A bifunctional lactoferrin-derived amyloid coating prevents bacterial adhesion and occludes dentinal tubules via deep remineralization

Abstract

Dentin hypersensitivity (DH) manifests as sharp and uncomfortable pain due to the exposure of dentinal tubules (DTs) following the erosion of tooth enamel. Desensitizing agents commonly used in clinical practice have limitations such as limited depth of penetration, slow remineralization and no antimicrobial properties. To alleviate these challenges, our study designed a lactoferrin-derived amyloid nanofilm (PTLF nanofilm) inspired by the saliva-acquired membrane (SAP). The nanofilm utilises Tris(2-carboxyethyl)phosphine (TCEP) to disrupt the disulfide bonds of lactoferrin (LF) under physiological conditions. The PTLF nanofilm modifies surfaces across various substrates and effectively prevents the early and stable adhesion of cariogenic bacteria, such as Streptococcus mutans and Lactobacillus acidophilus. Simultaneously, it adheres rapidly and securely to demineralized dentin surfaces, facilitating in-situ remineralization of HAP through a simple immersion process. This leads to the formation of a remineralized layer resembling natural dentin, with an occlusion depth of dentinal tubules exceeding 80 µm after three days. The in vivo and vitro results confirm that the PTLF nanofilm possesses good biocompatibility and its ability to exert simultaneous antimicrobial effects and dentin remineralization. Accordingly, this innovative bifunctional PTLF amyloid coating offers promising prospects for the management of DH-related conditions.

Statement of significance

• 1.
  We design a simple, fast, inexpensive, and easy-to-process PTLF nanofilm for nearly any material surface or shape.
• 2.
  The PTLF nanofilm modifies surfaces across various substrates and effectively prevents the adhesion of cariogenic bacteria, such as Streptococcus mutans and Lactobacillus acidophilus.
• 3.
  The abundant functional groups on the surface of PTLF nanofilm facilitate bioactive hydroxyapatite (HAP) formation and maintain stability at the HAP remineralization interface.