E Gingivalis Inflames the Oral Cavity and Destroys Tissues

Dentistry Today



A unicellular parasite commonly found in the mouth plays a role both in severe tissue inflammation and tissue destruction, according to researchers at Charité–Universitätsmedizin Berlin.

Most patients with severe and recurrent periodontitis showed an increased presence of the amoeba Entamoeba gingivalisin their oral cavities in the study. The effect of this amoeba is similar to that of Entamoeba histolytica, the parasite responsible for causing amebiasis.  

Once the parasite has invaded the gingival tissue, it feeds on its cells and causes tissue damage. According to the researchers, the two amoebae show similar mechanisms of tissue invasion and elicit a similar immune response in the host.

Periodontitis is an inflammation of the gums and supporting structures of the teeth. In patients with periodontitis, a decrease in the diversity of the oral flora coincides with an increase in the frequency of E gingivalis. In their study, the researchers showed that oral inflammation is associated with colonization by the oral parasite E gingivalis

Scientists have long been aware of the virulence potential of this genus of amoebae, according to the researchers. The gastrointestinal parasite E histolytica, for instance, causes a disease known as amebiasis, one of the most common causes of death from parasitic diseases worldwide.

“We have shown that an amoeba like E gingivalis, which colonizes the oral cavity, will invade the oral mucosa and destroy gingival tissue,” said Dr. Arne Schäfer, head of the Periodontology Research Unit at CharitéInstitute of Dental and Craniofacial Sciences and leader of the study. 

“This enables increased numbers of bacteria to invade the host tissue, which further exacerbates inflammation and tissue destruction,” said Schäfer.

The team of researchers was the first to describe precise roles of E gingivalis in the pathogenesis of inflammation. During their analysis of inflamed periodontal pockets, they detected evidence of the amoeba in about 80% of patients with periodontitis but only in 15% of healthy subjects.

The researchers’ observations revealed that, after invading the gums, the parasites move within the tissue, feeding on and killing host cells. Cell culture experiments showed that infection with E gingivalis slows the rate at which cells grow, eventually leading to cell death.

The researchers concluded that the amoeba’s role in inflammation shows distinct parallels to the pathogenesis of amebiasis. 

E gingivalis actively contributes to cell destruction inside the gingival tissue and stimulates the same host immune response mechanisms as E histolytica during its invasion of the intestinal mucosa,” said Schäfer.

“This parasite, which is transmitted by simple droplet infection, is one potential cause of severe oral inflammation,” said Schäfer. 

Treatment success often is short-lived in patients with periodontitis, the researchers said, possibly due to the high virulence potential of this previously unnoticed yet extremely common amoeba.

“We identified one infectious parasite whose elimination could improve treatment effectiveness and long-term outcomes in patients with gum disease,” said Schäfer. 

“Current treatment concepts for periodontitis fail to consider the possibility of infection by this parasite or its successful elimination,” Schäfer said.

A clinical trial is underway to determine the extent to which the elimination of this amoeba might improve treatment outcomes in patients with periodontitis. 

The study, “Entamoeba Gingivalis Causes Oral Inflammation and Tissue Destruction,” was published by the Journal of Dental Research.

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