The germicidal effect, biosafety and mechanical properties of antibacterial resin composite in cavity filling

Abstract

In recent years, dental resin materials have become increasingly popular for cavity filling. However, these materials can shrink during polymerization, leading to microleakages that enable bacteria to erode tooth tissue and cause secondary caries. As a result, there is great clinical demand for the development of antibacterial resins. The principle of antibacterial resin includes contact killing and filler-release killing of bacteria. For contact killing, quaternary ammonium salts (QACs) and antibacterial peptides (AMPs) can be added. For filler-release killing, chlorhexidine (CHX) and nanoparticles are used. These antibacterial agents are effective against gram-positive bacteria, gram-negative bacteria, fungi, and more. Among them, QACs has a lasting antibacterial effect, and silver nanoparticles even have a certain ability to kill viruses. Biocompatibility-wise, QACs, AMPs, and CHX have low cytotoxicity to cells when added into the resin. However, nanoparticles with smaller particle sizes have higher cytotoxicity. In terms of mechanical properties, QACs, AMPs, and CHX do not negatively affect the resin. However, the addition of magnesium oxide can have a negative impact. This paper reviews the types and antibacterial principles of commonly used antibacterial resins in recent years, evaluates their antibacterial effect, biological safety, and mechanical properties, and provides references for selecting clinical filling materials.

Keywords: Antibacterial peptides; Antibacterial resin; Chlorhexidine; Contact killing; Nano fillers; Quaternary ammonium salt.

Fig. 1

The chemical structure of MDPB (A) and MAE-DB (B).

Fig. 2

The effect of QACs on Staphylococcus aureus. (A) Confocal laser scanning microscopy showed that a large number of Staphylococcus aureus died after the application of QAC antibacterial agents (the green spots are living bacteria, while the red ones are dead bacteria). (B) Scanning electron microscope showed that the QAC antibacterial agent made the surface of bacteria shrink, indicating that the cell membrane had broken [111].

Fig. 3

The antibacterial mechanism of antimicrobial peptides (AMPs). AMPs have two secondary structures, namely α-helix and β-fold. (a) AMPs with positive charges adsorb onto negatively charged bacterial cell membranes, disrupting the cell membrane. (b) AMPs inhibit the synthesis of peptidoglycan, disrupting the bacterial cell wall. (c, d) AMPs can also inhibit bacterial DNA and enzyme synthesis, suppressing bacterial growth and metabolism. (e) Some AMPs can recruit immune cells, enhance phagocytic capability, and thereby eliminate bacteria.

Fig. 4

The antibacterial mechanism of chlorhexidine [94,117].

Fig. 5

Antibacterial mechanisms of antibacterial resin. (A)The process of contact killing occurs when the antibacterial component of the resin is quaternary ammonium salt (QAC), which can kill bacteria on contact. QAC molecules carry a positive charge, while bacteria are negatively charged; hence, electrostatic forces attract bacteria to the surface of the resin. The chemical structure of QAC contains one hydrophilic group and two hydrophobic groups. Hydrophobic groups can be directly inserted into the bacterial cell membrane - phospholipid bilayer. The structure of the phospholipid molecular layer changes, and then the permeability of the cell membrane changes. Finally, the cell membrane breaks, leading to bacterial death. (B)When the resin fillers are nanoparticles, they can be released around the resin to kill bacteria that are a little further away from the resin, known as filler-release induced bacterial death. Ag nanoparticles (Ag NPs) and ZnO nanoparticles (ZnO NPs) are the primary representatives of these nanoparticles. Ag⁺ is mainly released from Ag NPS to resist bacteria. Similarly, Zn⁺and radical oxygen species (ROS) are released from ZnO NPs. Metal ions can enter the cell membrane, destroy bacterial enzymes to affect bacterial metabolism, and break DNA to inhibit bacterial division. ROS can induce bacterial oxidative stress.