The nonperiodontopathic, the orange-complex, and the red-complex bacteria had different effects on the innate immune responses from gingival epithelial cells, which may affect the outcome of their host-microbial interaction in gingival sulcus.

Our results indicate that immune evasion may contribute to the pathogenicity of some periodontopathic bacteria.

Periodontitis is chronic inflammation of the periodontium caused by the host's inflammatory response to plaque biofilm, which destroys tooth-supporting soft and hard tissues. Periodontitis is a complex disease that involves interactions among three main features -microbial challenge, the host immune response, and environmental and genetic risk factors -in its pathogenesis. Although periodontitis has been regarded as the result of hyperimmune or hyperinflammatory responses to plaque bacteria, recent studies indicate that periodontal pathogens are rather poor activators and/or suppressors of the host immune response. This raises the question of how periodontal pathogens cause inflammation. To resolve this issue, in the present review we propose that bacterial invasion into gingival tissue is a key event in the initiation of periodontitis and that the persistence of these bacteria within host tissue results in chronic inflammation. In support of this hypothesis, we present the ways in which microbial, environmental and genetic risk factors contribute to bacterial invasion. It is hoped that the current model will instigate active discussion and new research to complete the puzzle of this complex disease process.

We previously reported that infection by

The role of Fusobacterium nucleatum in oral health and disease is controversial. We have previously shown that F. nucleatum invades gingival epithelial cells. However, the destiny of the internalized F. nucleatum is not clear. In the present study, the intracellular destiny of F. nucleatum and its cytopathic effect on gingival epithelial cells were studied. The ability of F. nucleatum and seven other oral bacterial species to invade immortalized human gingival epithelial (HOK-16B) cells were compared by confocal microscopy and flow cytometry. F. nucleatum had the highest invasive capacity, comparable to that of Porphyromonas gingivalis, a periodontal pathogen. Confocal microscopic examination revealed colocalization of internalized F. nucleatum with endosomes and lysosomes. Examination by transmission electron microscopy revealed that most intracellular F. nucleatum was located within vesicular structures with single enclosed membranes. Furthermore, F. nucleatum could not survive within gingival epithelial cells and had no cytopathic effects on host cells. Interestingly, endosomal maturation played a role in induction of the antimicrobial peptides human beta defensin (HBD)-2 and -3 by F. nucleatum from gingival epithelial cells. F. nucleatum is destined to enter an endocytic degradation pathway after invasion and has no cytopathic effect on gingival epithelial cells, which may cast new light on the role of F. nucleatum in the pathogenesis of periodontitis.