The authors declare no conflict of interest. N ovaMin ® is the trade name for a calcium sodium phosphosilicate bioactive glass that has been developed for use in oral health care. Originally developed for the treatment of hypersensitivity by the physical occlusion of dentinal tubules, recent studies have demonstrated a potential for this material to prevent demineralization and/or aid in remineralization of tooth surfaces. The mode of action of this material results from interactions with aqueous solutions. When introduced into the oral environment, the material releases sodium, calcium, and phosphate ions, which then interact with oral fluids and result in the formation of a crystalline hydroxycarbonate apatite (HCA) layer that is structurally and chemically similar to natural tooth mineral. This article will focus on the mechanisms of action of NovaMin and present results from a series of in vitro and in situ studies demonstrating the potential of this material in the areas of remineralization and caries prevention.
It was hypothesized that applying the polymer-induced liquid-precursor (PILP) system to artificial lesions would result in time-dependent functional remineralization of carious dentin lesions that restores the mechanical properties of demineralized dentin matrix. 140 µm deep artificial caries lesions were remineralized via the PILP process for 7–28 days at 37°C to determine temporal remineralization characteristics. Poly-L-aspartic acid (27 KDa) was used as the polymeric process-directing agent and was added to the remineralization solution at a calcium-to-phosphate ratio of 2.14 (mol/mol). Nanomechanical properties of hydrated artificial lesions had a low reduced elastic modulus (ER = 0.2 GPa) region extending about 70 μm into the lesion, with a sloped region to about 140 μm where values reached normal dentin (18–20 GPa). After 7 days specimens recovered mechanical properties in the sloped region by 51% compared to the artificial lesion. Between 7–14 days, recovery of the outer portion of the lesion continued to a level of about 10 GPa with 74% improvement. 28 days of PILP mineralization resulted in 91% improvement of ER compared to the artificial lesion. These differences were statistically significant as determined from change-point diagrams. Mineral profiles determined by micro x-ray computed tomography were shallower than those determined by nanoindentation, and showed similar changes over time, but full mineral recovery occurred after 14 days in both the outer and sloped portions of the lesion. Scanning electron microscopy and energy dispersive x-ray analysis showed similar morphologies that were distinct from normal dentin with a clear line of demarcation between the outer and sloped portions of the lesion. Transmission electron microscopy and selected area electron diffraction showed that the starting lesions contained some residual mineral in the outer portions, which exhibited poor crystallinity. During remineralization, intrafibrillar mineral increased and crystallinity improved with intrafibrillar mineral exhibiting the orientation found in normal dentin or bone.
Acid-etched dentin samples with a zone of demineralized dentin were remineralized via the polymer-induced liquid-precursor (PILP) process. Poly-L-aspartic acid was used as the polymeric process-directing agent. Samples were incubated in the mineralization solution for 1–4 weeks. Dentin samples remineralized by the PILP process presented a surface morphology very similar to the intact mineralized dentin’s architecture, in contrast to samples mineralized via the conventional nucleation and growth method (without polymer additive), which led to a superficial crust of randomly organized mineral crystals. Energy dispersive x-ray spectroscopy analysis of the PILP-mineralized samples showed the presence of calcium and phosphate ions at high levels. Since no hydroxyapatite (HA) clusters were observed on the surface of the PILP-mineralized samples, we could conclude the signal was produced from the mineral embedded within the dentin matrix. TEM and diffraction analyses suggest that both intrafibrillar and interfibrillar remineralization occurred in the demineralized dentin matrix.
In animal facilities, noises, often poorly controlled, occur over a wide range of frequencies and intensities. Evidence demonstrates that audible noise and ultrasound have deleterious effects on rodent physiology, but it is not known how they affect the autonomic nervous system (ANS). This study exposed 3 unrestrained, male, Sprague-Dawley rats daily to a 15-min white noise regime (90 dB), a quiet regime, or a 15-min ultrasound regime (90 dB at 4 frequencies in the range 20 to 40 kHz)--each for several weeks--and used radiotelemetry to monitor their cardiovascular responses. Exposure to audible noise increased heart rate and mean arterial pressure. Spectral analysis of HR variability showed diminished stimulation of the parasympathetic nervous system, shifting the sympathovagal balance. However, ultrasound, at the frequencies used, did not reproducibly affect cardiovascular parameters. The preliminary data obtained from this study indicate that audible noise, but not ultrasound (delivered using the same protocol), affects the ANS. Because the cardiovascular, respiratory, renal, and gastrointestinal systems are under autonomic control, such noise could have wide-ranging effects on animal physiology.
Background: Little is known about extensor tendon failure following drill injury at the time of volar plate fixation. Our goals were to analyze extensor tendon injury following simulated drill penetration, and change in tendon displacement during cyclic loading following simulated drill penetration injury. Methods: Extensor pollicis longus (EPL) and extensor carpi radialis brevis (ECRB) tendons were harvested from 9 fresh frozen cadaveric arms. Eighteen EPL and 18 ECRB samples were created from harvested tendons. Drill penetration injury was performed in either a continuous or an oscillating mode. Injured tendons were subjected to 1200 cycles at 1-to 15-kg cyclic load at a frequency of 1 Hz, and analyzed for failure at drill sites and change in displacement throughout the testing cycle. Results: Ten EPL samples and 16 ECRB samples completed testing without failure. Tendon type (ECRB, EPL), mode of injury (continuous, oscillating), and location (proximal, distal) did not affect tendon displacement during loading. A single EPL tendon failed following continuous drill penetration injury. Extensor carpi radialis brevis samples had a mean change in displacement of 2.8 (standard deviation [SD]: 1.5 mm) and 5.9 mm (SD: 4.7 mm) for oscillating and continuous modes, respectively. Six EPL samples had a mean change in displacement of 4.7 (SD: 2.7 mm) and 4.3 mm (SD: 1.8 mm) for oscillating and continuous modes, respectively. Conclusions: Complete extensor tendon failure due to drill penetration was rare. Drill mode did not affect the degree of elongation. Increasing cyclic loading of extensor tendons after drill injury caused modest extensor tendon elongation.
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