Potential mechanism for the laser-fluoride effect on enamel demineralization.

Laser-induced prevention of dental caries has been studied extensively. However, the cariostatic mechanisms of a combined fluoride-laser treatment are not well-understood. Using micro- computed tomography (micro-CT), we quantified the effect of fluoride and/or Er:YAG laser treatment on enamel demineralization. The mean mineral loss (%/V) for each group was 4,870 ± 1,434 (fluoride followed by laser treatment), 6,341 ± 2,204 (laser treatment), 7,669 ± 2,255 (fluoride treatment), and 10,779 ± 2,936 (control). The preventive effect of the laser (p < 0.001) and fluoride (p = 0.010) treatment was statistically significant. Characterized by micro-x-ray diffraction (XRD) analysis, the significant contraction in the a-axis after both laser and combined laser/fluoride treatment was revealed (both p < 0.05). In conclusion, subablative low-energy Er:YAG laser irradiation following fluoride treatment may instantaneously transform enamel hydroxyapatite into fluoridated hydroxyapatite to reduce enamel solubility as a preventive treatment for enamel demineralization.

Subablative Er:YAG laser effect on enamel demineralization.

OBJECTIVES: To characterize the cariostatic potential of a low-energy Er:YAG laser treatment. METHODS: Twelve sound premolars were selected. Two 2 × 1 mm windows were created on each tooth and randomly assigned to L(1) and L(2) groups. Three sites in each window were chosen with the middle site as the control and the left and right ones receiving Er:YAG laser treatment of 5.1 J/cm(2) (L(1)) or 2.0 J/cm(2) (L(2)), respectively. The teeth were further subjected to 4-day pH cycling to create caries-like lesions. After mineral quantification using a micro-computed tomography scanner, the preventive effects (ΔML = mineral loss of the control area minus that of the lased area) of L(1) and L(2) treatments were calculated based on the difference in the gray value of the control and lased sites. RESULTS: Significant inhibitory effects of L(1) and L(2) on enamel demineralization were demonstrated (both p ≤ 0.001), with the L(1) treatment having a greater effect (45.2%) than the L(2) treatment (25.2%, p = 0.004). CONCLUSIONS: Subablative low-energy Er:YAG laser irradiation can significantly prevent enamel demineralization potentially through the retardation of enamel diffusion. This study confirmed that high-energy laser treatment, which may damage the peripheral and underlying tissues, may not be needed for caries prevention.

Novel PCL-based honeycomb scaffolds as drug delivery systems for rhBMP-2.

This study investigated a novel drug delivery system (DDS), consisting of polycaprolactone (PCL) or polycaprolactone 20% tricalcium phosphate (PCL-TCP) biodegradable scaffolds, fibrin Tisseel sealant and recombinant bone morphogenetic protein-2 (rhBMP-2) for bone regeneration. PCL and PCL-TCP-fibrin composites displayed a loading efficiency of 70% and 43%, respectively. Fluorescence and scanning electron microscopy revealed sparse clumps of rhBMP-2 particles, non-uniformly distributed on the rods' surface of PCL-fibrin composites. In contrast, individual rhBMP-2 particles were evident and uniformly distributed on the rods' surface of the PCL-TCP-fibrin composites. PCL-fibrin composites loaded with 10 and 20 microg/ml rhBMP-2 demonstrated a triphasic release profile as quantified by an enzyme-linked immunosorbent assay (ELISA). This consisted of burst releases at 2 h, and days 7 and 16. A biphasic release profile was observed for PCL-TCP-fibrin composites loaded with 10 microg/ml rhBMP-2, consisting of burst releases at 2 h and day 14. PCL-TCP-fibrin composites loaded with 20 microg/ml rhBMP-2 showed a tri-phasic release profile, consisting of burst releases at 2 h, and days 10 and 21. We conclude that the addition of TCP caused a delay in rhBMP-2 release. Sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) and alkaline phosphatase assay verified the stability and bioactivity of eluted rhBMP-2 at all time points.

Compression-induced changes on physical structures and calcification of the aromatic polyether polyurethane composite.

It is generally accepted that stress causes calcification in both bio-prosthetic and polyurethane heart valves. However, simple uni-axially- and bi-axially-stretched samples did not yield a feasible model for the elaboration of the stress-induced calcification. In this study, heat compaction combined with the incorporation of polyethylene has been explored. Specimens of polyurethane were solution cast onto a porous bi-axially-drawn ultra-high-molecular-weight polyethylene film and then heat compacted under a pressure of 18 MPa at a chosen temperature for 1.5 h. The heat-compaction-induced calcification and physical changes of the polyurethane composite were evaluated using a 28-day in vitro calcification model and Attenuated Total Reflection-Fourier Transform-Infrared (ATR-FT-IR) spectroscopy. The calcification results indicated that heat-compaction-induced calcification was double that achieved without heat compaction. Heat-compacted polyurethane composite showed higher affinity to calcium ions than the non-heat compacted sample. The ATR-FT-IR results showed that the heat-compaction-induced physical changes include distortions of polymeric molecules and permanent changes of microstructures. The distortions of polymeric molecules could be deteriorated in contact with different media. The relaxation of the stressed structures of the polyether moiety might serve as a calcium trap and a heterogeneous nucleation site for calcification. The permanent changes of microstructures resulted from high distortions also served as affinity sites attracting calcification.