IADR Abstract Archives
Linoleic Acid and Competition between Streptococcus mutans-Streptococcus sanguinis. Experimental Caries-model.
Objectives: We previously reported an anticaries effect of the polyunsaturated linoleic acid. In the context of the current ecological conception of caries, how this fatty acid may create environmental conditions for the development of healthy biofilms has not been reported. The aim was to study the consequences of linoleic acid exposure on the competition between a commensal and a cariogenic species of the dental biofilm, under a cariogenic environment.
Methods: A dual-species caries-biofilm model with Streptococcus mutans UA159 (Sm) and Streptococcus sanguinis SK36 (Ss) was used. Saliva-coated enamel slabs were inoculated with equal amounts (1:1) of cells (1x108 CFU/mL) for both bacteria and distributed in 4 groups by inoculation sequences: 1) Ss followed by Sm (Ss-Sm), 2) Sm and Ss inoculated at the same time (Sm=Ss) and the controls 3) Sm followed by Sm (Sm-Sm) and 4) Ss followed by Ss (Ss-Ss). Mature dual-species biofilms were exposed 3x/day to 10% sucrose followed by either 100 mM linoleic acid, 0.05% NaF or 0.9% NaCl (caries-positive control). Acidogenicity and demineralization by microhardness were assessed and biofilms analyzed for biomass and viable cells. Triplicates for each condition in two independent experiments were assayed (n=6) and analyzed by ANOVA followed by post-hoc at p-value<0.05.
Results: Linoleic acid exposure after sucrose resulted in the lowest acidogenicity and demineralization in all inoculation sequences. The polyunsaturated fatty acid significantly reduced demineralization from 49.9%, 33.9%, 33.6% and 46.3% to 3.2%, 2.2%, 2.2% and 3.6% for Sm-Sm, Ss-Ss, Ss-Sm and Ss=Sm, respectively (p<0.05). Sucrose-induced demineralization in the linoleic acid groups was lower than that exhibited by 0.5% NaF and only slightly higher than the caries-negative control (p<0.05). Although biomass and viable microorganisms were lower in all inoculation sequences when compared to Sm-Sm, no significant differences were detected across the treatment groups, suggesting a metabolic rather than an antibacterial effect.
Conclusions: Linoleic acid seems to greatly reduce the cariogenic potential of sucrose and appears to create favorable conditions for the onset of commensal biofilms.
Methods: A dual-species caries-biofilm model with Streptococcus mutans UA159 (Sm) and Streptococcus sanguinis SK36 (Ss) was used. Saliva-coated enamel slabs were inoculated with equal amounts (1:1) of cells (1x108 CFU/mL) for both bacteria and distributed in 4 groups by inoculation sequences: 1) Ss followed by Sm (Ss-Sm), 2) Sm and Ss inoculated at the same time (Sm=Ss) and the controls 3) Sm followed by Sm (Sm-Sm) and 4) Ss followed by Ss (Ss-Ss). Mature dual-species biofilms were exposed 3x/day to 10% sucrose followed by either 100 mM linoleic acid, 0.05% NaF or 0.9% NaCl (caries-positive control). Acidogenicity and demineralization by microhardness were assessed and biofilms analyzed for biomass and viable cells. Triplicates for each condition in two independent experiments were assayed (n=6) and analyzed by ANOVA followed by post-hoc at p-value<0.05.
Results: Linoleic acid exposure after sucrose resulted in the lowest acidogenicity and demineralization in all inoculation sequences. The polyunsaturated fatty acid significantly reduced demineralization from 49.9%, 33.9%, 33.6% and 46.3% to 3.2%, 2.2%, 2.2% and 3.6% for Sm-Sm, Ss-Ss, Ss-Sm and Ss=Sm, respectively (p<0.05). Sucrose-induced demineralization in the linoleic acid groups was lower than that exhibited by 0.5% NaF and only slightly higher than the caries-negative control (p<0.05). Although biomass and viable microorganisms were lower in all inoculation sequences when compared to Sm-Sm, no significant differences were detected across the treatment groups, suggesting a metabolic rather than an antibacterial effect.
Conclusions: Linoleic acid seems to greatly reduce the cariogenic potential of sucrose and appears to create favorable conditions for the onset of commensal biofilms.