Demineralization Inhibition by High-Speed Scanning of 9.3 µm CO2 Single Laser Pulses Over Enamel.

BACKGROUND AND OBJECTIVE: In vitro studies were conducted to evaluate the use of an automated system for high-speed scanning of single 9.3 µm CO2 laser pulses in the inhibition of caries-like lesion formation in the enamel of extracted human molars. The effect of the laser in generating an acid-resistant layer and the effect of the layer on inhibiting surface mineral loss during pH cycling was explored. STUDY DESIGN/MATERIALS AND METHODS: Laser irradiation was performed with fluences of 0.6, 0.8, and 1.0 J/cm2 for single pulses of 1 mm diameter (1/e2 ), with pulse durations of 17, 22, and 27 microseconds, respectively. The laser was scanned at a 750 Hz pulse repetition rate in an automated pattern covering an area of 7 mm2 in 0.3 sec. Six treatment groups were investigated: three groups for each fluence for laser-only and three for laser irradiation with additional fluoride from a toothpaste slurry (sodium fluoride at 1100 ppm). Each group used non-irradiated areas, which included untreated controls for the laser-only groups and a fluoride-only treatment for the groups with additional fluoride. pH cycling was performed on both groups, followed by microhardness testing to determine the relative mineral loss (∆Z) from a caries-like formation and surface mineral loss (∆S). RESULTS: Laser irradiation with the 9.3 µm CO2 laser generated an acid-resistant layer of about 15 µm in depth. For the laser-irradiated samples with additional fluoride application, the relative mineral loss (∆Z) was 113 ± 63 vol%-µm, while for those with only fluoride application ∆Z was 572 ± 172 vol%-µm. At the highest fluence (1.0 J/cm2 ) used, an 80.2% inhibition of caries-like lesion was measured by ∆Z. Using only laser irradiation at the highest fluence resulted in an inhibition of caries-like lesion of 79.5% for the irradiated samples (∆Z = 374 ± 149 vol%-µm) relative to the control (∆Z = 1826 ± 325 vol%-µm). Surface microhardness tests resulted in an inhibition of surface softening, as measured by the Knoop Hardness Value (KHN) (108 ± 33 KHN for laser irradiated with additional fluoride, for non-irradiated controls with fluoride only 52 ± 16 KHN). Inhibition of surface loss was observed for all laser fluences, but the maximum surface loss for the untreated control group was only 2.2 ± 0.49 µm. CONCLUSIONS: The results demonstrate a significant benefit of the 9.3 µm CO2 laser at fluences of 0.6, 0.8, and 1.0 J/cm2 in caries-like lesion inhibition as measured by the relative mineral loss in depth and surface mineral loss, without significant damage to the enamel. Additionally, inhibition of surface softening and surface loss during pH cycling was observed. The surface loss was small compared with the overall lesion depth and thickness of the generated acid-resistant layer. Lasers Surg. Med. © 2020 Wiley Periodicals LLC.

Histopathological and biomechanical changes in soft palate in response to non-ablative 9.3-µm CO2 laser irradiation: an in vivo study.

The purpose of this study was to investigate in vivo the biomechanical and morphological changes in soft palates of Wistar rats from non-ablative irradiation with a 9.3-µm CO2 laser. A blinded, randomized, controlled study was designed with 45 Wistar rats categorized into treated and control sets. The treated set was exposed to 9.3-µm CO2 laser irradiation at an average power of 1.0 W and a single pulse fluence of 0.16 J/cm2 scanned using an automated system at a repetition rate of 315 Hz in a patterned area covering 0.4 cm2 in 6 s. The tissue of each animal was excised and divided into two halves. One-half was sectioned for histopathology, and the other half was used to measure tissue stiffness, which was reported as the effective Young's modulus. Measurements for both sets were taken at three time points: days 1, 21, and 35. There were no significant adverse events or changes in the behavior of the rats over the duration of the study. The treated set exhibited an order of magnitude increase in stiffness relative to the controls, which was maintained over the three time points. Histopathology showed a moderate contraction/disruption of the lamina propria collagen observed at day 1 and collagen accumulation observed at days 21 and 35 in the tissue remodeling phase. Non-ablative 9.3-µm CO2 laser irradiation can safely increase oral mucosal stiffness and can be used as an effective treatment to reduce tissue vibrations that are associated with snoring.

Thermal Testing of Titanium Implants and the Surrounding Ex-Vivo Tissue Irradiated With 9.3um CO2 Laser.

