No abstract

No abstract

Recent in vitro work and a short clinical study suggest that adding a bonding agent layer between sealant and saliva-contaminated enamel allows for adequate bond strength and retention of resin sealants and may improve success of all sealant applications. This five-year clinical study scored 617 occlusal and 441 buccal/lingual molar sealants, with use of a split-mouth design, with half receiving sealant alone and half bonding agent plus sealant. Treatment effects and potential risk factors for sealant failure were tested by means of a Cox regression model. Three bonding agent groups were analyzed for treatment effect: Tenure primer, Scotchbond Multi-Purpose, and 3 single-bottle dentin bonding agents as a third group. The single-bottle group was successful in reducing risk of sealant failure, with a hazard ratio (HR) of 0.53 (p = 0.014) for occlusal and 0.35 (p = 0.006) for buccal/lingual sealants. Scotchbond was detrimental to occlusal sealant success, with a HR of 2.96 (p = 0.0003). Tenure primer was neutral, showing HRs close to 1.0. Variables that affected success differed between occlusal and buccal/lingual sealants, suggesting that failures on these two surfaces may be dependent upon differing factors. Early eruption stage was a significant risk factor for both surfaces (HR = 2.91, p = 0.00001, occlusal; and HR = 1.52, p = 0.015, buccal/lingual). Behavior (HR = 1.96, p = 0.0007), salivary problems (HR = 1.73, p = 0.002), and visually apparent variations in enamel (HR = 1.51, p = 0.018) were significant risk factors for occlusal sealants only. In addition to completing detailed analyses of risk factors for sealant survival, this study shows that single-bottle bonding agents protect sealant survival, yielding half the usual risk of failure for occlusal sealants and one-third the risk of failure for buccal/lingual sealants.

Mutations in the human amelogenin gene (AMELX, Xp22.3) cause a phenotypically diverse set of inherited enamel malformations. We hypothesize that the effects of specific mutations on amelogenin protein structure and expression will correlate with the enamel phenotype, clarify amelogenin structure/function relationships, and improve the clinical diagnosis of X-linked amelogenesis imperfecta (AI). We have identified two kindreds with X-linked AI and characterized the AMELX mutations underlying their AI phenotypes. The two missense mutations are both in exon 2 and affect the translation initiation codon and/or the secretion of amelogenin (p.M1T and p.W4S), resulting in hypoplastic enamel. Primary anterior teeth from affected females with the p.M1T mutation were characterized by light and scanning electron microscopy. The thin enamel had defective prism organization, and the surface was rough and pitted. Dentin was normal. The severity of the enamel phenotype correlated with the predicted effects of the mutations on amelogenin expression and secretion.