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The speed of ultrasound at 20 MHz is measured for hard dental tissues inside human teeth. This includes the cementum, for which no data are available. The spatial distribution, extrema, and means of the longitudinal ultrasound velocity (LUV) are determined with an emphasis on the apical thirds and an extended spectrum. Tissue areas are investigated by optical means and by acoustical scanning, in order to compare apical regions-of-interest with the complete mineralized wet porous tissue that lies beneath the enamel cap. The maximal LUV in a single dentin specimen varies from 3903 m/s to 4226 m/s. The dentin's frequency distribution of LUV at 20 degrees C exhibits a predominant peak feature comprising several Voigt functions. Introducing standardized relative tooth width portions, the corono-apical decrease in LUV of 21 specimens is approximated by LUV=4224 - (257* ln(y)) along reduced distances in dentin. Abnormal teeth require a higher resolution and an approximate equation of the form LUV= (sigma(ai*yi))/(1 + sigma(bi+1*y(i+1. It can be used each time the corono-apical variation has to be quantified in each of the three tissues. Ten coefficients are numerically exemplified. An error evaluation is performed, which denotes errors of 0.2% +/- 1.3% (enamel), -0.1% +/- 1.6% (cementum), and acceptable residual errors for dentin.

The longitudinal velocity of sound in a specific material depends, amongst others, on the material's density and elasticity (Young's Modulus). Ultrasound therefore may be used for indirect characterization of materials. In this paper a method is described which allows high resolution measurements on coplanar ground sections of human teeth. The results are presented in two-dimensional velocity profiles. There is evidence from the first images, that longitudinal sound velocity (LSV) in dentin varies depending on the location. The use of LSV may be another way to characterize hard dental tissues physically, and to monitor induced changes.

We report on a neonate presenting with polyhydramnios; macrosomia; macrocephaly; visceromegaly including bilateral nephromegaly, hepatomegaly, cardiomegaly; thymus hyperplasia; cryptorchidism; generalized muscle hypotonia; and a distinctive facial appearance. The clinical course was marked by severe neurodevelopmental deficits combined with progressive respiratory decompensation leading to death at the age 6 months. Magnetic resonance imaging (MRI) disclosed a generalized cerebral atrophy with a marked deficit of the white matter. Renal ultrasound and MRI showed markedly enlarged kidneys with multiple small cystic lesions, a pattern indistinguishable from polycystic kidney disease. The postmortem kidney biopsy revealed dysplastic changes, microcysts, and a focal nephrogenic rest, characteristic features of the Perlman syndrome. In children with fetal gigantism, renal abnormalities, and neurological deficits, Perlman syndrome should be considered and may be confirmed by kidney biopsy.

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