes in the brain suggests that immunological mechanisms may play an important role in the development of the lesions.
    2. Uptake of inorganic mercury in the olfactory bulbs via olfactory pathways in rats. Henriksson and Tjalve (1998). Environ. Res. 77:130-140.(9600806)
    3. Neurobehavioral effects from exposure to dental amalgam Hg0: new distinctions between recent exposure and Hg body burden. Echeverria D, et al. (1998).  FASEB J. 12:971-980. (9707169)


  • Behavioral effects of low-level exposure to Hg0 among dental professionals: a cross-study evaluation of psychomotor effects. Bittner et al., (1998). Neurotoxicol. Teratol20:429-439. (9697969)
  • Behavioral effects of low-level exposure to elemental Hg among dentists. Echeverria et al., (1995). Neurotoxicol. Teratol. 17:161-168. (7760775)
  • Chronic neurobehavioural effects of elemental mercury in dentists. Ngim et al., (1992). Br. J. Ind. Med49:782-790. (1463679)
  • Chronic elemental mercury intoxication: neuropsychological follow-up case study. Hua et al., (1996). Brain Inj. 10:377-384. (8735667)
  • Mercury vapor inhalation inhibits binding of GTP to tubulin in rat brain: similarity to a molecular lesion in Alzheimer diseased brain. Pendergrass et. al., (1997). Neurotoxicology 18:315-324.(9291481)
  • Inhibition of brain tubulin-guanosine 5′-triphosphate interactions by mercury: similarity to observations in Alzheimer’s diseased brain. Pendergrass and Haley (1997). Met. Ions Biol. Sys. 34:461-478.(9046580)
  • Demonstration of mercury in the human brain and other organs 17 years after metallic mercury exposure. Opitz et al., (1996). Clin. Neuropathol15:139-144. (8793247)
  • Entry of low doses of mercury vapor into the central nervous system. Pamphlett and Coote (1998). Neurotoxicology 19:39-47.(9498219)
  • Neurological abnormalities associated with remote occupational elemental mercury exposure. Albers et. al., (1988). Ann. Neurol. 24:651-659.(2849369)
  • 90.(9705135)
  • Oxidative damage to nucleic acids in motor neurons containing mercury. Pamphlett et al., (1998). J. Neurol. Sci. 159:121-126. (9741394)




10. Metals and Occupational Exposure

  1. A study on the beryllium lymphocyte transformation test and the beryllium levels in working environment.
    Yoshida T; Shima S; Nagaoka K; Taniwaki H; Wada A; Kurita H; Morita K
    Ind Health, 35(3):374-9 1997 Jul
    The relationship between airborne concentration of beryllium in the working environment and workers’ beryllium lymphocyte transformation test (Be-LTT) values was examined based on data obtained from a four-year survey (1992-1995) conducted at beryllium-copper alloy manufacturing factories. This study showed that the T cells of workers continuously exposed to beryllium of more than 0.01 microgram/m3 could be activated and that the cell-mediated immune response of workers could be promoted. On the other hand, the Be-LTT of workers exposed to beryllium levels of less than 0.01 microgram/m3 was shown to be unaffected by beryllium. These findings suggest that beryllium sensitization is not manifested when level of beryllium in working environment are less than 0.01 microgram/m3. Therefore, in such cases workers do not develop Chronic beryllium disease (CBD). We concluded that the Be-LTT can be applied as a medical indicator to detect the development of CBD.
  2. Effects of occupational exposure to mercury vapors on T-cell and NK-cell populations. Moszczynski et al., (1996). Arch. Med. Res. 27:503-507. (8987185)
  3. Mercury sensitization induced by environmental exposure. Mori et al., (1998). Nippon Eisenigaku Zasshi 52:661-666.(9528265)
  4. An epidemiological study of factors relating to mercury sensitization. Sato et al., (1995). Arerugi 44:86-92. (7726753)
  5. Toxicological and neurophysiological findings in patients presenting to an environmental toxicology service. Koppel and Fahron (1995). J. Toxicol. Clin. Toxicol. 33:625-629.(8523483)
  6. The effect of occupational exposure to mercury vapour on the fertility of female dental assistants. Rowland et al., (1994). Occup. Environ. Med. 51:28-34.(8124459)
  7. L’absorption, les niveaux sanguins, et excrétion de mercure après une dose unique de vapeurs mercurielles chez les humains. Sandborgh-Englund et al., (1998). Toxicol. Appl. Pharmacol150:146-153.(9630463)
  8. The absorption, blood levels, and excretion of mercury after a single dose of mercury vapor in humans. Sandborgh-Englund et. al., (1998). Toxicol. Appl. Pharmacol150:146-153.(9630463)
  9. Mercury in saliva and feces after removal of amalgam fillings. Bjorkman et al., (1997). Toxicol. Appl. Pharamcol. 144:156-162. (9169079)



