Biofilm formation was evaluated on the following titanium and zirconia implants in vivo: machined titanium (Ti-m), modified titanium (TiUnite), modified zirconia (ZiUnite), machined alumina-toughened zirconia (ATZ-m), sandblasted alumina-toughened zirconia (ATZ-s), and machined zirconia (TZP-A-m). Bovine enamel slabs were used as controls. Surface morphologies were examined by atomic force (AFM) and scanning electron microscopy (SEM). The surface wettability was also determined. Twelve healthy volunteers wore a splint system with the tested materials. After 3 and 5 days the materials were examined by fluorescence in situ hybridization (FISH) and confocal laser scanning microscopy (CLSM). The levels of Streptococcus spp., Veillonella spp., Fusobacteriaum nucleatum, and Actinomyces naeslundii were quantitatively determined. The biofilm thickness was found to be between 19.78 and 36.73 μm after 3 days and between 26.11 and 32.43 μm after 5 days. With the exception of Ti-m the biofilm thickness after 3 days was correlated with surface roughness. In addition to Streptococcus spp. as the main component of the biofilm (11.23-25.30%), F. nucleatum, A. naeslundii, and Veillonella spp. were also detected. No significant differences in biofilm composition on the implant surfaces could be observed. In total, the influence of roughness and material on biofilm formation was compensated by biofilm maturation.
Four children, two girls and two boys, were found to have a short arm deletion of chromosome No. 18. Three of them exhibit a typical dysmorphy of the face showing retraction of the midface, broad-based, flat nose, hypertelorism, epicanthus, "carp mouth", big, protruding, and low set ears, as well as a variable number of Turner-like features, failure of growth, mental retardation, and muscular hypotonia. A newly born child, who died at 2 days of age exhibited severe brain defects of holoprosencephalic series. The clinical and cytogenetic findings are compared with the reviewed data of the 18 p deletion. The hypothesis of "gene-dosis compensation" is discussed in order to explain the variable phenotypical expression of 18 p-syndrome as there is obviously to correlation between the extent of the deficiency and the expression of malformations.
The cytogenetic analysis of a child with unspecific dysplastic signs revealed the karyotype: 46, XX, del(11) (q21). Two hypotheses could explain the mild phenotypical expression of this deletion:
1) The material of the deficient part of chromosome 11 is genetically inert or redundant (which seems unlikely);
2) “Gene‐dosis‐compensation” occurs for the loss of genes on the deficient part of chromosome 11.
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