2. The second mechanisms may be the cariostatic action
of the reaction products between SDF and mineral
component of the tooth. Selvig[35] showed that the
fluoride treatment increased the resistance of the
peri- and inter-tubular dentin to acid decalcification
and as a result, retarded the penetration of acid into
deeper layers of the dentin. Shimooka[36] pointed out
that F− ion of SDF applied to dentin under in vivo
conditions penetrated to a depth of 50–100 μ. It has
been reported that SDF (Ag(NH3)2F) reacts with the
tooth mineral hydroxyapatite (HA)(Ca10(PO4)6(OH)2)
to release calcium fluoride (CaF2) and silver
phosphate (Ag3PO4), which are responsible for
the prevention and hardening of dental caries.
A simplified chemical reaction was suggested as
shown below
Ca10(PO4)6(OH)2 + Ag(NH3)2 → CaF2 + Ag3PO4 +
NH4OH
CaF2 → Ca++ + 2F−
Ca10(PO4)6(OH)2 + 2F− → Ca10(PO4)6F2 + 2OH−
The Ag3PO4 that precipitates on the tooth surface is
insoluble. The CaF2 formed provides a reservoir of
fluoride for the formation of fluorapatite (Ca10(PO4)6F2),
which is more resistant to acid attack than HA
(Ca10(PO4)6(OH)2).[37] Fluorapatite is so stable that it
extremely resists decalcification by acid and chelating
agent.[17,33] In addition, it is known that F− promotes
calcification, and also restores lattice imperfection,[38]
and improves the crystallinity of HA.