11. Diagnostic Procedures in the Determination of Metal Toxicity

  1. Human Hapten-Specific Lymphocytes: Biomarkers of Allergy in Man
    Vera D. M. Stejskal, Ph.D.
    Drug Information Journal, Vol. 31, pp. 1379-1382, 1997
    Environmental pollutants and other chemicals may have increasing impact on the immune systems of human beings. Disregulation of the immune system by chemicals may be one of the reasons why the frequency of allergies and autoimmune diseases increases. Human hapten-specific memory lymphocytes can be detected in the blood from patients with drug-induced immunologic side-effects but not in similarly exposed healthy individuals. The immune reactivity of human lymphocytes in vitro to white coloring agent–titanium dioxide (TiO2), and to mercurial conservatives thimerosal and phenylmercury–has been studied. It was found that out of 650 patients tested, 3% reacted to titanium dioxide. The percentages for phenylmercury and thimerosal were 14% and 7%, respectively. Human memory cells can be used as markers of susceptibility in future choices of appropriate additives in pharmaceutic products.
  2. Mercury-specific lymphocytes: an indication of mercury allergy in man.
    Stejskal VD; Forsbeck M; Cederbrant KE; Asteman O
    Journal of Clinical Immunology, 16(1):31-40 1996 Jan
    In this study, 18 patients with oral lichen planus (OLP), adjacent to amalgam fillings, were tested in vitro with an optimized lymphocyte proliferation test, MELISA® (memory lymphocyte immunostimulation assay) and with a patch test. Twenty subjects with amalgam fillings but without oral discomfort and 12 amalgam-free subjects served as controls. The results show that patients with OLP have significantly higher lymphocyte reactivity to inorganic mercury, a corrosion product of amalgam, compared to control groups. Removal of amalgam fillings resulted in the disappearance of oral mucosal changes, thus indicating a causal relationship. Positive responses to phenylmercury (phenyl-Hg), a bactericidal agent in root fillings and in pharmaceutical preparations, were also noted in the oral lichen group but not in the control groups. Thus, low-grade chronic exposure to mercury may induce a state of systemic sensitization as verified by Hg-specific lymphocyte reactivity in vitro.
  3. Contact allergy to gold in dental patients.
    Räsänen L; Kalimo K; Laine J; Vainio O; Kotiranta J; Pesola I
    Br J Dermatol, 1996 Apr, 134:4, 673-7
    Gold sodium thiosulphate (GSTS) in patch test series commonly yields positive reactions. In this study of dental patients, the clinical relevance of these positive reactions, the suitability of gold compounds as patch test materials, and value of the lymphocyte proliferation test in gold contact allergy, were evaluated. The frequency of positive patch test reactions to GSTS was 12.4% in the dental series. Fifty-two patients, only two of whom were male, were studied. Thirteen (25%) had had symptoms from jewellery or dental restorations. However, in most cases gold allergy was subclinical. A 10% aqueous solution of gold sodium thiomalate (GSTM) was almost as good as 0.5% GSTS in petrolatum as a marker of gold contact allergy, but 0.001% potassium dicyanoaurate (PDCA) yielded a high percentage of false-negative results. Seventy-three per cent of the subjects with positive patch tests to GSTS responded to gold compounds in vitro in the lymphocyte proliferation test, whereas 13 controls without gold contact sensitivity were negative. Consistent results in skin and lymphocyte proliferation tests provide support for the concept that gold salt-induced ‘allergic-like’ reactions are truly allergic in nature.
  4. The relationship between IgE-mediated and cell-mediated hypersensitivities in an unselected Danish population: the Glostrup Allergy Study, Denmark.
    Nielsen NH; Menné T
    Br J Dermatol, 1996 Apr, 134:4, 669-72
    In this study, we have assessed the relationship between IgE-mediated and cell-mediated hypersensitivities in an unselected population living in western Copenhagen, Denmark. A total of 793 subjects, aged 15-69 years, were studied. Measurements of total serum IgE, prick tests with aero-allergens and patch tests with environmental haptens were performed in 561 (70.7% of 793) subjects. One or more positive prick tests were present in 28.4%, and contact sensitization occurred in 15.2%. When adjusted for the effects of sex and age, the probability of contact sensitization to one or more hapten was independent of serum IgE level (the odds ratio value (OR) = 1.0; 95% confidence interval (CI) = 0.7-1.4), and the probability of contact sensitization was independent of the number of positive prick tests (OR = 1.0; CI = 0.8-1.2). Contact sensitization appeared to be independent of enhanced IgE responsiveness in an unselected adult population.
  5. Contact allergies to nickel sulfate, gold sodium thiosulfate and palladium chloride in patients claiming side-effects from dental alloy components.
    Marcusson JA
    Contact Dermatitis, 1996 May, 34:5, 320-3
    397 patients claiming various subjective symptoms related to dental restoration materials have been tested for the presence of metal allergy. The resultant data have been compared with the corresponding allergies of eczematous patients. The frequency difference of metal allergy in the dental group is statistically significant or close to significance for nickel sulfate, potassium dichromate, cobalt chloride, palladium chloride and gold sodium thiosulfate. The findings suggest that the dental patient group represents a subgroup with a high frequency of metal allergy.
  6. Significance of the blood beryllium lymphocyte proliferation test.
    Newman LS
    Environ Health Perspect, 1996 Oct, 104 Suppl 5:, 953-6
    The blood beryllium lymphocyte proliferation test (BeLPT) is an in vitro measure of the beryllium antigen-specific cell-mediated immune response. This response to beryllium is now understood to play a central role in the immunopathogenesis of chronic beryllium disease (CBD). Although there remain some unresolved methodologic issues with testing, the blood BeLPT has already undergone sufficient development and field assessment to lead to a number of important conclusions: a) The BeLPT identifies beryllium sensitization and CBD earlier and better than any other clinical test presently available. b) The CBD cases identified with the blood test are clinically significant. c) A subset of the people identified by the BeLPT who do not yet have clinical disease will progress and require treatment with corticosteroids for impairing illness. d) The BeLPT can be used to improve clinical diagnostic accuracy and to correct mistaken diagnoses. e) The blood test can be used in screening large numbers of exposed workers because it is sensitive and specific and has high positive and negative predictive value for CBD. f) In every workforce studied to date, the BeLPT has identified beryllium sensitization and CBD that had been missed by conventional screening efforts. g) Worker populations that have been characterized using the BeLPT can help to elucidate the role of exposure genetics and dysregulated inflammation in the genesis of occupational lung disease.
  7. High frequency of contact allergy to gold sodium thiosulfate. An indication of gold allergy?
