Bacteria and pathogen may team up to trigger gum disease

A one-sided relationship between the bacteria Veillonella parvula and a pathogen in the mouth may lead to gum disease, a new study shows.

Friendly bacteria fills the human body. However, some of these microorganisms, such as Veillonella parvula, may be too nice. When these peaceful bacteria engage with the pathogen Porphyromonas gingivalis, it helps the germ multiply and cause gum disease, the researchers report.

The researchers wanted to understand how P. gingivalis colonizes the mouth. The pathogen is unable to produce its own growth molecules until it achieves a large population in the oral microbiome (the community of microorganisms that live on and inside the body).

The answer: It borrows growth molecules from V. parvula, a common yet harmless bacteria in the mouth whose growth is not population dependent.

In a healthy mouth, P. gingivalis makes up a minuscule amount of the bacteria in the oral microbiome and cannot replicate. But if dental plaque grows unchecked due to poor oral hygiene, V. parvula will multiply and eventually produce enough growth molecules to also spur the reproduction of P. gingivalis.

More than 47% of adults 30 and older have some form of periodontitis (also known as gum disease), according to the Centers for Disease Control and Prevention.

Understanding the relationship between P. gingivalis and V. parvula will help researchers create targeted therapies for periodontitis, says Patricia Diaz, professor of empire innovation at the University at Buffalo School of Dental Medicine and lead investigator of the study in ISME Journal.

“Having worked with P. gingivalis for nearly two decades, we knew it needed a large population size to grow, but the specific processes that drive this phenomenon were not completely understood,” says Diaz, who is also director of the University at Buffalo Microbiome Center. “Successfully targeting the accessory pathogen V. parvula should prevent P. gingivalis from expanding within the oral microbial community to pathogenic levels.”

The study tested the effects of growth molecules exuded by microorganisms in the mouth on P. gingivalis, including molecules from five species of bacteria that are prevalent in gingivitis, a condition that precedes periodontitis.

Of the bacteria researchers examined, only growth molecules secreted by V. parvula enabled the replication of P. gingivalis, regardless of the strain of either microbe. When researchers removed V. parvularom the microbiome, growth of P. gingivalis halted. However, the mere presence of any V. parvula was not enough to stimulate P. gingivalis. Only a large population of V. parvula incited the pathogen.

Data suggest that the relationship is one-directional as V. parvula received no obvious benefit from sharing its growth molecules, says Diaz.

“P. gingivalis and V. parvula interact at many levels, but the beneficiary is P. gingivalis,” says Diaz, noting that V. parvula also produces heme, which is the preferred iron source for P. gingivalis.

“This relationship that allows growth of P. gingivalis was not only confirmed in a preclinical model of periodontitis, but also, in the presence of V. parvula, P. gingivalis could amplify periodontal bone loss, which is the hallmark of the disease,” says George Hajishengallis, professor in the University of Pennsylvania School of Dental Medicine and co-investigator of the study.

“It is not clear whether the growth-promoting cues produced by P. gingivalis and V. parvula are chemically identical,” says Diaz. “Far more work is needed to uncover the identity of these molecules.”

Additional coauthors are from the University of Chile, the University of Connecticut, the Jackson Laboratory for Genomic Medicine, the National Institute of Dental and Craniofacial Research, the University of Leeds, and Penn. The National Institute of Dental and Craniofacial Research of the National Institutes of Health funded the work.

Source: University at Buffalo

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