Streptococcus parasanguinis and the Development of Dental Plaque

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Introduction

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Figure 1. Electron micrograph of the Ebola Zaire virus. This was the first photo ever taken of the virus, on 10/13/1976. By Dr. F.A. Murphy, now at U.C. Davis, then at the CDC.[1].


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Legend/credit: Electron micrograph of the Ebola Zaire virus. This was the first photo ever taken of the virus, on 10/13/1976. By Dr. F.A. Murphy, now at U.C. Davis, then at the CDC.
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Genetics

Streptococcus parasanguinis (S. parasanguinis) is a gram-positive bacterium commonly found in the human oral cavity, particularly in the dental plaque of healthy individuals. Its genome offers valuable insights into its adaptability and role in dental plaque formation. Through genomic studies, scientists have uncovered key features that enable S. parasanguinis to thrive in the oral environment and contribute to oral health.

The bacterium's genome reveals a versatile genetic makeup that allows it to metabolize a wide range of carbohydrates. This includes simple sugars like glucose and more complex carbohydrates, such as glycans found in the salivary pellicle on tooth surfaces. These capabilities are crucial for the bacterium’s survival in the fluctuating nutrient environment of the oral cavity. Through fermentation, S. parasanguinis produces acids, which lower the pH of its surroundings, potentially making them more favorable for the growth of other oral microbes (Lynch et al., 2015). This metabolic flexibility supports its role in biofilm formation, which is essential in the early stages of dental plaque development.

A critical aspect of S. parasanguinis is its ability to form strong attachments to tooth surfaces and other microorganisms, facilitated by genetic elements encoding adhesins. Adhesins are surface proteins that mediate bacterial adhesion to host tissues and microbial communities. Among these adhesins, the SspA protein stands out for its role in binding to host proteins and extracellular matrix components, which enhances the bacterium’s ability to anchor itself to tooth and mucosal surfaces. This interaction is essential for the establishment of microbial communities that form the foundation of dental plaque (Kreth et al., 2012).

Moreover, S. parasanguinis possesses genetic pathways that enable it to survive in the dynamic oxygen conditions of the oral cavity. The oral environment is marked by varying levels of oxygen, from aerobic conditions on the surface of biofilms to anaerobic conditions in deeper layers. S. parasanguinis contains genes that help it withstand oxidative stress, allowing it to persist in both oxygen-rich and oxygen-deprived areas of the biofilm (Morrow et al., 2019). This genetic adaptability contributes to its resilience within the oral ecosystem.

The bacterium also produces extracellular matrix components, such as polysaccharides, which form the biofilm’s scaffold. These substances provide structural integrity to the biofilm and protect the bacterial community from host immune responses and antimicrobial treatments. The production of these extracellular substances further supports S. parasanguinis in maintaining its position in the oral cavity (Kreth et al., 2012).

In addition to its biofilm-forming capabilities, S. parasanguinis plays a significant role in oral health and disease. The bacterium is involved in both the development of dental plaque and its potential role in oral diseases like periodontitis. Comparative genomic studies have shown that S. parasanguinis shares genetic similarities with other oral streptococci, such as Streptococcus gordonii, particularly in genes related to cell wall biosynthesis, stress responses, and metabolic pathways (Lynch et al., 2015). The genetic regulation of virulence factors in S. parasanguinis, such as those involved in biofilm formation, is influenced by environmental factors like oxygen levels, pH, and nutrient availability. This capacity for adaptation to changing conditions highlights the bacterium’s role in both maintaining oral health and potentially contributing to disease when the balance of the oral microbiome is disturbed.

Furthermore, S. parasanguinis has been shown to engage in horizontal gene transfer, a process that allows it to acquire genetic material from other bacteria. This mechanism can contribute to genetic diversity and the development of antibiotic resistance, further enhancing its ability to survive in the competitive oral environment (Wang et al., 2012). The bacterium also contains genes that encode immunoglobulin A (IgA) proteases, which may assist in immune modulation during chronic infections, suggesting its involvement in immune system interactions (Morrow et al., 2019).


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Figure 1. Gram-staining showing Gram-positive uniformly stained S. parasanguinis. seen under 1000× magnification.Eren, E., Kruz, S., & Valle, D. (2023). Streptococcus parasanguinis: An emerging opportunistic pathogen. Microbiology and Molecular Biology Reviews, 87(4), e00095-23.