    Björkner B; Bruze M; Möller H
    Contact Dermatitis, 1994 Mar, 30:3, 144-51
    When gold sodium thiosulfate was added to the patch test standard series, positive reactions were obtained in 8.6% of 823 consecutive patients with suspect contact allergy. The test reactions were clinically of an allergic type and, in several cases, long-lasting. There was no correlation with other allergens in the standard series. In a special study on 38 patients with contact allergy to gold sodium thiosulfate, the following principal findings were obtained: positive patch tests to the compound itself in dilute concentration; positive patch tests to potassium dicyanoaurate; negative patch tests to gold sodium thiomalate, sodium thiosulfate, and metallic gold; positive intradermal tests to gold sodium thiosulfate. Our findings make gold sodium thiosulfate the 2nd most common contact allergen after nickel sulfate. It is suggested that a positive skin test to gold sodium thiosulfate represents gold allergy.
    V. D. M. Stejskal, K. Cederbrandt, A. Lindvall, M. Forsbeck
    Toxicology in Vitro, Vol. 8; Number 5; pp. 991-1000, 1994
    The sensitizing properties of metals widely used in medical and dental care have been studied with the help of an optimized lymphocyte proliferative assay, MELISA®. MELISA® (memory lymphocyte immuno-stimulation assay) was originally developed for the screening of allergenic epitopes of drugs and other chemicals of low molecular weight, but has recently been adapted for the study of metal-induced sensitization. The patients studied suffered from various mucosal problems which were suspected to be caused by the release of metal ions from dental restorations. They were also troubled by chronic fatigue persisting over many years. One patient was also occupationally exposed to metals while working in a dental practice. Healthy subjects without any discomfort due to metal devices served as controls. In addition to metals used in dentistry, lymphocyte responses to organic mercurials used widely as preservatives in vaccines, eye/nose drops and contact lens fluids were studied. The results indicated that mercurials, as well as other metals such as gold or palladium, induce strong lymphocyte proliferative responses in patients with oral or systemic symptoms, but not in similarly exposed unaffected subjects. The results of MELISA® performed with a pair of identical twins with chronic fatigue syndrome (CFS) indicated that metal-specific responses may be dependent on the genetics of the patient. Thus, many metals that are today accepted for use in medicine and dentistry carry a definite sensitizing risk for certain genetically predisposed individuals. Therefore, the use of these metals should be limited in the future.
  9. Human exposure to mercury and silver released from dental amalgam restorations.
    Skare I; Engqvist A
    Arch Environ Health, 1994 Sep, 49:5, 384-94
    In 35 healthy individuals, the number of amalgam surfaces was related to the emission rate of mercury into the oral cavity and to the excretion rate of mercury by urine. Oral emission ranged up to 125 micrograms Hg/24 h, and urinary excretions ranged from 0.4 to 19 micrograms Hg/24 h. In 10 cases, urinary and fecal excretions of mercury and silver were also measured. Fecal excretions ranged from 1 to 190 micrograms Hg/24 h and from 4 to 97 micrograms Ag/24 h. Except for urinary silver excretion, a high interplay between the variables was exhibited. The worst-case individual showed a fecal mercury excretion amounting to 100 times the mean intake of total Hg from a normal Swedish diet. With regard to a Swedish middle-age individual, the systemic uptake of
  10. Diagnostic value of the lymphocyte proliferation test in nickel contact allergy and provocation in occupational coin dermatitis.
    Räsänen L; Tuomi ML
    Contact Dermatitis, 1992 Oct, 27:4, 250-4
    The lymphocyte proliferation test (LPT) was compared with the patch test in the diagnosis of nickel contact sensitivity. Of the 21 subjects with nickel contact allergy, the patch test detected 20 (95%). The subject remaining negative in the patch test was positive in the intradermal test. 18/21 subjects with nickel contact sensitivity were positive in the LPT, whereas in the control group 2/23 subjects were false positive. These results were obtained at nickel sulfate concentrations of less than 10 micrograms/ml, higher concentrations led to nonspecific lymphocyte stimulation. 3 nickel-sensitive cashiers with suspected coin contact-induced deterioration of their hand eczema were challenged by having them count nickel-containing coins daily for 15 min. 2 of them developed vesicular eczema on their palms and fingers in 2 to 3 days. The present results show that the LPT is a reliable additional test in the diagnosis of nickel contact sensitivity. Furthermore, provocation is a valuable procedure when assessing the relevance of nickel contact in occupational hand eczema in certain occupations.
  11. Lymphocyte Transformation test for Diagnosis of Isothiazoline Allergy in Man
    V. D. M. Stejskal, M. Forsbeck, R. Nilsson
    The Journal of Investigative Dermatology 94:798-802, 1990
    The lymphocyte transformation test (LTT) has been used for evaluation of in vitro lymphocyte responses in 18 patients with dermatitis and positive patch tests to 200 ppm of a combination of 5-chloro-2-methylisothiazolinone and 2-methtylisothiazolinone (MCI) in nine patients with dermatitis unrelated to MCI and in seven subjects without skin diseases. Two workers sensitized by occupational exposure to formulation containing 1,2-benzisothiazolin-3-one (BIT)were also studied. Lymphocytes from nine patch-test-positive patients proliferated vigorously to MCI in vitro. Lymphocytes from the remaining nine patients were not stimulated. Lymphocytes from two BIT-sensitized workers responded to BIT in vitro. The lymphocyte proliferation to isothiazolines indicates the presence of memory cells in the patients blood and confirms immunologic reaction to the inducing agent. To establish clinical relevance of LTT results, 12 MCI patch-test-positive patients underwent « use test » with lotion containing 15 ppm MCI. Four of five LTT-positive patients were use-test-positive, whereas seven of seven LTT-negative patients were use-test-negative. LTT-positive and lotion-positive patients responded to 100 ppm or lower concentrations of MCI on patch testing, whereas seven of eight LTT-negative and lotion-negative patients responded to 200 ppm only. In the case of MCI, proliferation was due to the chlorinated component, indicating that this part contains an allergenic epitome. Finally, MCI-specific lymphocyte proliferation was observed only in patients with MCI-positive skin test, but not in nine patients with dermatitis induced by other agents, or in seven subjects without skin diseases. Thus, the lymphocyte transformation test is able to distinguish between irritant and allergic responses. It may also be valuable in establishing the clinically relevant patch-test concentration of allergens with irritative properties.
  12. Development of low- and high-serum culture conditions for use of human oral fibroblasts in toxicity testing of dental materials. Liu et. al., (1991). J. Dent. Res. 70:1068-1073.



