Carbonated portions weaken the structure and render the tissue susceptible to attack.
Food remnants and debris mix with saliva and adhere to tooth surfaces as a slimy film
known as dental plaque. Oral bacteria, and most importantly certain types of
cariogenic bacteria (e.g. Mutans streptococci and Lactobacilli species), metabolize
dental plaque and produce acid which lowers the pH of the oral environment. When
the pH is below the critical pH for hydroxyapatite (<5.5), demineralization occurs
with a net outward flow of calcium and phosphorous ions from the enamel surface
into plaque and saliva. When the pH returns to 7.0, remineralization occurs with a net
inward flow of ions into the enamel surface. If fluoride is present during
remineralization, it is incorporated to form fluorapatite [Ca 10 .(PO 4 ) 6 .F 2 ], which is
more stable and resistant to further acid attacks. The process of demineralization and
remineralization is an ongoing one and frequently referred to as 'the ionic see-saw' or
'tug-of-war'. This is now widely believed to be the most important preventive action
of fluoride, and a constant post-eruptive supply of ionic fluoride is thought to be most
effective.
A number of mechanisms have been proposed to explain the action of fluoride (254HTable
6.7). The first is that fluoride has an effect during tooth formation by substitution of
hydroxyl ions for fluoride ions, thereby reducing the solubility of the tooth tissues.
Second, fluoride can inhibit plaque bacterial growth and glycolysis. At pH 7.0,
fluoride ions are precluded from entering bacteria. However, at pH 5.0, fluoride exists
as hydrofluoric acid, which crosses the bacterial cell membrane to interfere with its
metabolism, by specifically inhibiting the enzyme enolase in the glycolytic pathway.
Third fluoride inhibits the demineralization of tooth mineral when present in solution
at the tooth surface. Fourth, fluoride enhances remineralization by combining with
calcium and phosphate to form fluorapatite. Fluoride enhances crystal growth,
stabilizes and makes the tissue resistant to further acid attack. Enamel apatite
demineralizes when the pH drops to pH 5.5. However, when fluorapatite is formed
during remineralization, it is even more resistant to demineralization as the critical pH
for fluorapatite is pH 3.5. Therefore, it is most important to have an intraoral source of
fluoride when remineralization is taking place. Lastly, fluoride affects the morphology
of the crown of the tooth, making the coronal pits and fissures shallower. Such
shallower pits and fissures will be less likely to collect food debris, allow stagnation
and become decayed. The most important of these mechanisms is that when fluoride
is present in the oral environment at the time of the acid attack it inhibits
demineralization and promotes remineralization.
As early as 1890, Miller drew attention to the dissolutive process of dental caries and
directed efforts to inhibit dissolution. The clinical findings of the anti-caries activity
of drinking water with fluoride caused researchers to seek reasons for this. The
finding that fluoride-treated enamel had a lower solubility led many to consider this as
a cause and effect relationship. The anti-caries action of fluoride was thought to be
one of preventing dissolution of enamel, and efforts were made to incorporate more
and more amounts of fluoride into surface enamel. The first topical agent used, after
water fluoridation, was a 2% sodium fluoride solution and there was a greater uptake
of fluoride into enamel from acidified solutions. Numerous fluoride preparations with
varying concentrations of fluoride were employed for topical application and used as
anti-caries agents. It was noted that there was not much difference in the caries
reductions reported from the topical fluoride studies despite great variations in the
fluoride concentrations used. In addition, the difference in the levels of fluoride in