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About Gruppo R, Glueck CJ, Mcmahon RE, Bouquot J, Rabinovich BA, Becker A, Tracy T, Wang P.

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So far Gruppo R, Glueck CJ, Mcmahon RE, Bouquot J, Rabinovich BA, Becker A, Tracy T, Wang P. has created 991 blog entries.

The pathophysiology of alveolar osteonecrosis of the jaw: anticardiolipin antibodies, thrombophilia, and hypofibrinolysis.

We studied 55 patients (50 women, 5 men) with severe facial pain and biopsy-proven neuralgia-inducing cavitational osteonecrosis (NICO) of the alveolar bone of the jaws. Our aim was to assess the pathophysiologic contributions to NICO of anticardiolipin antibodies (aCLA), thrombophilia (increased tendency to intravascular thrombi), and hypofibrinolysis (reduced ability to lyse thrombi). Of the 55 patients, 43 (78%) had one or more tests positive for thrombophilia or hypofibrinolysis (or both), and only 12 (22%) were normal. Eighteen of 55 (33%) patients had high aCLA (> 2 SD above mean value for control subjects); immunoglobulin G (IgG) (p = 0.01) and immunoglobulin A (IgA)(p = 0.001) levels were higher in patients than in controls. The distribution of elevated aCLA immunoglobulin classes among patients was as follows: IgG alone, 5 (9%); IgA alone, 7 (13%); and IgM alone, 3 (5%). Three patients (5%) had high levels of both IgG and IgA aCLA. Other defects of the thrombotic or fibrinolytic systems in the 55 patients included high lipoprotein(a) in 36% (vs 20% in control subjects (p = 0.03)), low stimulated tissue plasminogen activator activity (tPA-Fx) in 22% (vs 7% in control subjects (p = 0.08)), high plasminogen activator inhibitor activity (PAI-Fx) in 18% (vs 8% in control subjects (p = 0.03)), resistance to activated protein C in 16% (vs 0% in control subjects (p = 0.007)), low antigenic protein C in 4+ (vs 0% in control subjects (p > 0.2)), and low antigenic protein S in 4% (vs 0% in control subjects (p > 0.2)). Anticardiolipin antibodies and other defects of the thrombotic and fibrinolytic systems appear to be common, potentially reversible pathogenetic risk factors associated with osteonecrosis of the jaw

Cardiac arrest caused by trigeminal neuralgia.

A 67-year-old man with a 12-year history of trigeminal neuralgia experienced multiple fainting episodes preceded by right facial pain. One episode resulted in cardiac arrest with successful resuscitation. Pacemaker insertion prevented further episodes of syncope despite the occurrence of pain. The fainting episodes and cardiac arrest are believed to be unusual manifestations of trigeminal neuralgia.

Thrombophilia, hypofibrinolysis, and alveolar osteonecrosis of the jaws. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology and Endodontics.

OBJECTIVES:

Our specific aim in 49 patients (42 women, 7 men) with osteonecrosis of the jaw was to determine whether thrombophilia (increased tendency to intravascular thrombosis) or hypofibrinolysis (reduced ability to lyse thrombi) were associated with this regional avascular necrosis.

STUDY DESIGN:

Determinants of thrombosis and fibrinolysis were compared in healthy controls and in 42 women and 7 men who had biopsy-proven idiopathic osteonecrosis of the jaw with severe chronic jaw or facial pain syndromes and failure to respond to conventional medical and dental treatments.

RESULTS:

Of the 49 patients, 35 (71%) had thrombophilia or hypofibrinolysis and only 14 were normal. Thrombophilia as a sole coagulation defect was found in 10 patients, 7 with resistance to activated protein C and 3 with low protein C (deficiency of an antithrombotic protein). Hypofibrinolysis with low stimulated tissue plasminogen activator activity and high lipoprotein (a) (an atherogenic, hypofibrinolytic lipoprotein) were found as sole coagulation defects in seven and eight patients, respectively. Ten patients had mixed defects; 7 of these 10 had thrombophilia with resistance to activated protein C. Sinusoidal dilatation was a constant feature in maxillary and mandibular bone biopsies, suggesting venous occlusion with intramedullary hypertension. Marrow fibrosis and occasional fibrin plugs were additional microscopic features believed to impair venous drainage and to contribute to ischemic necrosis of the alveolar bone.