12. Release of mercury and metals from dental feelings or from other source

    1. Mobilisation du mercure et de l’arsenic dans les être humains par le sodium 2,3-dimercapto-1-propane sulfonate (DMPS). Aposhian (1998). Environ. Health Perspect. 106:1017-1025. (9703487)
    2. Le mercure dans les fluides biologiques après la dépose d’amalgames dentaires. Sandborgh-Englund et al., (1998). J. Dent. Res. 77:615-624. (9539465)
    3. L’absorption, les niveaux sanguins, et excrétion de mercure après une dose unique de vapeurs mercurielles chez les humains. Sandborgh-Englund et al., (1998). Toxicol. Appl. Pharmacol150:146-153.(9630463)
    4. Aspects toxicologiques du relargage et ingestion systématique de mercure provenant des amalgames dentaires. Ekstrand et. al., (1998). Eur. J. Oral Sci. 106:678-686.(9584901)
    5. L’influence des amalgames dentaires sur le niveau de mercure dans les urines chez les sujets d’Apulia. Soleo et. al., (1998). G. Ital. Med. Lav. Ergon20:75-81.(9658238)
    6. Systemic transfer of mercury from amalgam fillings before and after cessation of emission. Halbach et. al., (1998). Environ. Res. 77:115-123.(9600804)
    7. Mercury as a potential hazard for the dental practitioner. Kostyniak (1998). N.Y. State Dent. J. 64:40-43.(9613096)
    8. Methylmercury and inorganic mercury in serum-correlation to fish consumption and dental amalgam in a cohort of women born in 1922. Bergdahl et. al., (1998). Environ. Res77:20-24.(9593624)
    9. Mercury and dental amalgam fillings. Lygre et. al., (1998). Tidsskr. Nor. Laegeforen 118:1698-1701.(9621758)
    10. The absorption, blood levels, and excretion of mercury after a single dose of mercury vapor in humans. Sandborgh-Englund et. al., (1998). Toxicol. Appl. Pharmacol150:146-153.(9630463)
    11. Mercury in saliva and feces after removal of amalgam fillings. Bjorkman et al., (1997). Toxicol. Appl. Pharamcol. 144:156-162. (9169079)
    12. Effect of Pd and In on mercury evaporation from amalgams. Okabe et. al., (1997). Dent. Mater. J. 16:191-199. (9555257)
    13. Mercury exposure from dental amalgam fillings: absorbed dose and the potential for adverse health effects. Mackert and Berglund (1997). Crit. Rev. Oral Biol. Med8:410-436.(9391753)
    14. The future of dental amalgam: a review of the literature. Part 2: Mercury exposure in dental practice. Eley (1997). Br. Dent. J182:293-297.(9154707)
    15. The future of dental amalgam: a review of the literature. Part 3: Mercury exposure from amalgam restorations in dental patients. Eley (1997). Br. Dent. J182:333-338.(9175289)
    16. Effect of Pd and In on mercury evaporation from amalgams. Okabe et. al., (1997). Dent. Mater. J. 16:191-199.(9555257)
    17. Patterns of mercury release from amalgam fillings into the oral cavity. Motorkina et. al., (1997). Stomatologiia (Mosk.) 76:9-11.(9381508)
    18. Compartmental transfer of mercury released from amalgam. Halbach et al., (1997). Hum. Exp. Toxicol.16:667-672. (9426369)
    19. Impact of nocturnal bruxism on mercury uptake from dental amalgams. Isacsson et. al., (1997). Eur. J. Oral. Sci. 105:251-257.(9249192)
    20. Dissolution of mercury from dental amalgam at different pH values. Marek (1997). J. Dent. Res. 76:1308-1315.(9168865)
    21. Intial mercury evaporation from amalgams made with In-containing commercial alloys. Nakajima et. al., (1996). Dent. Mater. J. 15:168-174.(9550014)
    22. Influence of chewing gum consumption and dental contact of amalgam fillings to different metal restorations on urine mercury content. Gebel and Dunkelberg (1996). Zentralbl. Hyg. Umweltmed. 199:69-75.(9409909)
    23. Long-term use of nicotine chewing gum and mercury exposure from dental amalgam fillings. Sallsten et. al., (1996). J. Dent. Res. 75:594-598.(8655765)
    24. Mercury exposure from « silver » tooth fillings: emerging evidence questions a traditional paradigm. Lorscheider et al., (1995). FASEB J. 9:504-508.   (7737458)
    25. Mercury levels among dental personnel in Isreal: a preliminary study. Steinberg et al., (1995). Isr. J. Med. Sci. 31:428-432. (7607870)
    26. People with high mercury uptake from their own dental amalgam fillings. Barregard et al., (1995). Occup. Environ. Med. 52:124-128. (7757165)
    27. Sodium 2,3-dimercaptopropane-1-sulfonate challenge test for mercury in humans: II. Urinary mercury, porphyrins and neurobehavioral changes of dental workers in Monterrey, Mexico. Gonzalez-Ramirez et. al., (1995). J. Pharmacol. Exp. Ther272:264-274.(7815341)
    28. Silver concentrations in human tissues. Their dependence on dental amalgam and other factors. Drasch et. al., (1995). J. Trace Elem. Med. Biol. 9:82-87.(8825980)
    29. An estimation of the uptake of mercury from amalgam fillings based on urinary excretion of mercury in Swedish subjects. Weiner and Nylander (1995). Sci. Total Environ. 168:255-265. (7644912)
    30. Mercury vaporization from amalgams with varied alloy compositions. Ferrancane et. al., (1995). J. Dent. Res. 74:1414-1417.(7560393)
    31. Combined estimation of mercury species released from amalgam. Halbach (1995). J. Dent. Res. 74:1103-1109.(7782541)
    32. Estimation of mercury dose by a novel quantitation of elemental and inorganic species released from amalgam. Halbach (1995). Int. Arch. Occup. Environ. Health 67:295-300.   (8543376)
    33. Human exposure to mercury and silver released from dental amalgam restorations. Skare and Engqvist (1994). Arch. Environ. Health 49:384-394. (7944571)
    34. Mercury concentrations in the urine of children with and without amalgam fillings. Schulte et al., (1994). Schweiz Monatsschr Zahnmed 104:1336-1340. (7984991)
    35. Amalgam tooth fillings and man’s mercury burden. Halbach (1994). Hum. Exp. Toxicol13:496-501.(7917507)
    36. Long-term mercury excretion in urine after removal of amalgam fillings. Begerow et. al., (1994). Int. Arch. Occup. Environ. Health 66:209-212.(7814102)
    37. Evaluation of the safety issue of mercury release from dental fillings. Lorscheider and Vimy. (1993). FASEB J. 7:1432-1433. (8262327)
    38. The relationship between mercury concentration in human organs and different predictor variables. Weiner and Nylander (1993). Sci. Total Environ138:101-115. (8259485)
    39. An in vitro and in vivo study of the release of mercury vapor from different types of amalgam alloys. Berglund (1993). J. Dent. Res. 72:939-946.(8501292)
    40. Mercury release from amalgam into saliva. An in-vitro study. Lussi (1993). Schweiz. Monatsschr. Zahnmed. 103:722-726.(8322057)
    41. Urinary mercury after administration of 2,3-dimercaptopropane-1-sulfonic acid: correlation with dental amalgam score. Aposhian et al., (1992). FASEB J6:2472-2476. (1563599)
    42. Mercury concentration in the mouth mucosa of patients with amalgam fillings. Willershausen-Zonnchen et. al., (1992). Dtsch. Med. Wochenschr. 117:1743-1747.(1425293)
    43. Side-effects: mercury contribution to body burden from dental amalgam. Reinhardt (1992). Adv. Dental Res. 6:110-113.(1292449)
    44. Dental amalgam: the materials. Marshall and Marshall (1992). Adv. Dent. Res6:94-99.(1292469)
    45. Quantitation of total mercury vapor released during dental procedures. Engle et. al., (1992). Dent. Mater.8:176-180.(1521706)
    46. Daily dose calculations from measurements of intra-oral mercury vapor. Olsson and Bergman (1992). J. Dent. Res71:414-423.(1556301)
    47. Mercury exposure of the population. IV. Mercury exposure of male dentists, female dentists and dental aides.  Zander et. al., (1992). Zentralbl. Hyg. Umweltmed193:318-328. (1290562)
    48. The mercury exposure of the population. III. Mercury mobilisation by DMPS (Dimaval) in subjects with and without amalgam fillings. Zander et. al., (1992). Zentralbl. Hyg. Umweltmed192:447-454.(1554403)
    49. Release of mercury vapor from dental amalgam. Berglund (1992). Swed. Dent. J. Suppl85:1-52.(1475757)
    50. Factors influencing mercury evaporation rate from dental amalgam fillings. Bjorkman and Lind (1992). Scand. J. Dent. Res. 100:354-360. (1465570)
    51. Amalgam fillings-a considerable source of exposure to heavy metals. Skare and Engqvist (1992). Lakartidningen 89:1299-1301. (1579001)
    52. Daily dose estimates of mercury from dental amalgams. Lorscheider and Vimy. (1991). J. Dent. Res. 70:233-237. (1999563)
    53. The dental amalgam issue. A review. Hanson and Pleva (1991). Experientia 47:9-22.(1999251)
    54. Significance of hydrogen ion concentration on the dissolution of mercury from dental amalgam. Soh et. al., (1991). Quintesence Int. 22:225-228.(2068263)
    55. Thermal effect on dissolution of mercury from two dental amalgams. Soh et. al., (1991). J. Oral Rehabil. 18:179-183.(2037941)
    56. Long-term dissolution of mercury from a non-mercury-releasing amalgam. Chew et. al., (1991). Clin. Prev. Dent. 13:5-7.(1860296)
    57. The mercury release of different amalgams in vitro. Lussi and Schoenberg (1991). Schweiz Monatsschr Zahnmed. 101:1405-1408.(1962164)
    58. Whole-body imaging of the distribution of mercury released from dental fillings into monkey tissues. Hahn et al., (1990). FASEB J4:3256-3260. (2227216)
    59. Estimation by a 24-hour study of the daily dose of intra-oral mercury vapor inhaled after release from dental amalgam. Berglund (1990). J. Dent. Res69:1646-1651.(2212208)
    60. Exposure to mercury in the population. I. Mercury concentrations in the urine of normal subjects.. Zander et. al., (1990). Zentralbl. Hyg. Umweltmed190:315-324. (2080963)
    61. Exposure to mercury in the population. II. Mercury release from amalgam fillings. Zander et. al., (1990). Zentralbl. Hyg. Umweltmed190:325-334. (2080964)
    62. Mercury release of silver amalgams in vitro. Hellwig et. al., (1990). Dtsch. Zahnarztl. Z45:17-19.(2257794)
    63. Mercury release from amalgam: a study in vitro and in vivo. Ahmed and Stannard (1990). Oper. Dent.15:207-218.(2095533)
    64. Mercury as a pollutant in the dental profession. I. Its biological cycle, toxicity and monitoring. Valerio et. al., (1990). Minerva Stomatol. 39:625-628.(2287331)
    65. Mercury exposure of different origins among dentists and dental nurses. Skare et al., (1990). Scand. J. Work Environ. Health 16:340-347. (2255875)
    66. Mercury, selenium, and glutathione peroxidase before and after amalgam removal in man. Molin et al., (1990). Acta Odontol. Scand48:189-202. (2368614)
    67. The influence of dental amalgam placement on mercury, selenium, and glutathione peroxidase in man. Molin et al., (1990). Acta Odontol. Scand48:287-295. (2220337)
    68. Dental « silver » tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis. Hahn et al., (1989). FASEB J. 3:2641-2646. (2636872)
    69. Mercury vapor from dental amalgams, an intro study. Derand (1989). Swed. Dent. J13:169-175.(2814828)
    70. Dental « silver » tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis. Hahn et. al., (1989). FASEB J. 3:2641-2646.(2636872)
    71. Dental amalgam: a review of the literature. Eggleston (1989). Compendium 10:500-505.(2700133)
    72. Comparison of release of mercury from three dental amalgams. Chew et. al., (1989). Dent. Mater. 5:244-246.(2638267)
    73. Dental amalgam and mercury. Aronsson et. al., (1989). Biol. Met2:25-30.(2485649)
    74. Effect of admixed indium on mercury vapor release from dental amalgam. Powell et. al., (1989). J. Dent. Res. 68:1231-1233.(2632609)
    75. Dissolution of metallic mercury in artificial saliva  and eleven other solutions. Takahashi et. al., (1989).Dent. Mater. 5:256-259.(2638269)
    76. Dental amalgam and mercury. Aronsson et al., (1989). Biol. Met2:25-30. (2485649)


