Background: Dental fluorosis requires aesthetic treatment to improve appearance and etching of enamel surfaces with phosphoric acid is a key step for adhesive restorations. The aim of this study was to evaluate surface roughness and a depth profile in healthy and fluorotic enamel before and after phosphoric acid etching at 15, 30 and 60 seconds. Methods: One hundred and sixty enamel samples from third molars with no fluorosis to severe fluorosis were evaluated by atomic force microscopy. Results: Healthy enamel showed a statistically significant difference (p < 0.05) between mean surface roughness at 15 seconds (180.3 nm), 30 seconds (260.9 nm) and 60 seconds (346.5 nm); depth profiles revealed a significant difference for the 60 second treatment (4240.2 nm). For mild fluorosis, there was a statistically significant difference (p < 0.05) between mean surface roughness for 30 second (307.8 nm) and 60 second (346.6 nm) treatments; differences in depth profiles were statistically significant at 15 seconds (2546.7 nm), 30 seconds (3884.2 nm) and 60 seconds (3612.1 nm). For moderate fluorosis, a statistically significant difference (p < 0.05) was observed for surface roughness for 30 second (324.5 nm) and 60 second (396.6 nm) treatments. Conclusions: Surface roughness and depth profile analyses revealed that the best etching results were obtained at 15 seconds for the no fluorosis and mild fluorosis groups, and at 30 seconds for the moderate fluorosis group. Increasing the etching time for severe fluorosis decreased surface roughness and the depth profile, which suggests less micromechanical enamel retention for adhesive bonding applications.

One adverse effect of nifedipine, a long‐acting vasodilator, is gingival overgrowth. Preexisting gingival inflammation and/or dental plaque has been suggested to be responsible for the progression of this side effect, but the precise mechanism is uncertain because of a lack of suitable animal models. A study was therefore done to establish an experimental model of gingival overgrowth in rats and to investigate the possible involvement of gingival inflammation and/or dental plaque in its development. Specific pathogen‐free Fischer rats (male, 14 days old) were used . Gingival inflammation and dental plaque accumulation were induced by infection with Streptococccus mutans MT8148R. The nifedipine‐treated rats (experimental group) were fed a caries‐inducing diet contai ning nifedipine either with or without infection, while the nifedipine‐untreated rats (control group) were fed the same diet, similarly with or with out the infection. Marked gingival overgrowth was induced in the mandibular molar region of nifedipine‐treated rats regardless of S. mutans infection, although the infection resulted in a further increase in the degree of gingival overgrowth. Histological examination of the gingival overgrowth revealed the presence of redundant subepithelial connective tissue in the treated rats, and inflammatory cell infiltration was apparent only in the tissue of the S. mutans‐infected rats regardless of the nifedipine administration. These findings suggest that nifedipine induces gingival overgrowth in rats either in the presence or absence of gingival inflammatio n and/or dental plaque, although these factors can augment the effect of the drug. Our experimental system seems to be a useful model for studying the mechanism of this side effect.