A cocoa (Theobroma cacao L.) extract impairs the growth, virulence properties, and inflammatory potential of Fusobacterium nucleatum and improves oral epithelial barrier function.

Amel Ben Lagha,Patricia Maquera Huacho,Daniel Grenier,David M Ojcius

doi:10.1371/journal.pone.0252029

Abstract

Fusobacterium nucleatum is associated with many conditions and diseases, including periodontal diseases that affect tooth-supporting tissues. The aim of the present study was to investigate the effects of a cocoa extract (Theobroma cacao L.) on F. nucleatum with respect to growth, biofilm formation, adherence, and hydrogen sulfide (H2S) production. The anti-inflammatory properties and the effect on epithelial barrier function of the cocoa extract were also assessed. The cocoa extract, whose major phenolic compound is epicatechin, dose-dependently inhibited the growth, biofilm formation, adherence properties (basement membrane matrix, oral epithelial cells), and H2S production of F. nucleatum. It also decreased IL-6 and IL-8 production by F. nucleatum-stimulated oral epithelial cells and inhibited F. nucleatum-induced NF-κB activation in monocytes. Lastly, the cocoa extract enhanced the barrier function of an oral epithelial model by increasing the transepithelial electrical resistance. We provide evidence that the beneficial properties of an epicatechin-rich cocoa extract may be useful for preventing and/or treating periodontal diseases.

Highlights

Periodontitis is a multifactorial chronic inflammatory disease that is initiated and maintained by a dysbiotic biofilm and that is characterized by the progressive destruction of the periodontal ligament and alveolar bone [1]
No minimum bactericidal concentration (MBC) value was obtained, suggesting that the cocoa extract has a bacteriostatic mode of action, concentrations > 2000 μg/mL may have a bactericidal effect
When cultivated in the presence of 500 μg/mL of the cocoa extract, the growth of F. nucleatum was not affected while the biofilm was reduced by 94.3% (Fig 1)

Summary

Introduction

Periodontitis is a multifactorial chronic inflammatory disease that is initiated and maintained by a dysbiotic biofilm and that is characterized by the progressive destruction of the periodontal ligament and alveolar bone [1]. A limited number of Gram-negative anaerobic bacteria with the ability to express virulence factors have been associated with the various stages of periodontitis [2, 3]. Of these periodontal pathogens, Fusobacterium nucleatum is believed to play a central role in periodontal biofilm maturation through its ability to act as a bridge between the early (streptococci, actinomyces) and late (Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia) colonizers of oral biofilms [4]. F. nucleatum has been associated with extra-oral infections, including appendicitis, osteomyelitis, atherosclerosis, pericarditis, and brain abscesses [5], and may play a role in preterm/low birth weight and colorectal cancer development [5, 6].

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