Throughout the history of medicine, lesions of the jaws have been described and named by those who thought were the first to observe them. My literature research revealed that the first recorded description of a NICO lesion was in the textbook,” DENTAL PHYSIOLOGY AND SURGERY,” written in 1848 by Surgeon- Dentist to the Middlesex Hospital in London, England, John Tornes.
Studies examining health consequences of the release of mercury from dental amalgams have concluded that there is insufficient mercury released from these restorations to cause a medical problem. Although the mercury vapor generated during removal of amalgams will cause a transient increase in the patient’s mercury level in tissue fluids, biochemical assays have demonstrated that the increase is too small to have a negative influence on organ systems. This is true even when patients have all their amalgams removed in a single session. Nevertheless, over the past decade, the release of mercury from dental amalgam has been frequently blamed for a variety of health complaints. A number of sensationalized media reports regarding the mercury issue have no doubt contributed to the public concern that has been aroused. Consequently, patients may present at the dentist’s office, either self-diagnosed or looking for a cause implicating mercury. In actuality, these patients may have symptoms of either medical problems or psychological disorders such as depression or anxiety. Unfortunately, the incorrect diagnosis may not only mislead, but actually place the patient in a dangerous situation. Two well-controlled studies have indicated that (1) 89% of the patients with self-reported “amalgam illness” had psychogenic disorders, whereas only 6% of the matched-pair manifested symptoms of these psychological disorders; and (2) these alleged “amalgam illness” patients had preneurotic reactive/defensive mechanisms that did not allow them to recognize aggressive and threatening situations which the control group would quickly and readily regard as potentially difficult to manage. Other studies involving psychological assessment seem to confirm that dental therapy (removal of amalgams) for people with alleged “amalgam illness” may, at best, provide a “placebo effect”.
Inflammatory cells in amalgam-associated, oral lichenoid contact lesions (OLL) were studied in 19 patients by immunocytochemistry 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.
In 111 women with repeated miscarriages, the urinary excretion of heavy metals was determined in a challenge test with the chelating agent 2,3-dimercaptopropane-1-sulphonic acid in addition to hormonal, chromosomal, immunological and uterine investigations. The heavy metal excretion was correlated to different immunological (natural killer cells, T cell subpopulations) and hormonal (progesterone, oestradiol, prolactin, thyroid stimulating hormone) parameters. We conclude that heavy metals seem to have a negative impact on ovarian as well as on pituitary function. The heavy metal-induced immunological changes may interfere with the physiological adaptation of the immune system to the state of pregnancy with the result of a miscarriage. The observed heavy metal-induced hormonal and immunological changes may be important factors in the pathogenesis of repeated miscarriages.
Before and after treatment scores on the Minnesota Multiphasic Personality Inventory – II (MMPI-II) were compared for 11 manic depression subjects with amalgams removed and for 9 subjects with amalgams who were told they were being given a placebo or sealant. Of the 87 scales, the amalgam removal group improved significantly more in 47 of them. Depression and hypomania scores improved significantly, as did anxiety, anger, schizophrenia, paranoia, and many others. Scores on the Million Clinical Multiaxial Inventory II found the scores in the amalgam removal group improved significantly more in the scales of avoidant, dependent, anitsocial and borderline, compared to the sealant / placebo group. The scores in the categories of Clinical Personality pattern category and severe Personality Pathology category also improved significantly more in the amalgam removal group. All scores of the nine dimensions tested in the Symptom Check List 90 improved significantly more in the group with amalgam removal. They included somatization, obsessive complusive, interpersonal sensitivity, depression, anxiety, hostility, phobic anxiety, paranoia, and psychotism. The amalgam removal group reported a 42% decrease in the number of somatic symptoms in the placebo / sealant group when comparing a before and after health questionnaire.
This paper on periodontal disease as a potential risk factor for systemic diseases was prepared by the Research, Science and Therapy Committee of The American Academy of Periodontology. It is intended to provide information regarding the role of periodontal disease in systemic diseases, including bacteremia, infective endocarditis, cardiovascular disease and atherosclerosis, prosthetic device infection, diabetes mellitus, respiratory diseases, and adverse pregnancy outcomes.
This study looked at the relationship between myopia and mercury from dental fillings. Hair mercury levels were found to be significantly higher in 25 nonmyopic children compared to 25 myopic children. The researchers hypothesized that if mercury was leaching from the silver dental fillings, then subjects without dental fillings would have a higher degree of myopia and poorer acuity. A study comparing 51 subjects without amalgams confirmed this hypothesis. The non-amalgam group had a 59 percent higher degree of myopia and significantly poorer acuity. Two additional studies also found that subjects without amalgams had a higher degree of myopia. All three studies found that significantly more subjects without amalgams wore glasses for distance when compared to subjects with amalgams. The authors hypothesize that mercury may increase the collagen fibrils of the sclera and thereby retard the progression of myopia.
