V.E. Dos Santos, Jr., de Vasconcelos, F.M., Ribeiro, A.G., and A. Rosenblatt. Paradigm shift in the effective treatment of caries in schoolchildren at risk. Int Dent J. 2012 Feb;62(1):47-51. doi: 10.1111/j.1875-595X.2011.00088.x.
Background: Silver diamine fluoride (SDF) is an effective agent for the arrest of caries in children, is easy to apply and can be used outside the clinical environment. Interim restorative treatment (IRT) using glass ionomer cement has also been claimed to be a simple and effective method to arrest caries in deciduous teeth.
Objective: To examine whether, for underprivileged schoolchildren with cavities, treatment with 30% SDF gives better results than IRT for carries arrest.
Method: This randomised controlled study compares the effect of IRT (FUJI IX) with 30% SDF in 91 children aged 5-6 years.
Results: After 1 year, treatment with SDF was more effective [relative risk (RR) = 66.9%] than IRT (RR = 38.6%) for the arrest of caries; this was statistically significant (P < 0.05).
Conclusion: The SDF technique showed better results than IRT for the arrest of cavities in deciduous teeth, indicating that its use for underprivileged communities may justify a paradigm shift in paediatric dentistry.
The following letter responds to a prior letter sent by Senator Inhofe Dec 6, 2011 (click here for prior post).
Click here or image below for source.
Denbesten, P., and W. Li. Chronic fluoride toxicity: dental fluorosis. Monogr Oral Sci. 2011;22:81-96. Epub 2011 Jun 23.
Abstract: Dental fluorosis occurs as a result of excess fluoride ingestion during tooth formation. Enamel fluorosis and primary dentin fluorosis can only occur when teeth are forming, and therefore fluoride exposure (as it relates to dental fluorosis) occurs during childhood. In the permanent dentition, this would begin with the lower incisors, which complete mineralization at approximately 2-3 years of age, and end after mineralization of the third molars. The white opaque appearance of fluorosed enamel is caused by a hypomineralized enamel subsurface. With more severe dental fluorosis, pitting and a loss of the enamel surface occurs, leading to secondary staining (appearing as a brown color). Many of the changes caused by fluoride are related to cell/matrix interactions as the teeth are forming. At the early maturation stage, the relative quantity of amelogenin protein is increased in fluorosed enamel in a dose-related manner. This appears to result from a delay in the removal of amelogenins as the enamel matures. In vitro, when fluoride is incorporated into the mineral, more protein binds to the forming mineral, and protein removal by proteinases is delayed. This suggests that altered protein/mineral interactions are in part responsible for retention of amelogenins and the resultant hypomineralization that occurs in fluorosed enamel. Fluoride also appears to enhance mineral precipitation in forming teeth, resulting in hypermineralized bands of enamel, which are then followed by hypomineralized bands. Enhanced mineral precipitation with local increases in matrix acidity may affect maturation stage ameloblast modulation, potentially explaining the dose-related decrease in cycles of ameloblast modulation from ruffle-ended to smooth-ended cells that occur with fluoride exposure in rodents. Specific cellular effects of fluoride have been implicated, but more research is needed to determine which of these changes are relevant to the formation of fluorosed teeth. As further studies are done, we will better understand the mechanisms responsible for dental fluorosis.
Click here for the full paper (fee).