CONCLUSIONS:

Primary thrombophilia and hypofibrinolysis appear to be common, heritable, pathophysiologic risk factors for idiopathic osteonecrosis of the jaws. These coagulation defects may also contribute to alveolar neuralgia, atypical odontalgia and facial neuralgia, idiopathic trigeminal neuralgia, and to treatment failures so often encountered in patients with alveolar osteonecrosis and disabling chronic facial and jawbone pain syndromes.

No evidence of renal toxicity from amalgam fillings.

Dental amalgam continuously releases mercury. Studies of sheep [Boyd et al., Am. J. Physiol. 261 (Regulatory Integrative Comp. Physiol. 30): R1010-R1014, 1991] showed decreased renal function after placement of amalgam fillings. In this study, renal function was investigated in 10 healthy volunteers before and after amalgam removal. The subjects had an average of 18 tooth surfaces filled with amalgam, which was removed during one dental session. One week before and sixty days after removal, the glomerular filtration rate (GFR) was determined by 51Cr-EDTA clearance technique. Blood and urine samples were collected for analysis of mercury, creatinine, beta 2-microglobulin, N-acetyl-beta-glucosaminidase (NAG), and albumin 1 wk before and 1, 2, and 60 days after amalgam removal. The plasma mercury concentration increased significantly 1 day after removal. Sixty days later, significantly lower mercury levels were found in blood, plasma, and urine. The GFR values were similar before and after mercury exposure (mean 94 and 94 ml/min per 1.73 m2, respectively). No detectable effects occurred on excretion of NAG, beta 2-microglobulin, or albumin. It is concluded that no signs of renal toxicity could be found in conjunction with mercury released from amalgam fillings.

Recent advances in the biomedicinal chemistry of fluorine-containing compounds. Chapter 1 in Ojima et al.; Biomedical Frontiers of Fluorine Chemistry. ACS Symposium Series.

In the first part of our review, biochemical aspects of the biomedicinal chemisty of fluorinated compounds will be covered.  Medicinal aspects of this field are then discussed, with emphasis on drugs that have been recently marketed, or are in the final phases of testing.

By |2018-07-24T19:26:12+00:00January 1st, 1996|Fluoride|

Resistance of the normal human microflora to mercury and antimicrobials after exposure to mercury from dental amalgam fillings.

The concentrations of mercury in saliva and feces and the resistance pattern of the gastrointestinal microflora were investigated for 20 subjects. Ten patients, with a mean number of 19 amalgam surfaces, had all amalgam fillings removed during one dental session. Ten subjects without amalgam fillings served as a control group. Saliva and fecal samples were collected before amalgam removal and 2, 7, 14, and 60 days afterward. Mercury levels in saliva and feces correlated significantly with the number of amalgam surfaces. No differences in the resistance pattern of the oral microflora were detected between the two groups. In the amalgam group there was an increase in the relative number of intestinal microorganisms resistant to mercury, ampicillin, cefoxitin, erythromycin, and clindamycin on days 7-14. This was not statistically significant in light of the normal variations of the control group. A significant correlation between the prevalence of mercury resistance and multiple antimicrobial resistance in intestinal bacterial strains was observed.

By |2018-07-20T17:22:13+00:00January 1st, 1996|Mercury|

Significant mercury deposits in internal organs following the removal of dental amalgam, & development of pre-cancer on the gingiva and the sides of the tongue and their represented organs as a result of inadvertent exposure to strong curing light (used to solidify synthetic dental filling material) & effective treatment: a clinical case report, along with organ representation areas for each tooth.