  • Prospective study on the mercury uptake of dental students. Part 1: Increase in mercury excretion during simulated training. Pieper et. al., (1989). Dtsch. Zahnarztl. Z44:714-716.(2637853)
  • Determination of the rate of release of intra-oral mercury vapor from amalgam. Berglund et. al., (1988). J. Dent. Res67:1235-1242.(3166008)
  • Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings. Nylander et. al., (1987). Swed. Dent. J11:179-187.(3481133)
  • Examination of blood levels of mercurials in practicing dentists using cold-vapor atomic absorption spectrometry. Chang et. al., (1987). J. Anal. Toxicol. 11:149-153.(3626527)
  • Potential health hazard of use of mercury in dentistry: critical review of the literaure. Enwonw (1987) Environ. Res. (1987). 42:257-274.(3542524)
  • Metal release from dental biomaterials. Brune (1986). Biomaterials 7:163-175.(3521750)
  • Estimation of mercury body burden from dental amalgam: computer stimulation of a metabolic compartment model. Vimy et. al., (1986). J. Dent. Res. 65:1415-1419.(3465771)
  • Intra-oral air mercury released from dental amalgam. Vimy and Lorscheider (1985). J. Dent. Res. 64:1069-1071. (3860538)
  • Serial measurements of intra-oral air mercury: estimation of daily dose from dental amalgam. Vimy and Lorscheider (1985). J. Dent. Res. 64:1072-1075. (3860539)
  • A model for recording mercury relaease from an amalgam surface. Brune (1985). Biomaterials 6:357-359.(4052550)
  • Man’s mercury loading from a dental amalgam. Brune and Evje (1985). Sci. Total Environ. 44:51-63.(4023695)
  • Initial corrosion of amalgams in vitro. Brune an Evje (1984). Scand. J. Dent. Res92:165-171.(6585923)
  • Mercury toxicity and dental amalgam. Wolff et. al., (1983). Neurotoxicology 4:201-204.(6361623)
  • Corrosion of amalgams. Brune (1981). Scand. J. Dent. Res89:506-514.(6951250)
  • Release of mercury from amalgam fillings into salival. Mayer and Diehl (1976). Dtsch. Zahnarztl. Z.31:855-859.(1068794)




13.  periodontal disease, genetic and metal causes

  1. Linkage disequilibrium of interleukin-1 genetic polymorphisms with early-onset periodontitis. Diehl SR, Wang Y, Brooks CN, et al. J Periodontol (United States), Apr 1999, 70(4) p418-30
  2. McDevitt MJ, Wang HY, Knobelman C, et al.Interleukin-1 genetic association with periodontitis in clinical practice.
    J Periodontol (United States), Feb 2000, 71(2) p156-63
  3. Kornman KS, di Giovine FS  Genetic variations in cytokine expression: a risk factor for severity of adult periodontitis.
    Ann Periodontol (United States), Jul 1998, 3(1) p327-38
  4. Kornman KS, Pankow J, Offenbacher S, et al. Interleukin-1 genotypes and the association between periodontitis and cardiovascular disease. J Periodontal Res (Denmark), Oct 1999, 34(7) p353-7
  5. Kornman KS, Knobelman C, Wang HY  Is periodontitis genetic? The answer may be Yes!.
    J Mass Dent Soc (United States), Autumn 2000, 49(3) p26-30
  6. Cullinan MP, Westerman B, Hamlet SM, et al.A longitudinal study of interleukin-1 gene polymorphisms and periodontal disease in a general adult population. J Clin Periodontol (Denmark), Dec 2001, 28(12) p1137-44
  7. Sandroff T  A genetic predisposition to periodontal disease.  CDS Rev (United States), Dec 1998, 91(9) p32-4
  8. Thomson WM, Edwards SJ, Dobson-Le DP, et al.  IL-1 genotype and adult periodontitis among young New Zealanders.
    J Dent Res (United States), Aug 2001, 80(8) p1700-3 
  9. Loss of mercury from amalgam fillings and abnormal oral bacterial flora as a cause of periodontal disease. Till (1978). ZWR 87:1076-1083.(282721) 



