Curcumin suppresses Streptococcus mutans adherence to human tooth surfaces and extracellular matrix proteins

Abstract

Streptococcus mutans is the key causative agent of caries and infective endocarditis. The first step in biofilm development and the consequent initiation of further disease is bacterial adherence to host cell surfaces. Therefore, the aim of this study was to evaluate the inhibitory effect of curcumin on S. mutans adherence to extracellular matrices and tooth surfaces. The effect of curcumin on the ability of S. mutans to adhere to glass surfaces coated with collagen and fibronectin was tested in order to determine whether the decrease of the bacterial adhesion by curcumin is achieved by hindering the bacteria in adhering to collagen and/or fibronectin. Also, human teeth inoculated with S. mutans were treated with curcumin in vitro in order to assess the relevance of the anti-adhesive effect to oral conditions in vivo. The minimum inhibitory concentration (MIC) at which curcumin completely inhibited bacterial growth was 128 μg/mL. The addition of curcumin below the MIC diminished bacterial adherence onto both collagen- and fibronectin-coated glass surfaces and human tooth surfaces. It appears that the anti-adhesive effect of curcumin against S. mutans is mediated through collagen and fibronectin. These results support the widespread use of curcumin as a food-based antimicrobial agent.

Synthetic versus natural curcumin: bioequivalence in an in vitro oral mucositis model

“…Since it appears somewhat more soluble in DMSO than nCUR, aqueous solutions for oral application can be produced with less DMSO (i.e., 0.04% vs. 0.1%, vol/vol). In this context, it is worth mentioning that CUR has recently also been shown to inhibit adherence to teeth and extracellular matrix of Streptococcus mutans , the major causative agent of human caries [14,15]. In the present study we found that antimicrobial activity of sCUR in standard time-kill analyses was indistinguishable from nCUR [5,16,17] on a weight per volume basis for 3 major pharyngeal species (Figure  2).…”

Synergistic Interactions of Pseudomonas aeruginosa and Staphylococcus aureus in an In Vitro Wound Model

“…The first critical step in the microbial colonization of host tissue is the adherence of bacteria to constituents of the host extracellular matrix, including fibronectin, laminin, and collagen (56,57). While many in vitro biofilm models have utilized host extracellular matrix factor-coated surfaces (e.g., collagencoated glass slides and collagen encapsulation to simulate biofilm) (58,59), the microbial biofilm dogma has historically considered only the role of the bacterium-derived matrix or EPS in antimicrobial tolerance. We found that being embedded in a matrix clearly protected S. aureus and P. aeruginosa from gentamicin.…”

Effect of brief cetylpyridinium chloride treatments during early and mature cariogenic biofilm formation

“…Bacterial adhesion and subsequent biofilm formation (early biofilm formation) is the first step of pathogenic biofilm formation (Song et al , ; Friedlander et al , ). Hence, strategies to inhibit early biofilm formation by cariogenic bacteria may be an effective means to control the development of cariogenic biofilms.…”