Viewed under a scanning electron microscope, the infiltrant material appeared to cover the adjacent apparently sound enamel more thickly and evenly compared with the MIH lesion surface, and although some surface porosities were still evident, these were less frequent and narrower than those on non-infiltrated MIH lesions (Fig. 2). These initial results demonstrate that caries infiltrant materials are capable of penetrating developmentally hypomineralised MAPK inhibitor enamel; however, this occurs in an inconsistent manner and is not as extensive as reported in carious lesions[7]. Based

on MIH characterisation studies, the pattern of infiltration is not explained easily by mineral content or porosity variation, indicating different lesion characteristic/s determine penetrability; with protein content a probable candidate. The failure of NaOCl pre-treatment to produce consistent or significantly improved results means consideration Tigecycline clinical trial must be given to other enamel properties but could also reflect that only the surface proteins are removed,

that this is not the most efficacious agent for the particular proteins present or, be a result of cross-linking by formaldehyde during sterilisation inhibiting protein removal. The recommended etch time is based on that required to penetrate the relatively hypermineralised surface layer of carious lesions: in MIH, this surface layer may have different properties, and the standard etching may be insufficient to allow full access to the lesion. The clinical history these of the teeth used in this study is unknown but use of remineralising agents, common in MIH management, and time in the oral environment

may influence surface layer properties or enamel penetrability. The inherent variability of MIH lesions may also be a confounding factor in achieving significant differences, particularly in terms of microhardness and given the small sample size. Similarly, given reports of higher protein content in brown lesions[13], different colour grouping of the lesions may yield different results; however, there were insufficient brown lesions for statistical analysis in this study. The surface changes observed under SEM confirm that microporosities in defective enamel can be occluded, although perhaps only partially. The sealing of surface defects and inter-rod diffusion pathways could reduce the susceptibility of the enamel to caries. This improved enamel seal may also reduce irritation to the pulp which may in turn decrease pulpal inflammation and sensitivity to evaporative, thermal, and osmotic stimuli common in MIH.