A 32 year old white female, in apparently good health, failed to respond to conservative wound care for alveolar osteitis after a routine mandibular first molar extraction. Curettage and biopsy of necrotic alveolar bone from the #30 socket escalated her pain such that hospitalization was necessary for pain management with intravenous morphine. Twelve months prior to admission she had been placed on exogenous estrogen (Premarin, 0.625 mg/day) after a partial oophorectomy. While hospitalized, she was found to have resistance to activated protein C (APCR). Premarin was discontinued. After discharge, weekly changes of an antibiotic impregnated dressing allowed for progressive regeneration of bone and epithelium with gradual reduction in her pain. She was found to be heterozygous for the mutant Factor V Leiden, a heritable factor for increased tendency to form thrombi, so-called thrombophilia. We speculate that the exogenous estrogen administration exacerbated the thrombophilia associated with the Factor V Leiden mutation by compounding the patient’s resistance to activated protein C thereby contributing to her development of osteonecrosis and severe alveolar neuralgia.
Treatment of dental diseases such as dental decay and periodontal disease cost the United States public an estimated USD 37 billion in 1994 (2). As such, the cost of dental treatment was higher than the cost of treating eye disease, diabetes or arthritis, among others. The highly individualized,labor intensive methods used to debride, repair and replace the involved teeth account for the enormity of this expense. This expense will increase, as more people, with more teeth, are living longer. The magnitude of this problem in terms of potential dental needs isillustrated by the relative and absolute numbers of older individuals who will be dentate in 2000 compared with 1900. In 1900, about 4% of the UnitedStates population was older than 64 years of age and about 60% were edentulous, giving a total of l.2 million dentate individuals. In 2000, 1 6% of the United States population will be older than 64 years and about 25% edentulous ( 1 18, 162), giving a total of 39 million dentate individuals. Thus, over a century the number of older dentate individuals at risk of developing dental caries and periodontal disease increased by 32 times.
OBJECTIVES:
In a preliminary pilot study of 30 treatments in 26 patients with osteonecrosis of the jaws and chronic disabling facial pain, our specific aim was to determine whether, to what degree, and how safely therapy of hypofibrinolysis and thrombophilia would ameliorate the chronic pain associated with osteonecrosis of the mandible and maxilla.
STUDY DESIGN:
Thrombophilia was treated with Coumadin (DuPont) in 10 patients; hypofibrinolysis was treated with Winstrol (Sanofi-Winthrop) in 20 patients, including 4 who had mixed thrombophilia and hypofibrinolysis and had previously been treated with Coumadin. The initial treatment period was targeted to be 4 months. Each patient was asked to keep a daily written pain-relief numeric rating score and side-effects diary and to provide a summary pain-relief numeric rating score and side effects compilation for the total treatment period.
RESULTS:
There were 4 men and 22 women in the study group; their mean age was 49 +/- 11 years. The mean onset of their osteonecrosis pain was at age 45 +/- 12 years, and the mean duration of their facial pain prior to therapy was 4.5 +/- 4.2 years. Ten patients had one or more thrombophilic traits (there were two patients with protein C deficiency, five with resistance to activated protein C and/or the mutant Factor V Leiden gene, and four with high anticardiolipin antibodies). The 10 patients who were thrombophilic were treated with Coumadin (the international normalized ratio was targeted to 2.5-3.0) for 22 +/- 9 weeks. By self-reported pain-relief numeric rating scores, 6 of the 10 patients with thrombophilia (60%) had > or = 40% pain relief, 2 (20%) had no change, and 2 (20%) had increased pain (30% and 80% worse). Nine of the 10 patients with thrombophilia (90%) had no Coumadin-related side effects; 1 patient (10%) stopped Coumadin therapy (after 28 weeks) because of nosebleeds. Winstrol (6 mg per day) was used for 16 +/- 9 weeks in 20 patients with hypofibrinolysis, some of whom had one or more hypofibrinolytic traits (10 had high levels of plasminogen activator/inhibitor activity, usually accompanied by low stimulated tissue plasminogen activator activity; 13 had high Lp[a] lipoprotein). Of these 20 patients with hypofibrinolysis, 9 patients (45%) had > or = 40% pain relief, 3 patients (15%) had 20% to 30% relief, 5 patients (25%) had no improvement, and 3 patients (15%) had increased pain (30% worse, 60% worse, and 70% worse). Six of the 20 patients with hypofibrinolysis (30%) had no Winstrol-related side effects, while 14 (70%) had side effects that could be attributed to Winstrol, including weight gain, peripheral edema, increased facial and body hair, and acne–all of which were reversed within 6 weeks of stopping Winstrol therapy.
CONCLUSIONS:
We postulate that thrombophilia and hypofibrinolysis lead to impaired venous circulation and venous hypertension of the mandible/maxilla with subsequent development of osteonecrosis and chronic facial pain. In many patients, facial pain can be ameliorated by treating the pathogenetic coagulation defects with Coumadin or Winstrol. Large, double-blind, placebo-controlled crossover studies will be required in the future to validate these preliminary results and to determine whether […]