PURPOSE: To measure the temperature rise and surface damage of titanium dental implants and the surrounding tissue in a pig jaw during 9.3-µm carbon dioxide (CO2) laser irradiation at various durations of time. MATERIALS AND METHODS: Thermal analysis tests were performed on 12 implants with the same surface. Twelve implants mounted alone or in pig jaws were laser-irradiated with a 9.3-µm CO2 laser using 3 different power settings. The temperature of the implant body and the proximal tissues was measured with a J-Type Thermocouple after being laser-irradiated with 3 different power setting for 30, 60 seconds, and 2 minutes. Scanning electron microscope (SEM) and digital microscope images were also taken of the all the implants before and after laser irradiation to detect the presence or absence of surface damage. RESULTS: Temperature analysis showed that in all cases the implant and the proximal tissue temperatures remained around the start temperatures of the implant and tissues with fluctuations of ±3°C but never reached the upper threshold of 44°C, the temperature at which thermal injury to bone has been reported. Digital and SEM images that were taken of the implants showed an absence of surface damage at the cutting speed of 20% (0.7 W); however, cutting speeds of 30% to 100% (1.0-4.2 W) did yield surface damage. CONCLUSIONS: Laser irradiation of titanium implant surfaces using a 9.3-µm carbon dioxide laser with an average power of 0.7 W showed no increase in thermal temperature of the implant body and tissue temperatures as well as no evidence of implant surface damage.

Detection of Amyloid ß Signature in the Lens and Its Correlation in the Brain to Aid in the Diagnosis of Alzheimer's Disease.

We report the findings from a clinical trial in which a group of patients clinically diagnosed with probable Alzheimer's disease (AD) were discriminated from an age-matched group of healthy volunteers (HVs) with statistical significance (P<.001). The results from 20 patients with AD and 20 HVs were obtained by a Fluorescent Ligand Eye Scanning (FLES) technique that measures a fluorescent signature specific to an exogenous ligand bound to amyloid-ß in the lens of the eye. Sensitivity and specificity of 85% and 95%, respectively, have been achieved in predicting clinical diagnosis. Additionally, amyloid brain imaging using florbetapir F18 positron emission tomography shows significant correlation with the results obtained in the eye. Results of the study demonstrate the safety of the FLES system.

Alzheimer's disease diagnosis by detecting exogenous fluorescent signal of ligand bound to Beta amyloid in the lens of human eye: an exploratory study.

We report results of a clinical exploratory human trial involving 10 participants using a combination of a fluorescent ligand and a laser scanning device, SAPPHIRE System, as an aid in the diagnosis of Probable Alzheimer's disease (AD). To the best of our knowledge, this is the first time that such a technique has been used in vivo of a human lens. The primary goal of the clinical trial, in addition to safety assessment, was to evaluate efficacy of the system. By detecting specific fluorescent signature of ligand bound beta amyloid in the supranucleus (SN) region of the human lens, a twofold differentiation factor between AD patients and Control groups is achieved. Data from our studies indicates that deeper regions of the SN provide the highest measures of ligand bound fluorescence signal from both controls and patients with AD. In addition, we present preclinical studies that were performed to investigate the binding affinity of the ligand to beta amyloid and evaluate the pharmacokinetics of the ligand in rabbit eyes. Further studies are underway involving a larger population for statistical evaluation of the method.

Spectrally balanced detection for optical frequency domain imaging.

In optical frequency domain imaging (OFDI) or swept-source optical coherence tomography, balanced detection is required to suppress relative intensity noise (RIN). A regular implementation of balanced detection by combining reference and sample arm signal in a 50/50 coupler and detecting the differential output with a balanced receiver is however, not perfect. Since the splitting ratio of the 50/50 coupler is wavelength dependent, RIN is not optimally canceled at the edges of the wavelength sweep. The splitting ratio has a nearly linear shift of 0.4% per nanometer. This brings as much as +/-12% deviation at the margins of wavelength-swept range centered at 1060nm. We demonstrate a RIN suppression of 33dB by spectrally corrected balanced detection, 11dB more that regular balanced detection.

Influence of scattering on transmission through long-period fiber gratings and tunable microstructure fibers.

Controlled optical scattering within or around an optical fiber provides a potentially useful mean for adjusting its transmission characteristic. This approach can complement conventional methods based on the establishment of well-defined variations in the index of refraction of the core or the cladding of the fiber. We describe the use of a highly scattering submonolayer of nanoparticles deposited onto the fiber surface for adjusting the resonance wavelength, depth, and width of an in-fiber long-period grating filter. We also introduce a polymer-dispersed liquid-crystal material that has a thermally tunable scattering cross section and can be incorporated into the channels of a microstructure optical fiber; this system may provide the means for a fiber-based scattering switch.