Toronto researchers say they’ve shown for the first time that the body’s own immune system likely plays a role in both the decay of teeth and the breakdown of fillings.
Bacteria remain the main culprit in tooth decay, but a recent study from a team at the University of Toronto shows in the laboratory that neutrophils, a type of white blood cell, contribute to the damage.
“What we found is neutrophils are capable of causing collateral damage while fighting the bacteria,” said Yoav Finer, a professor in the faculty of dentistry and one of the authors of the paper published in the journal Acta Biomaterialia.
Conventional wisdom based on decades of research held that bacteria alone caused both tooth decay and decay in the resin composites used in modern-day fillings and tooth restorations.
“The bacteria takes sugar and produces acid, and that acid dissolves the tooth structure,” explained co-author Michael Glogauer, a professor in the same faculty and the team’s immunology expert.
He said a maverick in the dental research field, John Gabrovsek of the Cleveland Clinic, first proposed the idea that immune cells also played a role in tooth decay, with a paper on the theory in the Journal of Dental Research in 1970.
“They thought he was crazy because it went against the dogma,” Glogauer said, adding that Gabrovsek got in touch with him about 15 years ago to share his idea.
“Based on what I know about neutrophils and what he knows about neutrophils, I thought there was a lot of credibility in that,” he said.
Glogauer then approached Finer and the two got to work.
Neutrophils are the only white blood cell that is routinely found in the mouth, Glogauer explained.
In the lab, the research team used neutrophils isolated from blood to coat either parts of extracted teeth or the resin used to restore teeth.
“We can actually see them breaking down using electron microscopy,” Glogauer said. The team also detected the breakdown byproducts that can only come from neutrophils, he said.
The neutrophils become activated by the presence of bacteria in the mouth and release enzymes that attack the bacteria but also degrade the structure of the tooth and the resin, he said.
Finer compared the white blood cells to a sledgehammer.
“It’s like trying to eliminate a fly on the wall by taking a sledgehammer,” Finer said. “You may hit the bug, but the damage to the wall is quite significant.”
Now the team is working on a variety of followups, including isolating the type of enzymes that damage teeth and translating the work to make it clinically applicable. For example, they said, a rinse could be developed that controls neutrophils to limit the damage they do to teeth.
And new restoration materials can be designed for dental work to resist the damage from the immune cells.
For Gabrovsek, now 85, the research is an important validation of his earlier work.
“We just heard this morning,” said his wife, Rita Gabrovsek, as her husband laughed in the background on a phone call from their home in Twinsburg, Ohio.
“He’s smiling, just smiling, a huge smile,” she said. “It bugged him all his life that his theory was totally brushed aside, so this is a big moment for us.”
Gabrovsek said he never wavered in his belief.
“I couldn’t believe for 50 years that scientists here in the United States didn’t believe me,” he said. “I thought, boy, they are very stupid scientists. Now others know I am right!”
The couple planned to celebrate the news with their grandchildren Thursday afternoon by telling them that their grandfather was right all along.
Liam Casey, The Canadian Press