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

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.

Antimicrobial efficiency and cytocompatibility of different decontamination methods on titanium and zirconium surfaces

“…To develop a peri‐implantitis‐biofilm model for testing implant‐decontamination conditions under harsh conditions, a new approach was applied combining microbial species with the most aggregation ( Aggregatibacter actinomycetemcomitans , Fusobacterium nucleatum ), adhesive ( Streptococcus sanguinis/oralis ), and net‐forming (mycelia by Candida albicans , pseudo‐mycelia by Actinomyces oris ) potential (Chen et al, 2022; D'Ercole et al, 2020; Hauser‐Gerspach et al, 2007). The primary goal was to create a manageable, reproducible, and robust, water‐insoluble biofilm to challenge any implant‐decontamination method to the most.…”

Bidirectional association between polycystic ovary syndrome and periodontal diseases

“…F.n serves as a bridge to assist the interspecies coaggregation, including Porphyromonas gingivalis ( P.g ), Treponema denticola ( T.d ), and Streptococcus gordonii ( S.g ), and accelerates biofilm formation via outer membrane proteins. In addition, F.n breaks the epithelial barrier and engages in attacking the lymphocytes, resulting in the host immune imbalance ( 37 ). Accumulating evidence suggests that the alteration of the oral microbial community in PCOS women might increase the risk of PDD.…”

Bioactive glass air‐abrasion promotes healing around contaminated implant surfaces surrounded by circumferential bone defects: An experimental study in the rat

“…F. nucleatum serves as a bridge between initial and late bacterial colonizers, including the red complex bacterial pathogens, Tannerella forsythia, Treponema denticola, and Porphyromonas gingivalis, which are actively associated with periodontal and peri-implant diseases. [7][8][9][10][11][12][13] The debridement of the implant surface is an essential step in treating peri-implant diseases. However, implant design and surface roughness may facilitate the development and retention of the bacterial biofilm and limit the effectiveness of mechanical debridement.…”

“…It starts with the adhesion of the initial colonizers, such as oral streptococci, to the acquired pellicle, which facilitates the adhesion of successive colonizers like Fusobacterium nucleatum. F. nucleatum serves as a bridge between initial and late bacterial colonizers, including the red complex bacterial pathogens, Tannerella forsythia, Treponema denticola , and Porphyromonas gingivalis , which are actively associated with periodontal and peri‐implant diseases 7–13 …”