Calcium Salt Precipitation and Mechanisms of Inhibition Under Oral Conditions

Abstract

Dental calculus contains a range of calcium phosphates, derived from plaque fluid and the saliva. Older deposits tend to contain more hydroxyapatite and 6 tricalcium phosphate. Compounds which inhibit the transformation of calcium phosphate nuclei to hydroxyapatite and its subsequent crystal growth are known to be effective in restricting calculus deposition in vivo. Such compounds include the diphosphonates, polyphosphates, and zinc. Under physiological conditions, apatites tend to be calcium-deficient with matching HP0₄ ^2- groups. If these groups are displaced, then crystal growth is inhibited. This can be demonstrated for heated apatite and FP0₃ ^2- treatment. The latter, however, subsequently hydrolyzes with reformation of the HPO₄ ^2- groups. Diphosphonates and polyphosphates adsorb upon nuclei, displacing surface phosphate in the process. The treated apatite nuclei will not grow until the adsorbed species are displaced or hydrolyzed. The cationic inhibitor, zinc, is acquired by the dental plaque and oral surfaces and is eluted in the saliva. Zinc is adsorbed upon apatite crystallites with displacement of calcium. When a surface coverage of approximately 3 μmol/m² is achieved, crystal growth is almost completely inhibited. Post-treatment with calcium desorbs the zinc. Inhibition of hydroxyapatite crystal growth and thence calculus formation thus depends upon displacement of surface ions from seed crystallites. The role of HPO₄ ^2- groups in this and other physiological apatite processes is of particular interest.