M Beerens

EFFECTS OF MI PASTE PLUS ® : A 3-MONTHS FOLLOW-UP 4 69 that lesions are not easily remineralised may require a different approach. New, upcoming techniques for lesion infiltration seem promising and provide an immediate aesthetic improvement (Paris et al. , 2010). The efficacy of these products still needs to be proven in long-term clinical studies to ensure that they do indeed protect the WSL from further demineralisation (Paris and Meyer-Lueckel, 2010). Another option would be to first open up the lesions by acid-etching before remineralisation treatment. Only an in situ study with very early decalcifications was reported (Al-Khateeb et al. , 2000). Given the fact that fixed appliances form a retention site for plaque, it was assumed that the amount of plaque sampled would be higher at the end of treatment with fixed appliance than after debonding. The fixed appliances hampered plaque sampling, resulting in similar amounts of plaque being collected before and after debonding. Also, the numbers of CFU counts per sample were similar at all time-points. Thus, in contrast to the expected decrease, the results showed no significant changes. Furthermore, it was expected that the proportions of aciduric bacteria, S . mutans , and Lactobacillus spp. Would have been high at the end of treatment with the fixed appliance and to decrease after the appliance was debonded. This was confirmed, as we found a high proportion of aciduric bacteria at T0 and a significant decrease at 6 and 12 weeks after debonding (T2 and T3, respectively). The use of CPP-ACPF paste did not show an additional beneficial effect. Also, the proportion of S. mutans was extremely high just before debonding. Based on the literature it was assumed that we would observe a greater reduction in the proportion of S. mutans in the CPP-ACPF group than in the control group, as a result of binding of the CPP-ACP nano-complexes to S. mutans (Schupbach et al. , 1996; Rose, 2000). This assumption was not supported by the results from our study. The proportion of S. mutans may simply be so high that a longer period is needed to reach the expected and desired reduction. The proportion of Lactobacillus spp. was low. In contrast to the reported correlation between S. mutans and Lactobacillus spp. with caries (Boersma et al. , 2005; Sanpei et al. , 2010), Lactobacillus spp. were frequently not detected at all just before debonding. In many cases the Rogosa agar was heavily colonized with S. mutans rather than with Lactobacillus spp. Although Rogosa agar favours the growth of Lactobacillus spp. over other species, other bacteria may still grow when abundant. When comparing our results with those from