However, these mercury deposits, which commonly occur in such cases, were successfully eliminated by the oral intake of 100 mg tablet of Chinese parsley (Cilantro) 4 times a day (for average weight adults) with a number of drug-uptake enhancement methods developed by the 1st author, including different stimulation methods on the accurate organ representation areas of the hands (which have been mapped using the Bi-Digital O-Ring Test), without injections of chelating agents. Ingestion of Chinese parsley, accompanied by drug-uptake enhancement methods, was initiated before the amalgam removal procedure and continued for about 2 to 3 weeks afterwards, and ECGs became almost normal. During the use of strong bluish curing light to create a photo-polymerization reaction to solidify the synthetic filling material, the adjacent gingiva and the side of the tongue were inadvertently exposed. This exposure to the strong bluish light was found to produce pre-cancerous conditions in the gingiva, the exposed areas of the tongue, as well as in the corresponding organs represented on those areas of the tongue, and abnormally increased enzyme levels in the liver. These abnormalities were also successfully reversed by the oral intake of a mixture of EPA with DHA and Chinese parsley, augmented by one of the non-invasive drug-uptake enhancement methods previously described by the 1st author, repeated 4 times each day for 2 weeks.

By |2018-11-13T23:21:39+00:00January 1st, 1996|Mercury|

Amalgam-associated oral lichenoid reactions: clinical and histologic changes after removal of amalgam fillings.

OBJECTIVE AND STUDY DESIGN:
Forty-nine consecutive patients with clinically diagnosed oral lichenoid reactions in contact with amalgam fillings were studied clinically and histologically. The long-term effect of replacement of these fillings was also examined.

RESULTS:
Seventeen (35%) patients showed positive reactions to mercury at the epicutaneous patch test that was carried out before treatment. After treatment, total regression of the lesions was found clinically in 33 (69%) and histologically in 26 (55%) patients. Most of the remaining lesions changed clinically and histologically to a less pronounced tissue reaction. Lesions in direct contact with amalgam fillings (group I) showed significantly better healing results than lesions that exceeded the contact area (group II). No difference in healing capacity was noted in the two groups between patients with positive patch reactions to mercury compared with those with negative reactions. Lesions that histologically were classified as benign oral keratosis showed a similar healing pattern as those classified as oral lichen planus.

CONCLUSION:
In group I all lesions changed histologically and clinically to a normal mucosa or to a less affected tissue reaction. In group II this change was less pronounced, which suggests that the fillings themselves were not the only factor involved in the cause of these lesions. The results suggest that various etiologic factors are involved in lichenoid reactions and that the effect of removal of amalgam fillings cannot be predicted by epicutaneous patch testing and biopsies.

By |2018-07-27T16:55:11+00:00January 1st, 1996|Mercury|

Sevoflurane versus isoflurane for maintenance of anesthesia: are serum inorganic fluoride ion concentrations of concern?

Sevoflurane administration can result in increased serum inorganic fluoride ion concentrations, which have been associated with inhibition of renal concentrating ability. We measured serum fluoride levels, renal function, and recovery variables as a function of time in ASA grade I-III patients administered general anesthesia with isoflurane or sevoflurane for at least 1 h. Fifty patients were exposed to sevoflurane (< or = 2.4% inspired concentration) or isoflurane (< or = 1.9% inspired concentration) for maintenance of anesthesia as part of a multicenter trial. Blood was collected for determination of serum fluoride ion concentration, electrolytes, blood urea nitrogen, and creatinine at various time points pre- and postoperatively. Mean serum fluoride levels were significantly increased in sevoflurane versus isoflurane groups at all time points; the mean peak serum levels were 28.2 +/- 14 mumol/L at 1 h for sevoflurane and 5.08 +/- 4.35 mumol/L at 12 h for isoflurane. Sevoflurane-mediated increases in serum fluoride levels peaked at 1 h and, in general, decreased rapidly after discontinuation of the anesthesia. Three of 24 patients exposed to sevoflurane had one or more fluoride levels > 50 mumol/L. One of these patients had a serum inorganic fluoride ion level > 50 mumol/L at 12 h after sevoflurane, and an additional patient had fluoride levels > 33 mumol/L for up to 24 h after sevoflurane discontinuation. Those two patients also demonstrated an increase in serum blood urea nitrogen and creatinine at 24 h after sevoflurane administration compared with baseline. The elimination half-life of serum fluoride ion was 21.6 h. The results of this study suggest the possibility of sevoflurane induced nephrotoxicity.

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