Caries Is a Threshold, Not a Dose

01The evidence

• The caries process has been described as beginning when dietary sugar is metabolised by acidogenic bacteria in the biofilm, with the resulting pH drop driving demineralisation of enamel.Journal of the American Dental Association

02The tension

Caries prevention is organised around sugar frequency and around bacterial counts. Both correlate with disease and both fail to predict individuals, because the same sugar exposure produces different pH excursions depending on the biofilm and on saliva, which are not captured by either measure.

03The theory

Enamel dissolves when the fluid around it is undersaturated with respect to hydroxyapatite. The pH at which that happens is the critical pH, and it depends on the calcium and phosphate concentrations and on the presence of fluoride.

Below the critical pH the tooth demineralises; above it, mineral is recovered. The relevant variable is therefore the time spent below a threshold that varies between patients, not the amount of sugar.

The prediction is that caries should be predicted by the critical pH and the time below it better than by sugar frequency or bacterial counts, and that raising the threshold, for instance by fluoride, should protect even when sugar exposure is unchanged.

The clinical consequence is that risk assessment should measure the threshold and the exposure below it, which is feasible with a pH telemetry test, rather than counting sugar or bacteria.

04What this is not

05Predictions

• P1Caries should be predicted by time below critical pH better than by sugar frequency.
• P2Raising the threshold should protect at constant sugar exposure.
• P3Patients with the same sugar intake but different thresholds should differ in caries.

06What would refute it

Caries tracking sugar exposure at controlled threshold would leave the dose model adequate.

07What it would change

It would make threshold measurement the basis of caries risk assessment.