Ultrasonic Monitoring of Dentin Demineralization.

Demineralization is a process of loss of minerals in the dental hard tissue that affects seriously the health of the patients, as it diminishes the tooth resistance, generating chewing problems by altering the occlusal structure, hypersensitivity, and pulpal problems. Demineralization can be produced by pathological processes as erosion or caries, or by surgical processes as etching. Due to the complexity of natural demineralization processes, it is mandatory to provide quantitative and standardized tests to allow their study in controlled laboratory conditions. Ultrasonic techniques are suitable for this purpose as they are nondestructive, quick, and provide localized mechanical information about the tissue, which is related with its degree of demineralization. In the present work, we evaluate the complete process of demineralization of the human dentin under controlled laboratory conditions using a pulse-echo ultrasonic technique. Up to 15 human dentin teeth have been demineralized with phosphoric acid at 10%. The time-of-flight measurements using the pulse-echo system allows to obtain the speed of sound in healthy (3415 m/s) and demineralized dentin tissue (1710 m/s), as well as to characterize the dynamical process of the acid penetration, which generates well-defined boundaries between two media (demineralized and mineralized dentin), showing very different mechanical properties. These boundaries advance in depth at an initial rate of [Formula: see text]/min, decelerating at -9.3 nm/min2 until the whole demineralization of the sample is achieved. In addition, the technique allows to measure the relevance of the demineralization produced by the acid residues inside the tooth once it has been removed from the acidic solution. Beyond the assessment of artificial demineralization lesions under laboratory conditions, as demonstrated in this article, the proposed technique opens new approaches to the assessment of demineralization caused by natural caries in vivo.

Monitoring the Setting of Calcium Sulfate Bone-Graft Substitute Using Ultrasonic Backscattering.

We report a method to monitor the setting process of bone-graft substitutes (calcium sulfate) using ultrasonic backscattering techniques. Analyzing the backscattered fields using a pulse-echo technique, we show that it is possible to dynamically describe the acoustic properties of the material which are linked to its setting state. Several experiments were performed to control the setting process of calcium sulfate using a 3.5-MHz transducer. The variation of the apparent integrated backscatter (AIB) with time during the setting process is analyzed and compared with measurements of the speed of sound (SOS) and temperature of the sample. The correlation of SOS and AIB allows us to clearly identify two different states of the samples, liquid and solid, in addition to the transition period. Results show that using backscattering analysis, the setting state of the material can be estimated with a threshold of 15 dB. This ultrasonic technique is indeed the first step to develop real-time monitoring systems for time-varying complex media as those present in bone regeneration for dental implantology applications.

Regulation of cell cycle transcription factor Swi5 by karyopherin Msn5.

Inactivation of S. cerevisiae ß-karyopherin Msn5 causes hypersensitivity to the overexpression of mitotic cyclin Clb2 and aggravates growth defects of many mutant strains in mitotic exit, suggesting a connection between Msn5 and mitotic exit. We determined that Msn5 controlled subcellular localization of the mitotic exit transcription factor Swi5, since it was required for Swi5 nuclear export. Msn5 physically interacted with the N-terminal end of Swi5. Inactivation of Msn5 caused a severe reduction in cellular levels of Swi5 protein. This effect occurred by a post-transcriptional mechanism, since SWI5 mRNA levels were not affected. The reduced amount of Swi5 in msn5 mutant cells was not due to an increased protein degradation rate, but to a defect in Swi5 synthesis. Despite the change in localization and protein level, Swi5-regulated transcription was not defective in the msn5 mutant strain. However, a high level of Swi5 was toxic in the absence of Msn5. This deleterious effect was eliminated when Swi5 nuclear import was abrogated, suggesting that nuclear export by Msn5 is important for cell physiology, because it prevents toxic Swi5 nuclear accumulation.