Managing oral biofilms to avoid enamel demineralization during fixed orthodontic treatment

Abstract

Enamel demineralization represents the most prevalent complication arising from fixed orthodontic treatment. Its main etiology is the development of cariogenic biofilms formed around orthodontic appliances. Ordinarily, oral biofilms exist in a dynamic equilibrium with the host's defense mechanisms. However, the equilibrium can be disrupted by environmental changes, such as the introduction of a fixed orthodontic appliance, resulting in a shift in the biofilm's microbial composition from non-pathogenic to pathogenic. This alteration leads to an increased prevalence of cariogenic bacteria, notably mutans streptococci, within the biofilm. This article examines the relationships between oral biofilms and orthodontic appliances, with a particular focus on strategies for effectively managing oral biofilms to mitigate enamel demineralization around orthodontic appliances.

Keywords: Biofilm; Biomaterial science; Enamel demineralization; Mutans streptococci.

Figure 1

Biofilm formation around orthodontic appliances. After the formation of salivary pellicles, the initial colonizers are attached, and then step-by-step biofilm maturation is achieved by the interaction between various microorganisms.

Figure 2

Biofilm formation of Streptococcus mutans (S. mutans) in the absence (A, B) and presence of sucrose (C, D). For biofilm formation, S. mutans UA159 was grown in a semi-defined biofilm medium with 20 mM glucose (A, B) or sucrose (C, D) for 24 hours after saliva-coating. The images were taken using a confocal laser scanning microscope (CLSM) at 200× magnification after biofilms were generated on eight-well Lab-Tek Chamber Permanox slides (Nagle Nunc International, Rochester, NY, USA). The bacterial cells (green) were stained with SYTO 13 fluorescent nucleic acid stain (Thermo Fisher Scientific, Madison, WI, USA) for 20 minutes before CLSM analyses. Biofilm developed by S. mutans was denser and deeper in the presence of sucrose (C, D) than in the absence of sucrose (A, B) due to the extracellular polysaccharide matrices.

Figure 3

Effects of orthodontic bonding procedures on biofilm formation Streptococcus mutans (S. mutans): A, E, untreated hydroxyapatite surface; B, F, etched hydroxyapatite surface; C, G, primed surface; D, H, adhesive surface. For biofilm formation, S. mutans UA159 was grown in a semi-defined biofilm medium with 20 mM glucose A–D, or sucrose E–H, for 24 hours after saliva-coating. The biofilm images were taken using a scanning electron microscope at 3,000× magnification. The presence of sucrose significantly promoted the biofilm formation of S. mutans, regardless of the orthodontic bonding procedures.

Figure 4

Scanning electron microscope images of the bovine enamel A–C, bracket materials D–F, and orthodontic adhesives G–I, at ×3,000 magnification: A, untreated surface; B, etched surface; C, primed surface; D, monocrystalline alumina (Hubit Co., Seoul, Korea); E, stainless steel (Hubit); F, polycarbonate (Hubit); G, composite adhesive (Tansbond XT, 3M, Monrovia, CA, USA); H, compomer (Tansbond Plus, 3M); I, resin-modified glass ionomer (Fuji Otho LC, GC, Tokyo, Japan). The adhesive surfaces G-I, are rougher than the bracket surfaces D-F, due to the filler and/or glass particles contained in the adhesives. In particular, the resin-modified glass ionomer has the roughest surface due to its larger glass particles I.

Figure 5

Effects of bisphenol A glycidyl methacrylate (bis-GMA) (B, E) and urethane dimethacrylate (UDMA) (C, F) on biofilm formation of Streptococcus mutans (S. mutans) in the absence (A–C) and presence of sucrose (D–F). For biofilm formation, S. mutans UA159 was grown in a semi-defined biofilm medium with 20 mM glucose or sucrose for 24 hours after saliva-coating. The images were taken using a confocal laser scanning microscope at ×1,000 magnification after biofilms were generated on 8-well Lab-Tek Chamber Permanox slides (Nagle Nunc International, Rochester, NY, USA). The bacterial cells (green) and polysaccharide biofilm matrices (red) were stained with SYTO 13 fluorescent nucleic acid stain (Thermo Fisher Scientific, Madison, WI, USA) and Alexa Flour 647-labeled dextran conjugate (Thermo Fisher Scientific), respectively. Bis-GMA (B, E) and UDMA (E, F) significantly increased the biofilm formation of S. mutans compared to control (A, D). In particular, both bis-GMA (E) and UDMA (F) significantly enhanced the biofilm formation of S. mutans in the presence of sucrose by facilitating the production of extracellular polysaccharide matrices.

Figure 6

The amount of fluoride ion released from a nonfluoride-releasing composite (Transbond XT, 3M, Monrovia, CA, USA), a fluoride-releasing composite (Light Bond, Reliance Orthodontics, Itasca, IL, USA), a compomer (Transbond Plus, 3M), and 2 resin-modified glass ionomers (Multi-Cure, 3M; and Fuji Ortho LC, GC, Tokyo, Japan). The highest level of fluoride ion release appears during the first 24 hours after exposure, followed by a low level of long-term fluoride ion release.

Figure 7

Fluoride uptake and re-release from various orthodontic adhesives after topical fluoride treatment for 1 minute: A, deionized water; B, acidulate phosphate fluoride gel (Oral-B, Belmont, CA, USA); C, a fluoridated dentifrice containing 1,000 ppm sodium fluoride (Regular Care, Crest, Cincinnati, OH, USA); D, sodium fluoride solution containing 900 ppm fluoride ion. Each fluoride treatment is performed in a 5-day cycle.

Figure 8

Chlorhexidine release from orthodontic adhesives in non-coated and saliva-coated groups after periodic exposure to a 1.0% chlorhexidine digluconate solution (Sigma-Aldrich, St. Louis, MO, USA); A, composite adhesive (Transbond XT, 3M, Monrovia, CA, USA); B, resin-modified glass ionomer (Fuji Ortho LC, GC, Tokyo, Japan) Each chlorhexidine treatment is performed in a 5-day cycle. Saliva-coating significantly increased chlorhexidine release from the composite adhesive.