14. Metals and Alzheiner’s disease, multiple sclerosis, Amyotrophic lateral sclerosis, Parkinson, Fibromyalgy


15. Study on animals

    1. A stereological study of dorsal root ganglion cells and nerve root fibers from rats exposed to mercury vapor. Schionning et al., (1998) Acta Neuropathol. 96:185-1
    2. Mercury in the rat hypothalamic arcuate nucleus and median eminence after mercury vapor exposure. Ernst et al., (1993). Exp. Mol. Pathol. 58:205-214. (8519347)
    3. Behavioral effects of neonatal metallic mercury exposure in rats. Frederickson et. al., (1992). Toxicology74:151-160.(1519238)
    4. Effect of subchronic mercury exposure on electrocorticogram of rats. Desi et al., (1996). Neurotoxicology17:719-723. (9086494)
    5. Detection of mercury in rat spinal cord and dorsal root ganglia after exposure to mercury vapor. Schionning et al., (1993). Exp. Mol. Pathol58:215-228.((8519348) 
    6. Pathological changes in the Brown Norway rat cerebellum after mercury vapour exposure. Hua et al., (1995). Toxicology 104:83-90. (8560505)
    7. Metallothionein induction in fetal rat brain and neonatal primary astrocyte cultures by in utero exposure to elemental mercury vapor (Hg0). Aschner et al., (1997). Brain Res778:222-232. (9462895)
    8. Does mercury from amalgam restorations constitute a health hazard. Weiner et al., (1990). Sci. Total Environ. 99:1-22.(2270464)


  • Behavioural effects of neonatal metallic mercury exposure in rats. Fredriksson et. al., (1992). Toxicology 74:151-160.(1519238)
  • Prenatal coexposure to metallic mercury vapour and methylmercury produce interactive behavioural changes in adult rats. Fredriksson et. al., (1996). Neurotoxicol. Teratol18:129-134.(8709923)
  • Behavioural effects of prenatal metallic mercury inhalation exposure in rats. Danielsson et. al., (1993). Neurotoxicol. Teratol15:391-396.(8302240)
  • Behavioral consequences of in utero exposure to mercury vapor: alterations in lever-press durations and learning in squirrel monkeys. Newland et. al., (1996). Toxicol. Appl. Pharmacol. 139:374-386.(8806855)
  • Mercury distribution in cortical areas and fiber systems of the neonatal and maternal adult cerebrum after exposure of pregnant squirrel monkeys to mercury vapor. Warfvinge et al., (1994). Environ. Res. 67:196-208. (7982394)
  • Distribution of mercury in guinea pig offspring after in utero exposure to mercury vapor during late gestation. Yoshida et al., (1986). Arch. Toxicol. 58:225-228. (3718224)
  • Exposure to mercury via breast milk in suckling offspring of maternal guinea pigs exposed to mercury vapor after parturition. Yoshida et. al., (1992). J. Toxicol. Environ. Health 35:135-139.(1542135)
  • Milk transfer and tissue uptake of mercury in suckling offspring after exposure of lactating maternal guinea pigs to inorganic or methylmercury. Yoshida et. al., (1994). Arch. Toxicol. 68:174-178.(8024464)
  • Kinetics of methylmercury and inorganic mercury in lactating and nonlactating mice. Sundberg et al., (1998). Toxicol. Appl. Pharmacol. 151:319-329. (9707508)  




16. Metals, fertility, embryogenesis

    1. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Vimy et. al., (1990).Am. J. Physiol. 258:R939-R945.(2331037)
    2. Maternal amalgam and prenatal mercury exposure. Halbach and Summer (1995). Eur. J. Pediatr. 154:498-499. (7671951)
    3. Mercury burden of human fetal and infant tissues. Drasch et al., (1994). Eur. J. Pediatr. 153:607-610. (7957411)
    4. Concentration of mercury, cadmium and lead in brain and kidney of second trimester fetuses and infants. Lutz et. al., (1996). J. Trace Elem. Med. Biol. 10:61-67.(8829128)
    5. Dental amalgam and pregnancy. Drasch and Roider (1995). Geburtshilfe Frauenheilkd 55:63-65.   (7657132)
    6. Heavy metals and fertility. Gerhard et al., (1998). J. Toxicol. Environ. Health 54:593-611. (9726782)
    7. Impact of heavy metals on hormonal and immunological factors in women with repeated miscarriages. Gerhard et al., (1998). Hum. Reprod. Update 4:301-309. (9741713)
    8. Environmental pollutants and fertility disorders. Heavy metals and minerals. Gerhard and Runnebaum (1992). Geburtshilfe Frauenheilkd 52:383-396. (1499949)
    9. Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption. Urbach et. al., (1992). Reprod. Toxicol. 6:69-75.(1562801)
    10. In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta. Boadi et. al., (1992). Environ. Res57:96-106.(1740099)
    11. In vitro effect of mercury on aryl hydrocarbon hydroxylase, quinone reductase, catecholamine-O-methyltransferase and glucose-6-phosphate dehydrogenase activities in term human placenta. Boadi et. al., (1991). Pharmacol. Toxicol. 68:317-321.(1946176)
    12. Toxic effects on embryos derived from amalgam restorations containing mercury. West German considerations. Strubelt et. al., (1989). Tandlakartidningen 81:283-290.(2623622)
    13. Breast-feeding exposure of infants to cadmium, lead, and mercury: a public health viewpoint. Abadin et al., (1997). Toxicol. Ind. Health 13:495-517. (9249931)
    14. Total and inorganic mercury in breast milk in relation to fish consumption and amalgam in lactating women. Oskarsson et al., (1996). Arch. Environ. Health 51:234-241.   (8687245)
    15. Exposure to toxic elements via breast milk. Oskarsson et al., (1995). Analyst 120:765-770.   (7741226)
    16. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Drexler and Schaller (1998). Environ. Res77:124-129.(9600805)


  • Mercury in human colostrum and early breast milk. Its dependence on dental amalgam   and other factors. Drasch et. al., (1998). J. Trace Elem. Med. Biol. 12:23-27.(9638609
  • Occupational mercury vapour exposure and testicular, pituitary and thyroid endocrine function. McGregor and Mason (1991). Hum. Exp. Toxicol. 10:199-203.(1678950)
  • Paternal exposure to mercury and spontaneous abortions. Cordier et. al., (1991). Br. J. Ind. Med. 48:375-381.(2064975)
  • Effect of organic and inorganic mercury on human sperm motility. Ernst and Lauritsen (1991). Pharmacol. Toxicol68:440-444.(1653954)
  • Autometallographic detection of mercury in testicular tissue of an infertile man exposed to mercury vapor. Keck et al., (1993). Reprod. Toxicol7:469-475. (8274823)    
  • Hong Kong male subfertility links to mercury in human hair and fish. Dickman et al., (1998). Sci. Total Environ. 214:165-174. (9646524)
  • Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Vimy et. al., (1990).Am. J. Physiol. 258:R939-R945.(2331037)



