Objective: To evaluate differences in the adhesion levels of the most common oral pathogens, Streptococcus mutans and Porphyromonas gingivalis, in human saliva-derived microcosm biofilms with respect to time and raw materials of orthodontic brackets. Methods: The samples were classified into three groups of bracket materials: 1) monocrystalline alumina ceramic (CR), 2) stainless steel metal (SS), and 3) polycarbonate plastic (PL), and a hydroxyapatite (HA) group was used to mimic the enamel surface. Saliva was collected from a healthy donor, and saliva-derived biofilms were grown on each sample. A realtime polymerase chain reaction was performed to quantitatively evaluate differences in the attachment levels of total bacteria, S. mutans and P. gingivalis at days 1 and 4. Results: Adhesion of S. mutans and P. gingivalis to CR and HA was higher than the other bracket materials (SS = PL < CR = HA). Total bacteria demonstrated higher adhesion to HA than to bracket materials, but no significant differences in adhesion were observed among the bracket materials (CR = SS = PL < HA). From days 1 to 4, the adhesion of P. gingivalis decreased, while that of S. mutans and total bacteria increased, regardless of material type. Conclusions: The higher adhesion of oral pathogens, such as S. mutans and P. gingivalis to CR suggests that the use of CR brackets possibly facilitates gingival inflammation and enamel decalcification during orthodontic treatment.

Concerns regarding unbound monomers in dental composites have increased with the increased usage of these materials. This study assessed the biological effects of urethane dimethacrylate (UDMA), a common monomer component of dental composite resins, on the cariogenic properties of Streptococcus mutans. Changes in the growth rate, biofilm formation, interaction with saliva, surface hydrophobicity, adhesion, glucan synthesis, sugar transport, glycolytic profiles, and oxidative- and acid-stress tolerances of S. mutans were evaluated after growing the cells in the presence and absence of UDMA. The results indicated that UDMA promotes the adhesion of S. mutans to the underlying surfaces and extracellular polysaccharide synthesis, leading to enhanced biofilm formation. Furthermore, UDMA reduced the acid tolerance of S. mutans, but enhanced its tolerance to oxidative stress, thus favoring the early stage of biofilm development. UDMA did not significantly affect the viability or planktonic growth of cells, but diminished the ability of S. mutans to metabolize carbohydrates and thus maintain the level of intracellular polysaccharides, although the tendency for sugar transport increased. Notably, UDMA did not significantly alter the interactions of bacterial cells with saliva. This study suggests that UDMA may potentially contribute to the development of secondary caries around UDMA-containing dental materials by prompting biofilm formation, enhancing oxidative tolerance, and modulating carbon flow.

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