Abstract
Zinc is an essential trace element. In the mouth, it is present naturally in plaque, saliva and enamel. Zinc is formulated into oral health products to control plaque, reduce malodour and inhibit calculus formation. It has good oral substantivity, and elevated concentrations can persist for many hours in plaque and saliva following delivery from mouthrinses and toothpastes. Although low concentrations of zinc can both reduce enamel demineralisation and modify remineralisation, during caries clinical trials, the addition of zinc to fluoride toothpastes has not affected their ability to reduce caries. Mechanistic studies may help explain this apparent contradiction. Zinc is readily desorbed from hydroxyapatite by calcium, which is plentiful in plaque and saliva. Where crystal-growth sites remain occupied by zinc despite this, they may simply be 'over-grown' by remineralisation initiated at unoccupied sites. Further, under certain conditions, low concentrations of zinc can enhance remineralisation of enamel lesions, by retarding lesion arrestment. Although this may help to explain the apparent lack of an overall zinc effect on caries, it seems unlikely that any negative effects would be countered exactly by positive effects. Further mechanistic studies, complementing well-designed in vitro and in situ caries studies, should lead to further understanding of the zinc-enamel interactions relevant to demineralisation and remineralisation.