17. Diabetes and periodontal disease

  1. American Academy of Periodonology. Position Paper : Diabetes and Periodontal Diseases. J Periodontol1999 ;70 :935-949.
  2. Aldbridge J.P., Lester V., Watts T.L.P., Collins A., Viberti G, Wilson R.F. Single-blind studies os the effects os improved periodontal health on metabolic control in type 1 diabetes mellitus. J. Clin. Periodontol.,1995,22 : 271-275
  3. Beck J., Garcia R., Heiss G., Vokonas P. & Offenbacher S. (1996). Periodontal disease and cardiovasculars disease. J periodontol 1996 ;67 :1123-1137.
  4. Belting CM, Hiniker JJ, Dummett CO. Influence of diabetes mellitus on the severity of periodontal disease. J Periodontol 1964 ;35 :476-480.
  5. Bernick SM, Cohen DW, Baker L, Laster L. Dental disease in children with diabetes mellitus. J Periodontol1975 ;46 :241-245.
  6. Brownlee M, Cerami A, Vlassara H. Advanced products of non-enzymatic glycosilation and the pathogenesis of diabetic vascular disease. Diabetes Metab Rev 1988 ;4 :437-451.
  7. Caenazzo A, Pietrogrande F, Polato G, Piva E, Sartori D, Girolami A. Devreased platelet mitogenic activity in patients with diabetes mellitus. Hematologia 1991 ; 24 :241-247.
  8. CHARBONNEL B. – La nouvelle classification et les nouveaux critères des anomales du métabolisme glucidique. Act. Med. Int. – Métabolisme – Hormones – Nutrition. 3, 1998, 6-10
  9. Cohen MP. Non-enzymatic glycosylation. Diabetes Annual 1988 ;4 :469-484.
  10. Collins J.G., Smith M.A., Arnold R.R. & Offenbacher S. Effects of Escherichia coli and Porphyromonas gingivalis liposaccharide on pregnancy outcome in the golden hamster. Infection and Immunity 1994 ; 62 :4652-4655.
  11. Delcourt C. et Papoz L. – Le diabète et ses complications dans la population française – Paris, INSERM,1996. Côté L9kDEL à la BU Reims Santé.
  12. DERSOT J-M., il n’y a pas de maladie parodontal en France ! – Inform. Dent., 1999, Vol. 81, 10, 661-669
  13. DeStefano F., Andra R.F., Kahn H.S., Willamson D.F. & Russell C.M. Dental disease and risk of coronay heart disease and mortality. British Medical Journal 1993 ;306 :688-691.
  14. Emrich L., Shlossman M., Genco RJ. Periodontal disease in non-insulino-dependant diabetes mellitus. J. Periodontol., 1991;62 :123-130.
  15. Ervasti T, Knuuttila M, Pohjamo L, Haukipuro K. Relation between control of diabetes and gingival bleeding. J periodontol 1985 ;56 :154-157.
  16. Gislen G, Nilsson KO, Matson L. Gingival inflammation in diaetic children related to degree of metabolic control.  Acta Odontol Scand 1980 ;38 :241-246.
  17.  Glavind L, Lund B, Löe H. The relationship between periodontal state and dibetes duration, insulin dosage and retinal changes. J Periodontol 1965 ;39 :341-347.
  18.  Golub LM, Scneir M, Ramamurthy NS. Enhanced collagenase activity in diabetic rat gingiva : in vitro ans in vivo evidence. J Dent Res 1978 ;57 :520-525.
  19.  Golub LM, Lee HM, Lehrer G, et al. Minocycline reduces gingival collagenolytic activity during diabetes. Preliminary observations and a proposed new mecanism of action. J Periodont Res 1983 ;18 :516-526.
  20. Golub LM, Nicoll GA, Iacono VJ, Ramamurthy NS. In vivo crevicular leucocyte response to a chemotactic challenge :Inhibition by experimental diabetes. Infect Immun 1982 ;37 :1013-1020.
  21. Grossi S.G., Skrepcinski F.B., Arnold R.R., DeCaro T., Zambon J.J., CumminsS D., Genco R.J. – Responses to periodontal therapy in diabetics and smokers. J. Periodontol., 1996, 67(suppl.), 1094-1102
  22.  Grossi Sara G., Genco RJ. Periodontal Disease and Diabetes Mellitus : a two-Way Relationship. Annals of Periodontology 1998 ;3 :54-60
  23.  Gusberti FA, Syed SA, Bacon G, Grossman N, Loesch WJ. Puberty gingivitis in insulin-dependent diabetic children. 1. Bross-sectional observations. J Periodontol 1983 ;54 :714-720
  24.  Hirschfeld I. Periodontal symptoms associated with diabetes. J Periodontol 1934 ;5 :37-46.
  25. Hugson A, Thorstensson H, Falk H, Kuylenstierna J. Periodontal conditions in insulin-dependent diabetics. J Clin Periodontol 1989 ;16 :215-223.
  26. Iacono Vj, Singh S, Golub LM, Ramamurthy NS, Kaslick R. In vivo assay of crevicular leucocyte migration. Its development and potential applications. J periodontol 1985 ;56(Suppl.2) :56-62
  27. Katz PP, Wirthlin MR Jr, Szpunar SM, Selby JV, Sepe SJ. Showstack JA. Epidemiology ans prevention of periodontol disease in individuals with diabetes. Diabetes Care 1991 ;14 :375-385.
  28. Kirstein M, Aston C, Hintz R, Vlassara H. Receptor specific induction of insulin-like growth factor I in human monocytes by advanced glycosylation end product-modified proteins. J Clin Invest 1992 ;90 :439-446.
  29. Kweider M., Lowe G.D., Muray G.D., Kinane D.F. & McGowan D.A. Dental disease, fibrinogen and white cell count ; links with myocardial infarction ? Scottish Medical Journal 1993 ;38 :73-74.
  30. LALLA E., LAMSTER IB., SCHMIDT AM. – Enhanced interaction of advanced glycation end products with their cellulae receptor RAGE : implications for the pathogenesis of accelerated periodontal disease in diabetes., Annals of Periodontology. 3(1) :13-9, 1998
  31. Listgarten MA, Laster L, Shapiro J, Cohen DW. Vascular basement lamina thickness in the normal and inflammed gingiva of diabetic and non-diabetic.  J Periodontol 1974 ;45 :676-684.
  32.  Manouchehr-Pour M, Spagnulo PJ, Rodman HM, Blissada NF. Comparison of neutrophil chemotactic response in diabetic patients with mild ans severe periodontal disease. J Periodontol 1981 ;52 :410-415.
  33. Matilla K.J. Dental infections as a risk factor for acute myocardial infarction. European Heart Journal1993 ;14 :51-53.
  34. Matilla K.J., Valle M.S., Nieminen M.S., Valtonen V.V. & Hietaniemi K.L. Dental infections and coronary atherosclerosis. Atherosclérosis 1993 ;103 :205-211.
  35. NELSON R.G., SHLOSSMAN M., BUDDING L.M, coll. – Periodontal disease and non-insulin-dependant diabetes mellitus in Pima Indians. Diabetes Care, 1990, 13, 836-840.
  36. Nishimura F, Takahashi K, Kurihara L, Takashiba S, Muramyama Y. Periodontol disease as a complication of diabetes mellitus. Annals of Periodontology 1998 ;3 :20-29.
  37. NOVAES A., PEREIRA A., DE MORAES N, NOVAES A. – Manifestations of insulin-dependant diabetes mellitus in the periodontium of youg brazilian patients. J. Periodontol, 1991, 62, 166-122.
  38. Offenbacher S, Katz V., Fertik G., Collins J, Boyd D, Maynor G., McKaig r., & Beck J. Periodontal infection as a risk factor for preterm low birth weight. J Periodontol 1996 ;67 :1103-1113.
  39. Paunio K., Impivaara O., Tiekso J. & Maki J.. Missing teeth and ischarmic heart disease in men aged 45-64 years. European Heart Journal 1993 ;14 :54-56.
  40. Piché Jon E., Swan RH, Hallmon William. The glycosylated Hemoglobin Assay for diabetes : Its value to the Periodontist. J Periodontol : 640-462.
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  45. Salvi GE, Collins JG, Yalda B, Arnold RR, Lang NP, Offenbacher S. Monocytic TNF-a secretion patterns in IDDM patients with periodontal diseases. J Clin Periodontol 1997 ;24 :8-16.
  46. Salvi GE, Yalda B, Collins JG, Jones BH, Smith FW, Arnold RR, Offenbacher S. Inflammatory Mediator Response as a Potential Risk Marker for Periodontal Diseases in Insulin-Dependent Diabetes Mellitus Patients. J Periodontol 1997 ;687 :127-135.
  47. Seppälä B., Seppälä M., Ainamo J. : A longitudianl study on non-insulin-dependant diabetes mellitus and periodontal disease. J. Clin. Periodontol.,1993, 20, 161-165
  48. Soskolne WA. Epidemiological an clinical aspects of periodontal diseases in diabetics. Annals of Periodontology 1998 ;3 :3-12.
  49. Taylor GW, Burt BA, Becker MP, Genco RJ, Shlossman M. Glycémic control and Alveolar bone loss progression in type 2 diabetes. Annals of Periodontology 1998 ;3 :30-39.
  50. Tervonen T, Karjalainen K. Periodontal disease related to diabetic status. A pilot study os the response to periodontal therapy in Type 1 diabetes. J Clin Periodontol 1997 ;24 :505-510.
  51. Tervonen T, Knuutila M, Pohjamo L, Nurkkala H. Immediate response to non-surgical periodontal treatment in subjects the diabetes mellitus. J Clin Periodontol 1991 ;18 :65-68.
  52. Tervonen T, Olivier R. Long-term control of diabetes mellitus and periodontitis. J Clin Periodontol1993 ;20 :431-435
  53. Tervonen T, Olivier R.C., Wolff et Coll. – Prevalence of periodontal pathogens with varying metabolic control of diabetes mellitux,, J. Clin. Periodontal., 1994, 21, 375-379.
  54. Vlassara H. Non-enzymatic glycosylation. Diabetes Annual 1991 :6 :371-389.
  55. Zambon J.J., Reynolds H, Fisher J.G., Shlossman M., Dunford R., Genco R.J. : Microbiological and immunological studies of adult periodontitis in patient with non-insulin-dependant diabetes mellitus. J ; Periodontol., 1988, 59, 23-31


