In the January 2014 issue (Volume 58, number 1), in the article “Caries Management by Risk Assessment Care Paths for Prosthodontic Patients: Oral Microbial Control and Management,” by Hamilton H. Le and Roy T. Yanase, the authors inadvertently failed to attribute information on pages 231 and 234 to reference 19. The authors apologize for this oversight and have provided new text to properly recognize the original source.

The new text should read:

Previous studies highlight a reduction in acid production in bacterial cells, by way of the inhibition of a key enzyme, enolase. Enolase, a glycolytic enzyme, has a crucial role in the conversion of 2-P-glycerate (2-PG) to P-enolpyruvate (PEP). Hamilton found a decrease in the production of PEP in the presence of the fluoride anion.

Hamilton goes on to show that the accumulation of F ⁻ in the bacterial cell cytoplasm is dependent on the transport of hydrogen fluoride (HF) through a transmembrane pH difference, or pH gradient, characteristic only in metabolically active cells. Once inside the cell, the basic environment of the cytoplasm leads to the dissociation of HF back to H ⁺ cations and F ⁻ anions, thereby acidifying the cytoplasm of the cell and reducing the pH gradient. Current studies have revealed that, in addition to enolase, F ⁻ also has an inhibitory effect on the membrane bound proton pump adenosine triphosphatase (ATPase). Inhibition of the pump results in the inability of a cell to reestablish a pH gradient, reducing the cell’s ability to transport solutes through mechanisms that are dependent on this gradient. Despite the dual versatility of fluoride to dissociate proton gradients as well as prevent their regeneration there remains a lack of consensus about the antimicrobial effects of F ⁻ and its contributions to caries management.