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About Liu Y, Cotgreave I, Atzori L, Grafström RC.

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So far Liu Y, Cotgreave I, Atzori L, Grafström RC. has created 991 blog entries.

The mechanism of Hg2+ toxicity in cultured human oral fibroblasts: The involvement of cellular thiols.

To study amalgam-related toxicity in a primary target cell type, human oral fibroblasts were grown in a low-serum medium containing 1.25% fetal bovine serum and exposed to Hg2+, a corrosion product of amalgam. A 1-h exposure to various concentrations of Hg2+ resulted in a dose-dependent loss of colony forming efficiency. Removal of the low-molecular-weight thiol cysteine from the medium increased the toxicity of Hg2+ almost 50-fold in comparison with complete medium or medium without fetal bovine serum. Accordingly, fetal bovine serum was not found to contain detectable levels of low-molecular-weight thiols. The levels of cellular free protein thiols were shown to be depleted Hg2+ at significantly lower concentrations of the metal ion than those required to decrease the levels of the major cellular low-molecular weight thiol glutathione. These decreases were dependent on the exposure conditions, i.e. the presence of serum and thiols, in a manner similar to the effect on colony forming efficiency. Other functions commonly related to cell viability, including the accumulation of the vital dye neutral red, the cytosolic retention of deoxyglucose and the mitochondrial reduction of tetrazolium were also inhibited by Hg2+, albeit at higher concentrations. Finally, the depletion of cellular glutathione, by pre-exposure of the cells to the glutathione synthesis inhibitor buthionine sulfoximine, somewhat increased the toxicity of Hg2+ and potentiated the depletion of protein thiols. Taken together, the toxicity of Hg2+ in human oral fibroblasts was demonstrated in several assays of which colony forming efficiency was the most sensitive, cell killing by this agent was related to its high affinity for protein thiols, whereas glutathione showed a significant, but limited, ability to protect the cells from Hg2+ toxicity.

By |2018-07-25T18:23:23+00:00January 1st, 1992|Mercury|

Comprehensive medical examination of a group of patients with alleged adverse effects from dental amalgams.

Mercury from dental amalgams does not seem to cause dose-related intoxications. However, animal studies have shown that high-dose exposure to mercury may support various types of immunologic reactions. Ten patients claiming that their symptoms were caused and aggravated by amalgam therapy were selected for a study of the effects of removal of one amalgam restoration followed by placing of a composite filling. Clinical symptoms and the result of laboratory tests were recorded. Six patients had contact allergies to metals, three of them to mercury ammonium chloride. The comparison of pre- and post-experimental test results showed significant reductions in p-IgE and dU-albumin and significant increases in p-C3d and dU-beta 2-microglobulin. There was no laboratory evidence of a direct toxic effect by mercury on the patients. The observed response by some of the studied factors to the low acute exposure to amalgam may imply that an activation of the immune system occurred.

Guest editorial: Focal infection revisited-the dentist as physician.

While not as attention-grabbing as some of the infections ofour time, we appear to be in danger ourselves of forgetting that the mouth constitutes a major portal of entry for a wide range of micro-organisms, whether inherently oral commensals or direct pathogens, the effects of which may be merely troublesome, as with the common oral infectious diseases, or more serious. There is an analogy with oral neoplasia which, though it may be as prevalent as cervical cancer, does not attract anything like the attention ofthe latter. One wonders why. Ever since the original concept of focal infection led to an excess of extractions over 70 years ago, the theory has been in relative disrepute. And yet to ignore focal infection is to refuse to recognize an abundant literature, all of medical significance.

By |2019-05-27T02:12:58+00:00January 1st, 1992|Other|

The effects of cleaning on the kinetics of in vitro metal release from dental casting alloys.

The kinetics of the release of elements from six dental casting alloys into cell-culture medium was assessed by means of atomic absorption spectroscopy. Alloys were evaluated in the polished and polished-cleaned conditions so that the effects of cleaning could be determined. Auger scanning microscopy was used for analysis of the surfaces of selected alloys before and after exposure to the cell-culture medium. Release patterns for each element were characterized by the shape of the dissolution vs. time curve, concentration of the element at 12 h as a percentage of the 72-hour concentration, and the relative slope of the curve from 48 to 72 h. Three patterns of release were observed for elements in these alloys. Type I patterns had logarithmic shapes with relatively large 12-hour concentrations and low 48-72-hour slopes. Type II patterns had logarithmic shapes but with moderate 12-hour concentrations and 48-72-hour slopes. Type III patterns were polynomial in shape, had relatively low 12-hour concentrations, and had large 48-72-hour slopes. Cleaning did not change the pattern of release but did generally significantly decrease the quantities of elements released (p = 0.05). The type of dissolution vs. time curve appeared to be dependent upon the element and the composition of the alloy. When cleaning reduced dissolution, surface analyses showed that the cleaning process increased the abundance of elements such as Au and Pd and reduced the abundance of Ag and Cu. Elements which were released from the alloys were more abundant on the surface than in the bulk in both polished and polished-cleaned conditions.

By |2018-09-01T01:14:54+00:00January 1st, 1992|Mercury|

Focal infection

Focal infection of oral origin may derive from closed or open sites. Open foci include caries lesions, periodontal pockets, and extraction sockets; closed foci, infection around root apices, unerupted but infected teeth, and infected pulps (Newman, 1968). Focal infection leading to infective endocarditis can even occur via a dens in dente (Whyman and MacFadyen, 1994). From the oral foci, microorganisms- bacterial, viral, or other-or their products may gain entry to the deeper tissues directly, by spreading along fascial planes, through bony cavities, or even along blood or lymph vessels or nerves, or via salivary gland mucous surfaces. Can one die of such simple chronic infection? One may cite the coroner’s court, but there is also extensive literature evidence.