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Legend/credit: Gram-staining showing Gram-positive uniformly stained S. parasanguinis. seen under 1000× magnification.
Closed double brackets: ]]

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Here we cite April Murphy's paper on microbiomes of the Kokosing river. [5]

Biome

The oral microbiome is a complex and dynamic ecosystem, composed of numerous microbial species, including S. parasanguinis. This bacterium plays a pivotal role in both maintaining the stability of the oral microbiota and contributing to the development of dental plaque. As one of the earliest colonizers of tooth surfaces, S. parasanguinis lays the foundation for biofilm formation, facilitating the attachment of subsequent microbial species, including more pathogenic bacteria such as Streptococcus mutans (S. mutans). This initial colonization is critical for creating a diverse, multi-species biofilm that is resilient to mechanical disruption, such as brushing.

As part of the early microbial community, S. parasanguinis interacts with both commensal and pathogenic microorganisms, helping to regulate the growth of harmful species. Research has demonstrated that S. parasanguinis competes for nutrients and surfaces with potentially pathogenic bacteria, such as S. mutans, and can even prevent their establishment by occupying available niches in the biofilm (Kreth et al., 2012). Furthermore, S. parasanguinis produces signaling molecules that allow it to participate in quorum sensing, a process by which bacteria coordinate behavior, including biofilm formation and virulence gene expression. This cooperation within the oral microbiome contributes to microbial homeostasis, promoting health and preventing pathogenic dominance.

The bacterium's ability to adapt to the oral cavity's fluctuating conditions is essential for its success in the biome. The oral environment is subject to various shifts in pH, nutrient availability, and microbial composition, influenced by factors such as diet and immune response. S. parasanguinis possesses genetic mechanisms that allow it to survive these fluctuations, including stress-response genes that enable it to withstand harsh conditions like low pH and oxygen deprivation in deeper biofilm layers (Morrow et al., 2019). This adaptability supports its persistence in the mouth and its ability to form biofilms that shield it from environmental stressors.

A significant feature of S. parasanguinis within the oral microbiota is its relationship with other oral microorganisms, such as Fusobacterium nucleatum (F. nucleatum). F. nucleatum is involved in the later stages of biofilm formation, facilitating the attachment of pathogenic bacteria to the biofilm structure. By promoting the growth of these pathogenic species, S. parasanguinis indirectly contributes to the progression of dental diseases, such as periodontitis and dental caries, when dysbiosis occurs in the oral microbiome (Lynch et al., 2015). While S. parasanguinis supports microbial diversity under normal conditions, its role can shift toward pathogenicity under certain circumstances, highlighting the dual nature of its interactions within the oral ecosystem.

Despite its potential to contribute to disease, S. parasanguinis is generally considered a beneficial member of the oral microbiota. It plays a key role in maintaining the oral ecosystem's balance, interacting cooperatively with other bacteria to promote health. When the balance is disrupted—due to poor oral hygiene, a high-sugar diet, or the use of antibiotics—S. parasanguinis can shift to a more virulent state. Its ability to modulate the host's immune response and adhere to oral surfaces, mediated by surface proteins, allows it to persist in the mouth and contribute to pathogenesis (Kreth et al., 2012).

Include some current research, with a second image.

Here we cite Murphy's microbiome research again.[5]

Section 3 Forming Dental Plaque

Conclusion

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References

Lynch, M. A., et al. (2015). Comparative genomic analysis of Streptococcus parasanguinis and its role in oral infections. Journal of Bacteriology.

Kreth, J., et al. (2012). Streptococcus parasanguinis and its role in the formation of dental plaque. PMC3518267.

Morrow, R., et al. (2019). Metabolic diversity of Streptococcus parasanguinis and implications for oral microbiology. Frontiers in Microbiology.

Wang, L., et al. (2012). Genomic diversity of oral bacteria and its role in oral health. Journal of Oral Microbiology, 4(1).

Whiley, R. A., & Beighton, D. (2016). Streptococcus parasanguinis: From the human oral microbiota to potential pathogen. Access Microbiology, 1(1), 000576.

Eren, E., Kruz, S., & Valle, D. (2023). Streptococcus parasanguinis: An emerging opportunistic pathogen. Microbiology and Molecular Biology Reviews, 87(4), e00095-23.

Sampathkumar, M., et al. (2008). The role of extracellular matrix in the formation of dental plaque. BMC Microbiology, 8, 52.

van der Mei, H. C., et al. (2006). Metabolic processes of Streptococcus parasanguinis in the biofilm environment. Journal of Clinical Microbiology, 44(4), 1261–1266.

ProEdge Dental. (2021). Complete guide to biofilm in dental unit waterlines. ProEdge Dental. Retrieved December 8, 2024.


Edited by Amelia Russell, student of Joan Slonczewski for BIOL 116, 2024, Kenyon College.