Τόμος 5 (1987) – Τεύχος 3 – Άρθρο 2 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Ελληνική Έκδοση – Volume 5 (1987) – Issue 3 – Article 2 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-Greek Edition

5: 155-166 (1987)

PHARMAKON-Press: Epitheorese Klin. Farmakol. Farmakokinet.

5: 155-166 (1987)

Dental caries is the progressive destruction, by bacteria and their products, of the calcified tissues of the teeth exposed to the oral environment. Caries can only develop by the favorable confluence of three factors: (1) microorga­nisms that adhere to the tooth surface, (2) carbohydrates that the microorganisms can readily metabolize to acid, and (3) a susceptible host or tooth surface that will dissolve in the acid. In this dynamic pro­cess of demineralization and proteolytic breakdown of the collagen matrix, several bacterial species have been indicated as cariogenic. Streptococcus mutans has been especially implicated in the initiation of lesions of the smooth coronal surfaces. Actinomyces viscosus and naeslundii have been associated with the development of root caries, while lactobacilli appear to be the main organisms involved in dentine caries. Pits and fissures offer a favorable site for colonization of streptococci, actino­myces and lactobacilli; all these microor­ganisms have been associated with le­sions on the occlusal surface. Many fer­mentable carbohydrates can be metabolized by oral microorganism. Nevertheless, the caries-inducing potential of sucrose is considered higher than that exhibited by any other carbohydrate in the human diet. It is readily diffusible into plaque; it serves as a substrate for acid production; and it is a precursor of the polyglycans that give the plaque its adherent properties. Dietary habits can influence cariogenicity. The choice of carbohydrate foods whose physi­cal properties make them retentive and frequent snacking are both habits that in­crease a diet’s capability to induce den­tal decay. Last years caries have been considered as a dynamic process, its pha­ses shifting between demineralization, eq­uilibrium, and remineralization. This reco­gnition resulted in several recently esta­blished associations between sweeteners and natural defense mechanisms related to salivary secretion and buffering. Α further protective mechanism relates to the main­tenance of a concentration gradient ad­vancing the diffusion of calcium and phos­phate ions from the saliva into dental enamel. This remineralizing mechanism is enhanced by strong complex formation be­tween calcium ions and polyols, especially mannitol, sorbitol and xylitol. Several stu­dies have shown that little or no pH de­crease occurs in dental plaque at exposure to some sweeteners, eg, mannitol, sorbitol, L-sorbose, xylitol and lycesin. In addition, xylitol provokes a direct inhibition of S-mutans through degeneration and autoly­sis of the bacterial cells. On the other hand, adaptation of the oral flora to meta­bolize xylitol was not shown after a long use of this polyol.

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