The prevalence of dental caries has been reduced significantly in some segments of the population over the past 25 years. The observed reduction has been attributed largely to increased exposure to fluoride in drinking water and use of fluoridated dentrifrices. During the same time period the use of food preservatives e.g. benzoates, sorbates, propionates, salicylates has also increased dramatically. For example the consumption of benzoate in the U.S. has increased from 1.8 million tons in 1970 to 25.5 million in 1995. Thus humans are exposed to preservatives constantly; persons in the U.S. consuming the average amount of soda ingest 800 mg of benzoate daily. Food preservatives are weak acids and exert their anti-microbial effect in a manner similar to that of fluoride i.e. at low pH values they diffuse undissociated through the bacterial cell membrane and acidify the cytoplasm, rendering microorganisms sensitive to acid. Acid tolerance is a characteristic of cariogenic organisms. Weak acids may also affect bacterial membranes. We have preliminary data which show that benzoates reduces the production of glycosyltransferase by microorganisms without affecting the enzymatic activity. This observation is consistent with an earlier report (Bowen and Hewitt, 1971) which showed that fluoride in growth medium influences the production of glucosyltransferase by mutans streptococci. Data from preliminary studies conducted in rats show that benzoate and non-steroidal anti- inflammatory agents e.g. ketoprofen (weak-acid) enhances the cariostatic effect of fluoride and also many suppress mutans populations. The purpose of the present study is to explore the effects of well-recognized food preservatives alone or in combination with fluoride on caries in our animal model. The outcome of this research could result in identifying a novel method of enhancing the effectiveness of fluoride.
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