In vitro evaluation of fluorescein for testing the permeability of white spots on tooth enamel.

This investigation demonstrates the reliability of fluorescein for detecting the permeability of incipient dental caries (white spots). Artificial white spots were created on the buccal surface of 12 human bicuspids by viscous lactic acid (pH 4). Permeability of these lesions was assessed and reassessed before and after 24 and 48 hr of acid challenge using two disclosants: sodium iodide and sodium fluorescein. Estimates obtained from both disclosants showed that the microvoid volume approximately doubled as the decalcification time doubled. The two disclosants exhibited good intraclass reliability and their scores were correlated (r = 0.69 to r = 0.91). However, only fluorescein disclosed the extent of porous white spot lesions. Thus, fluorescein should be considered when the objective is to detect the location and permeability of incipient lesions.

Fluoride concentrations in whole saliva following use of fluoride tablets and a rinse.

This clinical investigation is comprised of two studies. The first monitored the oral clearance of fluoride following the use of an oral rinse and two types of tablets: one that was chewed, swished, and swallowed, and another that was allowed to dissolve undisturbed at a specific site in the oral vestibule. Fluoride from the rinse and tablets exhibited similar rapid clearance patterns with a mean concentration of 1.2 ppm or less within 1 hr and returned to baseline concentrations within 24 hr. Data from the second study indicated fluoride was distributed unevenly to various areas of the mouth from the slowly dissolving undisturbed tablet. Information concerning oral clearance of fluoride may be used to rationalize various treatment regimens.

A point mutation in the coding region of uroporphyrinogen decarboxylase associated with familial porphyria cutanea tarda.

Familial porphyria cutanea tarda (PCT) is inherited as an autosomal dominant trait caused by decreased activity of uroporphyrinogen decarboxylase (URO-D). In most families with PCT, URO-D mRNA levels are normal but both catalytic activity and immunologic reactivity of URO-D are half normal. We have cloned and sequenced 8 URO-D cDNA transcripts derived from a pedigree member with familial PCT. Three of the cDNAs had sequences encoding normal URO-D but five cDNA's contained a point mutation resulting in a gly----val substitution at amino acid position 281. An oligonucleotide probe complementary to the mutant sequence hybridized to DNA from affected individuals within the pedigree, but not to DNA from normal individuals. Measurements of pulse labeled URO-D in Epstein-Barr virus transformed lymphocytes indicated that the mutant protein has a half-life in vivo of less than four hours. In vitro measurements utilizing labeled URO-Ds generated in a reticulocyte lysate system revealed a 12-hour half-life for the mutant protein compared with a 102-hour half-life for normal URO-D. This is the first URO-D mutation to be characterized in a pedigree with familial PCT. This mutation was not detected in affected individuals from seven other PCT pedigrees, suggesting that PCT can result from different mutations.

Steady-state levels of uroporphyrinogen decarboxylase mRNA in lymphoblastoid cell lines from patients with familial porphyria cutanea tarda and their relatives.

Familial porphyria cutanea tarda (PCT) results from a generalized deficiency of uroporphyrinogen decarboxylase (URO-D) activity. The molecular defect responsible for this disorder has not been characterized. To determine whether decreased levels of URO-D mRNA are responsible for subnormal URO-D activity, steady-state levels of URO-D mRNA in lymphoblastoid cells were determined. Northern blots were hybridized with a URO-D cDNA probe and quantified by densitometry. No difference in the levels of URO-D mRNA was detected between affected individuals and their normal relatives. Thus, the deficiency of URO-D activity in two familial PCT pedigrees characterized here does not arise from a deficiency of URO-D mRNA.

Effects of octenidine on dental plaque and gingivitis in monkeys.

This investigation monitored the effects of daily oral rinses with octenidine on plaque and gingivitis in five monkeys. Formulations containing 0.5% or 1.0% octenidine or the rinse vehicle placebo were provided daily for 2 weeks. Each week the dentition of each monkey was examined, photographed, and sampled for plaque. All responses exhibited a numerical decrease in mean scores following treatments with each concentration of octenidine, whereas the placebo treatment exerted negligible effects. Decreases in plaque mass were observed after 2 weeks of treatment with 1% octenidine (58%) or 0.5% octenidine (55%) compared with the corresponding baseline values. Similar trends were noted in the extent and thickness of supragingival plaque and its ability to decrease the pH of a sucrose solution. Octenidine treatments reduced the proportions of motile forms in samples of subgingival plaque and also restricted its ability to produce H2S. Slight numerical decreases were seen in the Gingival Index and flow rate of the crevicular fluid. These consistent protective trends suggest that octenidine decreases the pathogenic potential of established plaque.

Cell and platelet stability in disodium and tripotassium edta.

The relative stability of blood cells and platelets from 25 donor samples collected in both Na2EDTA and K3EDTA was examined. Twenty-one samples were from normal donors. At designated intervals over a five hour period cell counts and mean cell volumes were determined for each specimen. The separation of plasma from whole blood for future potassium determinations, as well as the preparation of blood smears for determining cellular morphology, were also performed at the designated intervals. The results indicate that no significant changes were observed in the areas investigated. Additional tests should be performed on pathological samples.