Prevalence of enamel defects and dental caries among 9-year-old Auckland children.
Schulter PJ, Kanagaratnam S, Durward CS, Mahood R
NZ Dental Journal December 2008 (p145-152)
This study found that water fluoridation increases the incidence of dental fluorosis, but has no lasting benefit in reducing tooth decay.
The study concluded that there had not been a significant increase in fluorosis incidence since the 1980s (which was already 3 times higher than predicted when fluoridation was first proposed). The levels reported then were around 25% to 28% (Colquhoun, 1985).
Dental fluorosis incidence
- 29.1% of fluoridated children had dental fluorosis compared with 14.7% of unfluoridated children
- Diffuse opacities (dental fluorosis) were the predominant tooth defects
Tooth decay rates
- There was no difference in tooth decay rates in the permanent teeth (this differs from the Southland study, but at age 9 there is often an apparent benefit, likely due to delayed tooth eruption caused by fluoridation, that disappears by age 12 to 15 – see Armfield and Spencer, 2004)
- There was no statistically significant difference in tooth decay rates in deciduous (“baby”) teeth based on affected tooth surfaces (dmfs score)
- Fluoridated children had less tooth decay in deciduous teeth on a per tooth basis (dmft) and number of children caries free (62% v 55%)
The study noted that:
- international research shows that the increase in dental fluorosis levels is directly related to total fluoride intake, and detectable even at small differences in intake
- the swallowing of fluoride toothpaste by very young children (perhaps 50% of that placed on the toothbrush) is a risk factor (note – the Ministry of Health, NZ Dental Association, and Plunket advocate practices that significantly increase the amount of fluoride swallowed by young children)
- the effect of fluoride in (allegedly) reducing tooth decay is primarily due to topical effect after the tooth has erupted (i.e. not from swallowing it).
- fluoride tablets taken before tooth eruption have little effect on tooth decay but “present a clear risk for fluorosis”.
This study examined 310 fluoridated and 302 unfluoridated children, based on current fluoridation status.
About half the children had intermittent residence in fluoridated areas, and some were unknown. It is not stated when the exposure occurred, even though international studies show that it is the time of exposure that is critical in causing fluorosis – the first 6 months is most critical if bottle fed, with reducing but significant risk up to age 4. The 2005 Southland study also showed a higher incidence of fluorosis in those who had lived in fluoridated areas up to age 4.
The study did not separate out those who had had lifelong exposure to fluoridation, though it utilised a complex statistical modelling to counteract, in part, this shortfall. We do not consider the other “justifications” tenable if the purpose was to determine the effects of water fluoridation.
Socio economic status was determined by the school decile rating, rather than the SES status of each child. Although this approach is not considered appropriate, the results suggest it has not significantly impaired the study.
There was a significant difference in SES status between fluoridated and unfluoridated children (the unfluoridated children has the lower SES status, which international studies show is the main factor in higher levels of tooth decay).
Many of the first molar permanent teeth, at higher risk of decay than other teeth, were fissure-sealed. This would corrupt the caries results, but, if so, seems to demonstrate that fissure-sealing is a more effective method of caries prevention than fluoridated water.