Caries inhibition in vital teeth using 9.6-μm CO2-laser irradiation

Peter Rechmann, Daniel Fried, Charles Q Le, Gerald Nelson, Marcia Rapozo-Hilo, Beate M T Rechmann, John D B Featherstone, Peter Rechmann, Daniel Fried, Charles Q Le, Gerald Nelson, Marcia Rapozo-Hilo, Beate M T Rechmann, John D B Featherstone

Abstract

The aim of this study was to test the hypothesis that in a short-term clinical pilot trial short-pulsed 9.6 μm CO(2)-laser irradiation significantly inhibits demineralization in vivo. Twenty-four subjects scheduled for extraction of bicuspids for orthodontic reasons (age 14.9 ± 2.2 years) were recruited. Orthodontic brackets were placed on bicuspids (Transbond XT, 3M). An area next to the bracket was irradiated with a CO(2)-laser (Pulse System Inc, Los Alamos, New Mexico), wavelength 9.6 μm, pulse duration 20 μs, pulse repetition rate 20 Hz, beam diameter 1100 μm, average fluence 4.1 ± 0.3J∕cm(2), 20 laser pulses per spot. An adjacent nonirradiated area served as control. Bicuspids were extracted after four and twelve weeks, respectively, for a quantitative assessment of demineralization by cross-sectional microhardness testing. For the 4-week arm the mean relative mineral loss ΔZ (vol% × μm) for the laser treated enamel was 402 ± 85 (mean ± SE), while the control showed significantly higher mineral loss (ΔZ 738 ± 131; P = 0.04, t-test). The difference was even larger after twelve weeks (laser arm ΔZ 135 ± 98; control 1067 ± 254; P = 0.002). The laser treatment produced 46% demineralization inhibition for the 4-week and a marked 87% inhibition for the 12-week arm. This study shows, for the first time in vivo, that the short-pulsed 9.6 μm CO(2)-laser irradiation successfully inhibits demineralization of tooth enamel in humans.

Figures

Figure 1
Figure 1
Orthodontic bracket placed on the study bicuspids using a composite resin (Transbond XT); an area to be irradiated cervical to the bracket is marked.
Figure 2
Figure 2
Four or twelve weeks after irradiation the bicuspids were extracted; for quantitative assessment of demineralization by cross-section microhardness testing to evaluate the relative mineral loss ΔZ (vol% × μm), the teeth were cut into halves separating the laser irradiated area (L) from the nonirradiated control area (C).
Figure 3
Figure 3
Cross-section microhardness testing: The cross-section of a bicuspid is shown, presenting dentin (D), enamel (E), and the composite (Transbond XT) (C), which was used to glue the orthodontic bracket (B) onto the enamel surface; the lines of micro-indentations (M) were placed right below the enamel surface following a distinct distribution pattern; they are located directly below the area where the metallic orthodontic bracket (B) was fixed to the tooth with a composite (C); this area is where the microbial plaque challenge is most likely to cause demineralization.
Figure 4
Figure 4
Depth profile of vol% mineral loss for the controls (square symbols) in comparison to the laser treated areas (triangular symbols) from the bicuspids four weeks after treatment.
Figure 5
Figure 5
Depth profile of vol% mineral versus depth from the outer surface for the control group (square symbols) in comparison to the laser treated group (triangular symbols) from the bicuspids twelve weeks after treatment.
Figure 6
Figure 6
Mean relative mineral loss ΔZ (vol% × μm) for the laser treated enamel and for the controls (n = 12, SE) four weeks after treatment.
Figure 7
Figure 7
Mean relative mineral loss ΔZ (vol% × μm) for the laser treated enamel group and for the control group (n = 12, SE) twelve weeks after treatment.

Source: PubMed

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