IADR Abstract Archives
Competition for Arginine as a Tipping Point for Caries Development
Objectives: The major route for arginine metabolism in supragingival oral biofilms is via the arginine deiminase pathway (ADS), which is expressed by many commensal oral streptococci. Ammonia production via the ADS can neutralize acids and enhance the fitness of health-associated streptococci, thus serving as a caries protection factor. Arginine can also be converted by arginine decarboxylase (ADC) into agmatine, which can be catabolized by the agmatine deiminase system (AgDS) that is present in Streptococcus mutans. Agmatine catabolism by the AgDS can enhance acid tolerance of oral bacteria by raising cytoplasmic pH, but agmatine levels and AgDS expression by S. mutans appear insufficient to moderate biofilm acidification. This study explored whether measurements of ADS and AgDS in dental plaque could be used to differentiate caries risk.
Methods: A total of 124 children were recruited and grouped as caries-free (CF, n=53), caries-active with enamel carious lesions (CAE; n=36), and caries-active with dentinal lesions (CA; n=35). Supragingival plaque was collected from caries-free tooth surfaces (PF) and from enamel (PE) and dentinal (PD) carious lesions. ADS and AgDS activity were measured in plaque using established protocols.
Results: Plaque ADS activity ranged from 0.00 to 39.7 units (mg protein)-1. ADS activity of CA-PD samples was significantly lower than that of CF-PF samples (p=0.005) and CAE-PF samples (p<0.001). Plaque AgDS activity ranged from 0.00 to 2.8 units (mg protein)-1. Although not statistically significant, AgDS activity of CA-PD samples trended higher compared to the other plaque groups. Supragingival biofilms of caries-active children and tooth surfaces exhibited lower ADS and higher AgDS activities, compared to caries-free children and tooth surfaces.
Conclusions: Our results confirm that higher ADS activity may decrease caries risk, and we propose that ADC and AgDS may increase the cariogenic potential of dental biofilms by diverting arginine from the ADS and augmenting acid tolerance of S. mutans.
Methods: A total of 124 children were recruited and grouped as caries-free (CF, n=53), caries-active with enamel carious lesions (CAE; n=36), and caries-active with dentinal lesions (CA; n=35). Supragingival plaque was collected from caries-free tooth surfaces (PF) and from enamel (PE) and dentinal (PD) carious lesions. ADS and AgDS activity were measured in plaque using established protocols.
Results: Plaque ADS activity ranged from 0.00 to 39.7 units (mg protein)-1. ADS activity of CA-PD samples was significantly lower than that of CF-PF samples (p=0.005) and CAE-PF samples (p<0.001). Plaque AgDS activity ranged from 0.00 to 2.8 units (mg protein)-1. Although not statistically significant, AgDS activity of CA-PD samples trended higher compared to the other plaque groups. Supragingival biofilms of caries-active children and tooth surfaces exhibited lower ADS and higher AgDS activities, compared to caries-free children and tooth surfaces.
Conclusions: Our results confirm that higher ADS activity may decrease caries risk, and we propose that ADC and AgDS may increase the cariogenic potential of dental biofilms by diverting arginine from the ADS and augmenting acid tolerance of S. mutans.