Search

The application of a self-assembling peptide on noncavitated caries lesions is supposed to be a feasible approach to facilitate remineralization and mask their unfavorable appearance. However, demineralizing conditions are common in the oral environment, so the aim of this pH-cycling study was to compare recommended and novel treatment methods regarding their ability to hamper demineralization and as a consequence mask artificial enamel caries lesions. Artificial caries lesions were prepared in bovine enamel and randomly allocated to 11 groups (n = 22). Treatments before pH-cycling were as follows: the application of a self-assembling peptide (Curodont™ Repair [C]), a low-viscosity resin (Icon® [I]), 2 fluoride solutions (10,000 ppm F-: Elmex fluid [E] and 43,350 ppm F-: Tiefenfluorid® [T]), and no intervention (N). During pH-cycling (28 days, 6 × 60 min demineralization/day) half of the specimens in each group were brushed (10 s; 2 ×/day) with either fluoride-free (named e.g., C0) or NaF (1,100 ppm F-; e.g., C1) dentifrice slurry. In another subgroup specimens were pH-cycled but not brushed (NNB). Differences in integrated mineral loss (ΔΔZ), lesion depth (ΔLD), and colorimetric values (ΔΔE) were calculated between values after pre-demineralization, surface treatment, and pH-cycling. Specimens of C0, C1, NNB, N0, N1, T0, and E0 showed significantly increased ΔZ and LD values after pH-cycling (p ≤ 0.003; paired t test). C0, C1, NNB, and N0 showed significantly higher changes in ΔΔZ than E1, I0, I1, and T1 (p < 0.001; ANOVA). Significantly reduced colorimetric values could only be observed for I1, I0, E1, and E0 after treatment and after pH-cycling (p ≤ 0.027; paired t test). In conclusion, under the conditions chosen only the application of a low-viscosity resin could mask caries lesions significantly, whereas self-assembling peptides could neither inhibit lesion progression nor mask the lesions considerably., (© 2017 S. Karger AG, Basel.)

Adult age-specific colorectal cancer incidence rates increase exponentially from maturity, reach a maximum, then decline in extreme old age. Armitage and Doll (1) postulated that the exponential increase resulted from "n" mutations occurring throughout adult life in normal "cells at risk" that initiated the growth of a preneoplastic colony in which subsequent "m" mutations promoted one of the preneoplastic "cells at risk" to form a lethal neoplasia. We have reported cytologic evidence that these "cells at risk" are fetal/juvenile organogenic, then preneoplastic metakaryotic stem cells. Metakaryotic cells display stem-like behaviors of both symmetric and asymmetric nuclear divisions and peculiarities such as bell shaped nuclei and amitotic nuclear fission that distinguish them from embryonic, eukaryotic stem cells. Analyses of mutant colony sizes and numbers in adult lung epithelia supported the inferences that the metakaryotic organogenic stem cells are constitutively mutator/hypermutable and that their contributions to cancer initiation are limited to the fetal/juvenile period. We have amended the two-stage model of Armitage and Doll and incorporated these several inferences in a computer program CancerFit v.5.0. We compared the expectations of the amended model to adult (15-104 years) age-specific colon cancer rates for European-American males born 1890-99 and observed remarkable concordance. When estimates of normal colonic fetal/juvenile APC and OAT gene mutation rates (∼2-5 × 10(-5) per stem cell doubling) and preneoplastic colonic gene loss rates (∼8 × 10(-3)) were applied, the model was in accordance only for the values of n = 2 and m = 4 or 5.

Cisplatin was administered as a single i.p. dose of 5 mg/kg to WAG/Rij rats at intervals of 7 days or 0.5 h before, or 7 days after graded X-ray doses to the left kidney. The right kidney was surgically removed 4 weeks after irradiation. Renal function was determined by measuring total urine volume excreted in 24 h, urine osmolality and serum urea. The severity of alterations in the various anatomic compartments of the kidney induced by the various treatments were graded histologically. The administration of 2 or 5 mg/kg cisplatin alone did not alter any of the kidney function parameters. Isoeffective radiation doses calculated for each of the functional parameters continuously decreased with increasing time after treatment. Differences between the isoeffective doses for the three combined treatments and for treatment with irradiation alone were only observed for urine osmolality and urine volume which primarily are tubular-related functional parameters. The histopathological grading studies also indicated that enhancement by cisplatin of radiation-induced damage was almost entirely confined to the tubules. The results of this study indicate that the sequence and length of time between treatments is an important variable in the development of cisplatin plus radiation-induced renal injury, but that none of the tested combinations showed a more than additive toxicity.