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24 I I research _ bleaching cosmeticdentistry 2_2011 (10X/0.3 objective). High-resolution confocal mi- croscopic images were then obtained. _Results Figures 3 to 6 show representative confocal micrographs of treated sections and untreated sections. Figure 3a shows 6 µm subsurface of 10 % carbamide peroxide control area and Figure 3b shows the treated 10 µm subsurface. In Figure 3b, a subsurface crack is visible. As evident from Figures 3a, 4a, 5a and 6a, there was an uptake of dyes in the control groups. From all our observations, there were no signifi- cant subsurface porosities observed up to a depth of 100 µm, the limit of our methodology. The dye was associated mainly with enamel cracks as the depthofobservationincreased.Theperipheryofthe superficialenamelprismshowsincreaseduptakeof the marker, indicating a possible route for the oxi- dation product to diffuse through enamel surface. Generalobservationsindicatethatthedyefollowed inherent cracks to deep areas in the enamel sub- surface (Figs. 3b, 4a, 6a & b). _Discussion Whilemoststudieshaveevaluatedtheeffectof whitening on the morphological effect of enamel and dentine, the present study focused on the significance of subsurface enamel pores and de- fects. In our study, we did not find any significant subsurface porosities, observed up to a depth of 100 µm. The cycling treatment methodology with artificial saliva storage for 17 hours may have re- paired some of the initial damage done by the bleaching. We also did not find any difference be- tween the ACP and the OP groups. Opalescence PF 10 % contains fluoride and potassium nitrate, but it is unknown whether these two ingredients per- form the same desensitising function as claimed by ACP. Iwamoto et al. showed similar negative results when silver nitrate was used as the staining agent. Inthatstudy,nopenetrationwasseenintheenamel of any of the groups.18 However, we did see pene- tration of the dye in the periphery of the enamel prism in both the control and the treatment groups for both whitening materials. The increased uptake may be due to the removal of the organic compo- nents from the superficial enamel layers by the bleaching agent. The uptake of dyes in the control groups was not expected. This may be explained by the fact that exposed enamel is under constant attackintheoralenvironment.Theweakenedpores may be the inroad for chromopores and peroxide alike. The penetration of the dyes was especially no- ticeablewhenwefollowedsurfacecrackstoadepth of 100 µm (Fig. 4a). The uptake of dyes through the cracks may be clinically significant, since it may explainwhycertainpatientsareespeciallysensitive to bleaching. If diffusion through the enamel inter- crystallinespacesisthesolecauseofsensitivity,one wouldexpecttofindhigherincidenceofseveresen- sitivity.19 However, if subclinical defects/cracks are the cause, the clinical picture of severe sensitivity reported to be around 4 % can be better explained. Enamel cracks or lamellae have been suggested to be initiation sites for caries.20 AsseeninFigure4b,theperipheryoftheenamel prism shows increased uptake of the marker, in- dicating a possible route for the oxidation prod- uct to diffuse through the enamel surface. Based on our findings, we hypothesise that peroxide initially penetrated into and through the enamel intercrystallinespacestoreachtheenameldentine junction and dentine regions. Indeed, in vitro ex- periments by a number of authors have demon- strated the penetration of low levels of peroxide, from a range of peroxide products and solutions, into the pulp chambers of extracted teeth after exposure times of 15 to 30 minutes.21–23 One would expect that diffusion of peroxide through Figs. 4a & b_OP control area 28 µm subsurface (a). The dye penetrated via the crack. OP-treated 24 µm subsurface (b). Figs. 5a & b_ACP control area 12 µm subsurface (a). ACP-treated 48 µm subsurface (b). Fig. 4a Fig. 4b Fig. 5a Fig. 5b