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Fusobacterium nucleatum: The Opportunistic Pathogen of Periodontal and Peri-Implant Diseases

Chen, Yanchi, Shi, Tao, Li, Yiling, Huang, Linyang, Yin, Derong·2022·Frontiers in Microbiology
DOI 10.3389/fmicb.2022.860149PMC PMC8966671
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Abstract

Peri-implant diseases are considered to be a chronic destructive inflammatory destruction/damage occurring in soft and hard peri-implant tissues during the patient’s perennial use after implant restoration and have attracted much attention because of their high incidence. Although most studies seem to suggest that the pathogenesis of peri-implant diseases is similar to that of periodontal diseases and that both begin with microbial infection, the specific mechanism of peri-implant diseases remains unclear. As an oral opportunistic pathogen, Fusobacterium nucleatum ( F. nucleatum ) has been demonstrated to be vital for the occurrence and development of many oral infectious diseases, especially periodontal diseases. More notably, the latest relevant studies suggest that F. nucleatum may contribute to the occurrence and development of peri-implant diseases. Considering the close connection between peri-implant diseases and periodontal diseases, a summary of the role of Fusobacterium nucleatum in periodontal diseases may provide more research directions and ideas for the peri-implantation mechanism. In this review, we summarize the effects of F. nucleatum on periodontal diseases by biofilm formation, host infection, and host response, and then we establish the relationship between periodontal and peri-implant diseases. Based on the above aspects, we discuss the importance and potential value of F. nucleatum in peri-implant diseases.

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Figure 1 The bridging function of Fusobacterium nucleatum in biofilm formation. Fusobacterium nucleatum is a bridging organism that has a great ability to bind to many other microorganisms. In the oral cavity, Fusobacterium nucleatum adheres to both early and late colonizers, promoting the coaggregation of periodontal disease-related pathogens. In addition, it can bind to Candida albicans and Clostridioides difficile. RadD is one of the most profoundly studied adhesions of Fusobacterium nucleatum and contributes to the binding between Fusobacterium nucleatum and Candida albicans, Streptococcus cristatus, Streptococcus gordonii, Streptococcus mutans, Actinomyces naeslundii, Porphyromonas gingivalis, and Clostridioides difficile via an arginine-inhibitable method. Several other Fusobacterium nucleatum outer membrane proteins are also vital in bacterial coaggregation and biofilm formation, including Fap2, FomA and CmpA. Moreover, the Fusobacterium nucleatum outer membrane lectin also contributes to dual-species biofilm formation in a galactose-inhibitable method.
Figure 1 The bridging function of Fusobacterium nucleatum in biofilm formation. Fusobacterium nucleatum is a bridging organism that has a great ability to bind to many other microorganisms. In the oral cavity, Fusobacterium nucleatum adheres to both early and late colonizers, promoting the coaggregation of periodontal disease-related pathogens. In addition, it can bind to Candida albicans and Clostridioides difficile. RadD is one of the most profoundly studied adhesions of Fusobacterium nucleatum and contributes to the binding between Fusobacterium nucleatum and Candida albicans, Streptococcus cristatus, Streptococcus gordonii, Streptococcus mutans, Actinomyces naeslundii, Porphyromonas gingivalis, and Clostridioides difficile via an arginine-inhibitable method. Several other Fusobacterium nucleatum outer membrane proteins are also vital in bacterial coaggregation and biofilm formation, including Fap2, FomA and CmpA. Moreover, the Fusobacterium nucleatum outer membrane lectin also contributes to dual-species biofilm formation in a galactose-inhibitable method.CC BY · PubMed Central
Figure 2 The mechanism by which Fusobacterium nucleatum induces host responses. (1) Under healthy conditions, one of the most important factors is that Fusobacterium nucleatum uses FAD-I to stimulate gingival epithelial cells to express human beta-defensin-2 via gingival epithelial cell Toll-like receptors. Stimulated human beta-defensin-2 helps to defend against invading microbes, including Fusobacterium nucleatum itself, and maintains homeostasis in the complex oral environment. (2) In a state of disease, Fusobacterium nucleatum destroys the epithelial barrier and affects human gingival fibroblasts. It not only induces cell autophagy but also stimulates the secretion of several cytokines and chemokines. When challenged by Fusobacterium nucleatum, the immune system is activated to eliminate invasive bacteria. However, Fusobacterium nucleatum could restrain the human immune system to reduce this removal effect. Moreover, the production of TNF-α from activated NK cells may lead to periodontal tissue destruction.
Figure 2 The mechanism by which Fusobacterium nucleatum induces host responses. (1) Under healthy conditions, one of the most important factors is that Fusobacterium nucleatum uses FAD-I to stimulate gingival epithelial cells to express human beta-defensin-2 via gingival epithelial cell Toll-like receptors. Stimulated human beta-defensin-2 helps to defend against invading microbes, including Fusobacterium nucleatum itself, and maintains homeostasis in the complex oral environment. (2) In a state of disease, Fusobacterium nucleatum destroys the epithelial barrier and affects human gingival fibroblasts. It not only induces cell autophagy but also stimulates the secretion of several cytokines and chemokines. When challenged by Fusobacterium nucleatum, the immune system is activated to eliminate invasive bacteria. However, Fusobacterium nucleatum could restrain the human immune system to reduce this removal effect. Moreover, the production of TNF-α from activated NK cells may lead to periodontal tissue destruction.CC BY · PubMed Central
Figure 3 The relationship between Fusobacterium nucleatum periodontal diseases and peri-implant diseases. Biofilms are universally accepted as mutual and critical factors in the initiation of periodontal and peri-implant diseases. The varied substrate for bacterial colonization and probably elevated function of Fusobacterium nucleatum in biofilm formation may be responsible for the reported discrepancies in its composition. With the succession of dental plaque, on the one hand, Fusobacterium nucleatum adheres to and/or invades host cells to induce mixed infection; on the other hand, invaded Fusobacterium nucleatum activates the human immune system to secrete inflammatory factors and accumulate inflammatory cells. These two effects cooperate with each other to elicit the ultimate inflammatory response. Detected differences between periodontal diseases and peri-implant diseases in histological structure and inflammatory response might indicate the specific pathogenesis of Fusobacterium nucleatum in these two diseases individually between the host infection and host response.
Figure 3 The relationship between Fusobacterium nucleatum periodontal diseases and peri-implant diseases. Biofilms are universally accepted as mutual and critical factors in the initiation of periodontal and peri-implant diseases. The varied substrate for bacterial colonization and probably elevated function of Fusobacterium nucleatum in biofilm formation may be responsible for the reported discrepancies in its composition. With the succession of dental plaque, on the one hand, Fusobacterium nucleatum adheres to and/or invades host cells to induce mixed infection; on the other hand, invaded Fusobacterium nucleatum activates the human immune system to secrete inflammatory factors and accumulate inflammatory cells. These two effects cooperate with each other to elicit the ultimate inflammatory response. Detected differences between periodontal diseases and peri-implant diseases in histological structure and inflammatory response might indicate the specific pathogenesis of Fusobacterium nucleatum in these two diseases individually between the host infection and host response.CC BY · PubMed Central

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Chen, Y., Shi, T., Li, Y., Huang, L., & Yin, D.
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Frontiers in Microbiology
Publisher
Frontiers Media SA
Published
2022-03-11
Volume
13
ISSN
1664-302X
DOI
10.3389/fmicb.2022.860149
PMC
PMC8966671
Cited by
75
References
7
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
Sichuan University (RCDWJS2021-6, RD-02-202009)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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