Biofilms and oral health: nanotechnology for biofilm control

Abstract

Dental biofilms are complex microbial communities enclosed by a self-produced extracellular matrix, leading to dental caries, periodontitis, and other oral diseases. These biofilms are often resistant to conventional antibiotics and result in persistent infections that negatively impact oral health. Recent advances in nanotechnology have demonstrated nanoparticles as a promising therapeutic alternative for controlling dental biofilms. In addition, such nanoparticles possess unique physicochemical properties such as high surface area-to-volume ratio, enhanced reactivity, and ability to penetrate biofilm structures. Therefore, this review explores the potential of various nanoparticles, such as silver, zinc oxide, and titanium dioxide, in disrupting biofilm formation and removal of pathogenic oral biofilm forming bacteria. Additionally, this review critically examines various strategies for surface functionalization of nanoparticles to enhance their antimicrobial efficacy and biofilm-targeting capabilities. Furthermore, the article also presents various applications of dental materials coated with nanoparticles in preventing biofilm adhesion and growth. In essence, this review article will provide collective information on various approaches in using nanoparticles to reduce the risk of recurrent oral infections and enhance overall dental health.

Keywords: Antimicrobial coating; Biofilm disruption; Dental biofilm; Nanoparticles; Oral health.

Fig. 1

Virulence factors of P. gingivalis. Type IX secretion system (T9SS) is responsible for secreting gingipains and other effector molecules. Gingipains contribute to the degradation of host proteins, while fimbriae facilitate adhesion to oral epithelial surfaces and other bacterial species. P. gingivalis also produces additional virulence factors, including the capsule, lipopolysaccharides (LPS), hemagglutinins, peptidylarginine deiminase (PPAD), and outer membrane vesicles (OMVs), all of which contribute to bacterial attachment and virulence [325]

Fig. 2

Stages of C. albicans colonization on dental surfaces. C. albicans initially adheres to the dental surface and transitions into its more virulent hyphal form. As the biofilm matures, cells can disperse and colonize new sites. Various adhesins play crucial roles at each stage, facilitating adhesion to tooth surfaces and interactions with bacterial species such as S. oralis and S. gordonii [14]

Fig. 3

A Biofilm formation of S. mutans on dental surfaces. In sucrose-mediated adhesion, Glycosyltransferases synthesize glucans that promote bacterial attachment. Additional surface proteins involved in adhesion include Gbps, Cnm, and PacI adhesin [384]. B Virulence factors of F. nucleatum. F. nucleatum serves as a bridging organism between early and late colonizers in dental biofilms, facilitated by RadD and FomA adhesins. Its LPS activates Toll-like receptors, triggering NF-κB pathway and cytokine release, leading to inflammation and tissue damage [19]

Fig. 4

Process of biofilm degradation by reactive oxygen species (ROS) generation: A Carboxymethyl-dextran-coated iron oxide nanoparticles attach to the bacterial biofilm on the tooth surface. B In the presence of hydrogen peroxide (H₂O₂) and an acidic environment, the iron oxide core catalyzes the generation of ROS. ROS initiate oxidative stress, leading to bacterial cell damage and biofilm disruption. As a result, the biofilm matrix degrades, causing the release of dead bacterial cells and reducing microbial colonization on the tooth surface

Fig. 5

a The surface coating with zwitterionic materials possesses a neutral surface charge on dental materials and potentially shows a reduced Streptococcus mutans, Staphylococcus aureus, Klebsiella oxytoca, and Klebsiella pneumoniae colonization, b glass nanoparticles on the titanium implants reduces the porous membrane structures which eliminate bacterial adhesion. c, d the hydroxyl and thoil side chain molecules were used as linker molecules between the nanoparticles and protein of interest to combat microbial infections

Fig. 6

Translational Research Process and Challenges in Clinical Studies: A The translational research pathway from preclinical to clinical research, highlighting key study types such as in vitro studies, in vivo (animal model) studies, case reports, case–control studies, cohort studies, and randomized controlled trials. The transition from promising preclinical results to clinical product development is marked by a gap that requires strategic planning. B A network diagram illustrating clinical study limitations (red nodes) and corresponding strategies to overcome them (green nodes). Blue arrows indicate direct relationships between limitations, while green arrows show solutions addressing specific challenges. Key limitations include lack of long-term clinical data, ethical and patient safety concerns, toxicity, regulatory challenges, and limited sample sizes. Strategies such as enhancing biocompatibility testing, increasing sample sizes, and addressing regulatory issues are proposed to mitigate these challenges. The solutions highlighted in (B), such as enhancing biocompatibility testing, improving cost-effectiveness, and ensuring ethical compliance, are critical for bridging the gap in (A), ensuring that innovative products successfully navigate the complexities of clinical research and reach patients effectively