There is considerable evidence for an association between dental carie
s and food starches. However, the intraoral utilization of starch may
be quite complex, giving rise to conflicting results. Demineralization
induced by unsweetened cookies was examined in an intraoral model sys
tem that utilized palatal appliances containing blocks of bovine ename
l. The enamel surfaces were covered with either a filter paper disc to
trap sugars or a layer of Streptococcus mutans to metabolize the suga
rs and bring about enamel demineralization. Demineralization was deter
mined as an increase in porosity with respect to iodide ions (delta Ip
). Measurements revealed a rapid elevation and maintenance of high lev
els of maltose in the plaque space after ingestion of the unsweetened
or sweet cookies. Entrapped food particles appeared to serve as a rese
rvoir of maltose. Unsweetened cookies brought about enamel demineraliz
ation, but the pH of the streptococcal plaque fell slowly and the init
iation of demineralization was delayed. Thus, delta Ip and plaque pH w
ere -0.3+/-1.3 U and 6.1+/-0.3, respectively, after 15 min. The delay
was shown to be related to the need to induce the acidogenic streptoco
cci to metabolize maltose. Once induced, delta Ip rose rapidly and rea
ched a maximum at 45 min. Sweet cookies released sucrose and maltose a
nd brought about a rapid onset of demineralization. In summary, the da
ta demonstrated (1) that maltose was released rapidly from unsweetened
cookie particles and diffused into the plaque space of the model syst
em and (2) that maltose-dependent demineralization of enamel required
time for the induction of the streptococcal cells. The present observa
tions may help in understanding earlier conflicting reports on the car
iogenic potentials of starch-containing foods.