Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 11 (9)

Potential Oral Health Care Agent From Coffee Against Virulence Factor of Periodontitis

Affiliations

Potential Oral Health Care Agent From Coffee Against Virulence Factor of Periodontitis

Sing-Hua Tsou et al. Nutrients.

Abstract

Background: Coffee is a major dietary source of polyphenols. Previous research found that coffee had a protective effect on periodontal disease. In this study, we aimed to investigate whether coffee extract and its primary phenolic acid, chlorogenic acid, affect the growth and protease activity of a periodontopathogen Porphyromonas gingivalis (P. gingivalis).

Methods: Coffee extract and chlorogenic acid were prepared by a two-fold serial dilution. The turbid metric test and plate count method were used to examine the inhibitory effects of chlorogenic acid on P. gingivalis. The time-kill assay was used to measure changes in the viability of P. gingivalis after exposure to chlorogenic acid for 0-24 h. The protease activity of P. gingivalis was analyzed using the optical density of a chromogenic substrate.

Results: As a result, the minimum inhibitory concentration (MIC) of chlorogenic acid was 4 mg/mL, and the minimum bactericidal concentration was 16 mg/mL. Chlorogenic acid at concentrations above MIC resulted in a longer-lasting inhibitory effect on P. gingivalis viability and significantly reduced associated protease activity. The coffee extract showed antibacterial activity as observed by the disk diffusion test, whereas these inhibitory effects were not affected by different roast degrees of coffee.

Conclusions: Collectively, our novel findings indicate that chlorogenic acid not only has antimicrobial activity but also reduced the protease activity of P. gingivalis. In addition, coffee extract inhibits the proliferation of P. gingivalis, which may partly be attributed to the effect of chlorogenic acid.

Keywords: Porphyromonas gingivalis; chlorogenic acid; disk-diffusion test; protease activity; time-kill test.

Conflict of interest statement

The authors declare no competing financial interest. The sponsors had no role in the design, execution, interpretation, or writing of the study

Figures

Figure 1
Figure 1
The minimum inhibitory concentration of chlorogenic acid against Porphyromonas gingivalis. The visualizing turbidity measurement method was used to determine the MIC. The test samples contained (a) 32 mg/mL, (b) 16 mg/mL, (c) 8 mg/mL, (d) 4 mg/L, and (e) 2 mg/mL chlorogenic acid dissolved in 10% dimethyl sulfoxide (DMSO). (f) 10% DMSO and (g) 5.25% sodium hypochlorite represented the negative and positive control groups, respectively.
Figure 2
Figure 2
The minimum bactericidal concentration of chlorogenic acid against Porphyromonas gingivalis. The counting colony method was used to determine the MBC. Agar plates were treated with bacterial and (a) 32 mg/mL, (b) 16 mg/mL, (c) 8 mg/mL, and (d) 4 mg/mL chlorogenic acid dissolved in 10% dimethyl sulfoxide (DMSO), respectively. (e) 10% DMSO and (f) 5.25% sodium hypochlorite represented the positive and negative control groups, respectively.
Figure 3
Figure 3
The time-kill effect of chlorogenic acid against Porphyromonas gingivalis. The cumulative change in the growth of the P. gingivalis strain after treatment with different concentrations of chlorogenic acid. The results show the antibacterial effect of chlorogenic acid at concentrations of (△) 2 mg/mL, (○) 4 mg/mL, (+) 8 mg/mL, (×) 16 mg/mL, and (□) 10% dimethyl sulfoxide of the negative control group, respectively. Chlorogenic acid at the MBC concentration showed a bactericidal effect after 3 h treatment.
Figure 4
Figure 4
Chlorogenic acid inhibited the protease activity of Porphyromonas gingivalis (ATCC 33277) by the bacterial protease activity test. Percentage value changes in the protease activity of the P. gingivalis strain after treatment with chlorogenic acid at concentrations of 32, 16, 8, and 4 mg/mL, respectively, and treated with 10% dimethyl sulfoxide (DMSO) as the negative control group. The test indicated a significant difference between each concentration of the chlorogenic acid groups and 10% DMSO of the negative control group (* p < 0.001).

Similar articles

See all similar articles

References

    1. Petersen P.E., Baehni P.C. Periodontal health and global public health. Periodontol. 2000. 2012;60:7–14. doi: 10.1111/j.1600-0757.2012.00452.x. - DOI - PubMed
    1. Ezzo P.J., Cutler C.W. Microorganisms as risk indicators for periodontal disease. Periodontol. 2000. 2003;32:24–35. doi: 10.1046/j.0906-6713.2003.03203.x. - DOI - PubMed
    1. Hajishengallis G., Darveau R.P., Curtis M.A. The keystone-pathogen hypothesis. Nat. Rev. Microbiol. 2012;10:717–725. doi: 10.1038/nrmicro2873. - DOI - PMC - PubMed
    1. Cohen J. The immunopathogenesis of sepsis. Nature. 2002;420:885. doi: 10.1038/nature01326. - DOI - PubMed
    1. Imamura T. The role of gingipains in the pathogenesis of periodontal disease. J. Periodontol. 2003;74:111–118. doi: 10.1902/jop.2003.74.1.111. - DOI - PubMed
Feedback