By |2019-05-26T01:25:59+00:00January 1st, 1992|Other|

More about neuralgia-inducing cavitational osteonecrosis (NICO).

The substantial intolerance exhibited by Dr. Donlon’s’ commentary on our article that dealt with the histopathology of jawbone osteomyelitis (neuralgiainducing cavitational osteonecrosis, NICO) in facialneuralgia patients is disappointing. It is enticing, I know, to blithely accept one’s own suppositions as science and the other chap’s as drivel. In this case we are accused of generating considerable drivel, excluding science from our research, creating facts from fantasy, and possessing no diagnostic skills worthy of mention. These charges are especially intriguing because
the political controversy that surrounds NICO led me to the unusual action of referring our paper to several international experts before it was submitted for publication. I truly thought I had addressed its major deficiencies!

By |2018-08-25T01:27:14+00:00January 1st, 1992|Periodontal Disease|

Neuralgia-inducing cavitational osteonecrosis (NICO): osteomyelitis in 224 jawbone samples from patients with facial neuralgia.

A somewhat obscure etiologic theory for facial neuralgias presumes a low-grade osteomyelitis of the jaws that produces neural degeneration with subsequent production of inappropriate pain signals. Animal investigations and treatment successes with human patients based on this theory lend it credence. The present study examined 224 tissue samples removed from alveolar bone cavities in 135 patients with trigeminal neuralgia or atypical facial neuralgia. All tissue samples demonstrated clear evidence of chronic intraosseous inflammation. The most common microscopic features included dense marrow fibrosis or “scar” formation, a sprinkling of lymphocytes in a relative absence of other inflammatory cells (especially histiocytes), and smudged, nonresorbing necrotic bone flakes. Very little healing or new bone formation was visible. These lesions were able to burrow several centimeters to initiate distant cavities. The present preliminary investigation cannot prove etiology, but the presence of intraosseous inflammation in every single jawbone specimen in these patients and certain clinical and treatment aspects of these lesions (to be reported later) has led the authors to recommend the term neuralgia-inducing cavitational osteonecrosis or NICO for these lesions.

Cavitational bone defect: a diagnostic challenge.

A patient with a history of trauma to the maxillary left anterior region presented with chronic pain of unknown etiology. Root canal therapy and periradicular surgery failed to resolve the persistent pain. A second surgical procedure revealed a bone cavity superior and distopalatally to the apex of the maxillary left lateral incisor. The suspected etiology was necrotic bone removed from the bone cavity.

By |2018-08-29T22:54:51+00:00January 1st, 1991|Periodontal Disease|

Long-term fluoride release from glass ionomer-lined amalgam restorations.

This in vitro study evaluated the amount of fluoride released from glass ionomer-lined amalgam restorations over a period of 1 year. Class V cavities (2 x 2 x 7 mm) were prepared on the facial and lingual surfaces of 50 extracted human molars randomly distributed into 5 groups: Group 1: No restorations; Group 2: Dispersalloy amalgam alone; Group 3: same as Group 2 except 1 mm of Ketac-Silver was placed on the axial wall before amalgam insertion; Group 4: GC Lining/amalgam; and Group 5: Miracle Mix/amalgam. After restoration, each tooth was thermocycled (100x) at 5 degrees C and 55 degrees C with a dwell time of 30 seconds for baseline fluoride release levels. The teeth were placed in a polyethylene vial containing 4 ml of deionized water. At weekly intervals, each tooth was transferred to a fresh vial. Fluoride release was measured with a fluoride ion specific electrode for 10 consecutive weeks and then again at the end of 1 year. Calibration curves for low level measurements were prepared so the readings could be expressed in micrograms/ml F. At 1 year, fluoride released in micrograms/ml was: Group 1: less than 0.08; Group 2: less than 0.08; Group 3: 0.28; Group 4: 0.68; Group 5: 1.12. An ANOVA was used to evaluate the statistical difference between the groups. At the end of 1 year, measurable amounts of fluoride were recorded for all glass ionomer-lined groups with Miracle Mix and GC Lining releasing significantly more fluoride than Ketac-Silver (P less than 0.002).

By |2018-07-20T21:59:51+00:00January 1st, 1991|Fluoride|

Aureobasidium infection of the jaw.

A 32-yr-old white North American male resident of Norway presented with an asymptomatic radiolucency first identified 3 yr after the removal of an impacted mandibular right third molar in Southern California 16 yr previously. Surgical exploration revealed an intraosseous cavity filled with a black, homogeneous, gelatinous substance thought to be foreign material, but which was diagnosed histologically as containing black yeasts. Cultivation of a microbiologic sample for 6 wk grew black yeast-like colonies. The yeast isolate was identified as an Aureobasidium species different from the typical A. pullulans. A blood sample was negative with regard to antibodies both with double diffusion technique and ELISA. Also, examination with respect to dermatologic manifestations gave negative results. Flucytocin 10 g/d was administered systemically for 30 d. Six months postoperatively bone regeneration was satisfactory radiologically.

By |2018-08-27T20:19:39+00:00January 1st, 1991|Periodontal Disease|
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