Biofilm formation by <i>Porphyromonas gingivalis</i> and <i>Streptococcus gordonii</i>

Cook, Guy S.; Costerton, J. William; Lamont, R. J.

doi:10.1111/j.1600-0765.1998.tb02206.x

Cited by 107 publications

(57 citation statements)

References 26 publications

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“…Alternatively, a wide range of oral bacteria which principally live in biofilm might be capable of invasion as a means of persisting when they happen to encounter a shedding surface. Since species interaction appears to be widespread in oral biofilm (Cook et al, 1998;Fong et al, 2001;Palmer et al, 2001Palmer et al, , 2003McNab et al, 2003), another alternative could be that non-invasive species gain entrance to cells by forming consortia with invasive species.…”

Section: Discussionmentioning

confidence: 98%

Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythensis are Components of a Polymicrobial Intracellular Flora within Human Buccal Cells

2005

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Previously, we used in situ hybridization and confocal microscopy to detect the periodontal pathogens Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythensis within buccal epithelial cells taken directly from the mouth. This study tested the hypothesis that the intracellular flora of buccal cells is polymicrobial. Mixtures containing a red fluorescent universal probe paired with green fluorescent versions of either A. actinomycetemcomitans-, P. gingivalis-, or T. forsythensis-specific probes were hybridized with buccal cells collected from each of 38 healthy humans. We verified co-localization of probe pairs within cells by generating three-dimensional reconstructions. Intracellular bacteria were detected in every subject. Each cell that was labeled with a species-specific probe also contained bacteria recognized only by the universal probe. Bacteria labeled with specific probes often occupied smaller regions within larger masses of bacteria. Those findings suggest that future studies of invasion by oral bacteria may need to include microbial consortia.

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Section: Discussionmentioning

confidence: 98%

Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythensis are Components of a Polymicrobial Intracellular Flora within Human Buccal Cells

2005

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“…Without S. gordonii, P. gingivalis can barely establish biofilm under a low challenging shear force. However, with S. gordonii, P. gingivalis successfully establishes biofilm under the same shear force (16). P. gingivalis fimbriae, S. gordonii autoinducer 2, and streptococcal surface protein B (SspB) have been reported to be involved in the S. gordonii-P. gingivalis interaction (17)(18)(19).…”

Section: Discussionmentioning

confidence: 99%

Effects of Nicotine on Streptococcus gordonii Growth, Biofilm Formation, and Cell Aggregation

Huang

et al. 2014

Appl Environ Microbiol

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e Streptococcus gordonii is a commensal species of human oral flora. It initiates dental biofilm formation and provides binding sites for later colonizers to attach to and generate mature biofilm. Smoking is the second highest risk factor for periodontal disease, and cigarette smoke extract has been reported to facilitate Porphyromonas gingivalis-S. gordonii dual-species biofilm formation. Our hypothesis is that nicotine, one of the most important and active components of tobacco, stimulates S. gordonii multiplication and aggregation. In the present study, S. gordonii planktonic cell growth (kinetic absorbance and CFU), biofilm formation (crystal violet stain and confocal laser scanning microscopy [CLSM]), aggregation with/without sucrose, and 11 genes that encode binding proteins or regulators of gene expression were investigated. Results demonstrated planktonic cell growth was stimulated by 1 to 4 mg/ml nicotine treatment. Biofilm formation was increased at 0.5 to 4 mg/ml nicotine. CLSM indicated bacterial cell mass was increased by 2 and 4 mg/ml nicotine, but biofilm extracellular polysaccharide was not significantly affected by nicotine. Cell aggregation was upregulated by 4, 8, and 16 mg/ml nicotine with sucrose and by 16 mg/ml nicotine without sucrose. Quantitative reverse transcriptase PCR indicated S. gordonii abpA, scaA, ccpA, and srtA were upregulated in planktonic cells by 2 mg/ml nicotine. In conclusion, nicotine stimulates S. gordonii planktonic cell growth, biofilm formation, aggregation, and gene expression of binding proteins. Those effects may promote later pathogen attachment to tooth surfaces, the accumulation of tooth calculus, and the development of periodontal disease in cigarette smokers.

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“…In this report, coatings with the antimicrobial peptide GL13K were tested in a drip-flow reactor against Streptococcus gordonii, a primary colonizer on oral surfaces that provides attachment for the subsequent pathogenic biofilm formation by P. gingivalis [23]. Adherence of P. gingivalis to surfaces in the developed biofilm depends on deposition of S. gordonii cells on the salivary pellicle at the colonized surface [23].…”

Section: Introductionmentioning

confidence: 99%

Antimicrobial GL13K Peptide Coatings Killed and Ruptured the Wall of Streptococcus gordonii and Prevented Formation and Growth of Biofilms

Chen

Hirt

et al. 2014

PLoS ONE

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Infection is one of the most prevalent causes for dental implant failure. We have developed a novel antimicrobial peptide coating on titanium by immobilizing the antimicrobial peptide GL13K. GL13K was developed from the human salivary protein BPIFA2. The peptide exhibited MIC of 8 µg/ml against planktonic Pseudonomas aeruginosa and their biofilms were reduced by three orders of magnitude with 100 µg/ml GL13K. This peptide concentration also killed 100% of Streptococcus gordonii. At 1 mg/ml, GL13K caused less than 10% lysis of human red blood cells, suggesting low toxicity to mammalian cells. Our GL13K coating has also previously showed bactericidal effect and inhibition of biofilm growth against peri-implantitis related pathogens, such as Porphyromonas gingivalis. The GL13K coating was cytocompatible with human fibroblasts and osteoblasts. However, the bioactivity of antimicrobial coatings has been commonly tested under (quasi)static culture conditions that are far from simulating conditions for biofilm formation and growth in the oral cavity. Oral salivary flow over a coating is persistent, applies continuous shear forces, and supplies sustained nutrition to bacteria. This accelerates bacteria metabolism and biofilm growth. In this work, the antimicrobial effect of the coating was tested against Streptococcus gordonii, a primary colonizer that provides attachment for the biofilm accretion by P. gingivalis, using a drip-flow biofilm bioreactor with media flow rates simulating salivary flow. The GL13K peptide coatings killed bacteria and prevented formation and growth of S. gordonii biofilms in the drip-flow bioreactor and under regular mild-agitation conditions. Surprisingly the interaction of the bacteria with the GL13K peptide coatings ruptured the cell wall at their septum or polar areas leaving empty shell-like structures or exposed protoplasts. The cell wall rupture was not detected under regular culture conditions, suggesting that cell wall rupture induced by GL13K peptides also requires media flow and possible attendant biological sequelae of the conditions in the bioreactor.

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Biofilm formation by Porphyromonas gingivalis and Streptococcus gordonii

Cited by 107 publications

References 26 publications

Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythensis are Components of a Polymicrobial Intracellular Flora within Human Buccal Cells

Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Tannerella forsythensis are Components of a Polymicrobial Intracellular Flora within Human Buccal Cells

Effects of Nicotine on Streptococcus gordonii Growth, Biofilm Formation, and Cell Aggregation

Antimicrobial GL13K Peptide Coatings Killed and Ruptured the Wall of Streptococcus gordonii and Prevented Formation and Growth of Biofilms

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