Diabetes and Periodontal Bone Loss

Diabetes-induced changes in oral microbiome promote periodontal bone lossDiabetes-induced-changes-in-oral-microbiome-promote-periodontal-bone-loss

The following article explains the loss of bone density in a person who has Diabetes and relates the research and studies done to collaborate the research.  I found this very interesting and had to include the link for anyone interested in reading the article.  I am also including a link for the pdf file so that you can download it if you wish.

The beginning of the article states:

“A new study led by University of Pennsylvania researchers has found that the

oral microbiome is affected by diabetes, causing a shift to increase its

pathogenicity. The research, published in the journal Cell Host & Microbe this

week, not only showed that the oral microbiome of mice with diabetes shifted

but that the change was associated with increased inflammation and bone loss.”

The article goes on state,

“Up until now, there had been no concrete evidence that diabetes affects the

oral microbiome,” said Dana Graves, senior author on the new study and vice

dean of scholarship and research at Penn’s School of Dental Medicine. “But the

studies that had been done were not rigorous.”

“Just four years ago, the European Federation of Periodontology and the

American Academy of Periodontology issued a report stating there is no

compelling evidence that diabetes is directly linked to changes in the oral

microbiome. But Graves and colleagues were skeptical and decided to pursue

the question, using a mouse model that mimics Type 2 diabetes.”

“My argument was that the appropriate studies just hadn’t been done, so I

decided, We’ll do the appropriate study,” Graves said.

Graves coauthoredthe study with Kyle Bittinger of the Children’s Hospital of

Philadelphia, who assisted with microbiome analysis, along with E Xiao from

Peking University, who was the first author, and coauthors from the University

of São Paulo, Sichuan University, the Federal University of Minas Gerais and

the University of Capinas. The authors consulted with Daniel Beiting of Penn

Vet’s Center for HostMicrobial Interactions and did the boneloss

measurements at the Penn Center for Musculoskeletal Diseases.

The researchers began by characterizing the oral microbiome of diabetic mice

compared to healthy mice. They found that the diabetic mice had a similar oral

microbiome to their healthy counterparts when they were sampled prior to

developing high blood sugar levels, or hyperglycemia. But, once the diabetic

mice were hyperglycemic, their microbiome became distinct from their normal

littermates, with a less diverse community of bacteria.

The diabetic mice also had periodontitis, including a loss of bone supporting

the teeth, and increased levels of IL17, a signaling molecule important in

immune response and inflammation. Increased levels of IL17 in humans are

associated with periodontal disease.

“The diabetic mice behaved similar to humans that had periodontal bone loss

and increased IL17 caused by a genetic disease,” Graves said.

The findings underscored an association between changes in the oral microbiome

and periodontitis but didn’t prove that the microbial changes were responsible for

disease.  To drill in on the connection, the researchers transferred microorganisms

from the diabetic mice to normal germfree mice, animals that have been raised

without being exposed to any microbes.  These recipient mice also developed bone

loss. A microCT scan revealed they had 42 percent less bone than mice that had

received a microbial transfer from normal mice. Markers of inflammation also went

up in the recipients of the diabetic oral microbiome.  “We were able to induce the

rapid bone loss characteristic of the diabetic group into a normal group of animals

simply by transferring the oral microbiome,” said Graves.

With the microbiome now  implicated in causing the periodontitis, Graves and

colleagues wanted to know how. Suspecting that inflammatory cytokines, and

specifically IL17, played a role, the researchers repeated the microbiome

transfer experiments, this time injecting the diabetic donors with an antiIL17

antibody prior to the transfer. Mice that received microbiomes from the treated

diabetic mice had much less severe bone loss compared to mice that received

a microbiome transfer from untreated mice.  The findings “demonstrate

unequivocally” that diabetesinduced changes in the oral microbiome drive

inflammatory changes that enhance bone loss in periodontitis, the authors wrote.

Though IL17 treatment was effective at reducing bone loss in the mice, it is

unlikely to be a reasonable therapeutic strategy in humans due to its key role

in immune protection. But Graves noted that the study highlights the

Diabetes-induced changes in oral microbiome promote periodontal bone loss

importance for people with diabetes of controlling blood sugar and practicing

good oral hygiene.

“Diabetes is one of the systemic disease that is most closely linked to

periodontal disease, but the risk is substantially ameliorated by good glycemic

control,” he said. “And good oral hygiene can take the risk even further down.”