18. Quelques résumés divers The activities of coenzyme Q10 and vitamin B6 for immune responses

Folkers K, Morita M, McRee J Jr.

Institute for Biomedical Research, University of Texas, Austin 78712.

Coenzyme Q10 (CoQ10) and vitamin B6 (pyridoxine) have been administered together and separately to three groups of human subjects. The blood levels of CoQ10 increased (p < 0.001) when CoQ10 and pyridoxine were administered together and when CoQ10 was given alone. The blood levels of IgG increased when CoQ10 and pyridoxine were administered together (p < 0.01) and when CoQ10 was administered alone (p < 0.05). The blood levels of T4-lymphocytes increased when CoQ10 and pyridoxine were administered together (p < 0.01) and separately (p < 0.001). The ratio of T4/T8 lymphocytes increased when CoQ10 and pyridoxine were administered together (p < 0.001) and separately (p < 0.05). These increases in IgG and T4-lymphocytes with CoQ10 and vitamin B6 are clinically important for trials on AIDS, other infectious diseases, and on cancer.

Publication Types:

  • Clinical Trial
  • Controlled Clinical Trial

PMID: 8503942 [PubMed – indexed for MEDLINE]


  • Increased blood mercury levels in patients with Alzheimer’s diseases. Hock et. al., (1998). J. Neural. Transm105:59-68.(9588761)
  • Imbalances of trace elements related to oxidative damage in Alzheimer’s diseases brain. Cornett et. al., (1998). Neurotoxicology 19:339-345.(9621340)
  • Metals and trace elements in plasma and cerebrospinal fluid in normal aging and Alzheimer’s disease. Basun et. al., (1991). J. Neural Transm. Park. Dis. Dement. Sect3:231-258.(1772577)
  • Brain trace elements in Alzheimer’s disease. Ehmann et. al., (1986). Neurotoxicology 7:195-206.(3714121)
  • Regional brain trace-element studies in Alzheimer’s disease. Thompson et. al., (1988). Neurotoxicology9:1-7.(3393299)
  • Trace element imbalances in isolated subcellular fractions of Alzheimer’s disease brains. Wenstrup et. al., (1990). Brain Res533:125-131.(2085723)
  • Trace element imbalances in hair and nails of Alzheimer’s diseases patients. Vance et. al., (1988). Neurotoxicology 9:197-208.(3205430)
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    Sivri A; Cindas A; Dinçer F; Sivri B
    Clin Rheumatol, 1996 May, 15:3, 283-6
    Fibromyalgia and irritable bowel syndrome are both common conditions which account for most of the referrals to physical medicine and rehabilitation-rheumatology and gastroenterology clinics, and they frequently coexist. In this study, we utilized a previously validated questionnaire to assess the prevalence of symptoms of bowel dysfunction and irritable bowel syndrome, and to survey the range of bowel pattern in 75 patients with fibromyalgia as compared to 50 normal controls. Symptoms associated with irritable bowel syndrome (p < 0.05) were reported in 41.8% of the fibromyalgia patients and 16% of the normal controls. In conclusion, we found that patients with fibromyalgia have a high prevalence of gastrointestinal complaints confirming the results indicating that fibromyalgia and irritable bowel syndrome frequently coexist. This may suggest a common pathogenic mechanism for both conditions.