The newly discovered bacterium that causes gum disease delivers a
one-two punch by also triggering normally protective proteins in the mouth
to actually destroy more bone, a University of Michigan study found.
Scientists and oral health care providers have known for decades that
bacteria are responsible for periodontitis, or gum disease. Until now,
however, they hadn’t identified the bacterium.
“Identifying the mechanism that is responsible for periodontitis is a major
discovery,” said Yizu Jiao, a postdoctoral fellow at the U-M Health System,
and lead author of the study appearing in the recent issue of the journal
Cell Host and Microbe.
Jiao and Noahiro Inohara, research associate professor at the U-M Health
System, worked with William Giannobile, professor of dentistry, and Julie
Marchesan, formerly of Giannobile’s lab.
The study yielded yet another significant finding: the bacterium that causes
gum disease, called NI1060, also triggers a normally protective protein in
the oral cavity, called Nod1, to turn traitorous and actually trigger
bone-destroying cells. Under normal circumstances, Nod1 fights harmful
bacterium in the body.
“Nod1 is a part of our protective mechanisms against bacterial infection. It
helps us to fight infection by recruiting neutrophils, blood cells that act
as bacterial killers,” Inohara said. “It also removes harmful bacteria
during infection. However, in the case of periodontitis, accumulation of
NI1060 stimulates Nod1 to trigger neutrophils and osteoclasts, which are
cells that destroy bone in the oral cavity.”
Giannobile, who also chairs the Department of Periodontics and Oral Medicine
at the U-M School of Dentistry, said understanding what causes gum disease
at the molecular level could help develop personalized therapy for dental
patients.
“The findings from this study underscore the connection between beneficial
and harmful bacteria that normally reside in the oral cavity, how a harmful
bacterium causes the disease, and how an at-risk patient might respond to
such bacteria,” Giannobile said.
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