Study investigates cellular mechanism behind dental fluorosis
February 21, 2020
— Results from an NYU College of Dentistry study
suggest how excess fluoride exposure affects the cells forming tooth enamel — possibly explaining how dental fluorosis arises.
Science Signaling, a peer-reviewed scientific journal published weekly by the American Association for the Advancement of Science, published the study Feb. 18.
“The benefits of fluoride for oral health considerably outweigh the risks,” said Rodrigo Lacruz
, Ph.D., associate professor of basic science and craniofacial biology at the NYU College of Dentistry and the study’s senior author. “But given how common dental fluorosis is and how poorly understood the cellular mechanisms responsible for this disease are, it is important to study this problem.”
Fluoride, a naturally occurring mineral, helps prevent caries in children and adults by making the outer surface of teeth more resistant to acid attacks that cause tooth decay. It is added to community water systems around the world, with the U.S. Department of Health and Human Services recommending a level of 0.7 parts per million.
The level of fluoride the NYU researchers studied was more than 20 times greater than that used in community water fluoridation, according to the ADA Science & Research Institute. The researchers used about 19 parts per million in their study, a concentration found in waters that cause fluorosis.
Safe levels of fluoride, like the low levels found in fluoridated drinking water, help strengthen and protect tooth enamel. However, exposure to too much fluoride from any source, over long periods when teeth are developing under the gums during childhood, can cause dental fluorosis. Mild fluorosis shows the appearance of faint white lines or opaque zones on the teeth, but more severe cases show brown staining, poor mineralization and porous enamel.
The researchers analyzed the effects of exposing tooth enamel cells from rats to excessive amounts of fluoride and then examined how the cells were affected, including calcium signaling and calcium ions released from intracellular stores.
Researchers then examined whether human kidney cells were similarly affected. Human kidney cells were not affected by exposure to excess fluoride in the same manner. This suggests the impact of excess fluoride is characteristic only of enamel cells and also that excess fluoride exposure does not disrupt calcium regulation in kidney cells.
Dr. Lacruz said he was surprised.
“You would think that if you expose the enamel cells and kidney cells to the same stressor — treating them with the same amount of fluoride for the same period of time — that you’d have more or less similar responses,” said Dr. Lacruz. “But that was not the case. Under the same circumstances, enamel cells react to coping with stress in vastly different ways than kidney cells.”
This suggests that fluoride responsiveness is in some ways unique to enamel-producing cells, he said.
Dr. Lacruz said he and others will pursue future research on the subject, which could include testing fluoride’s cellular effects on live rodents to validate what they observed in vitro.
“Now we know what to look for,” he said.
Dr. Lacruz acknowledged that fluoride studies can be subject to controversy, but emphasized his support for community water fluoridation, backed by decades of research that illustrate its value in preventing caries.
“It’s black and white for us,” he said. “I understand what the others are saying, but the facts are the facts. There’s so much benefit that it’s hard to argue with it.”
The National Institute of Dental and Craniofacial Research, NYU Abu Dhabi and a support grant to NYU Langone’s Laura and Isaac Perlmutter Cancer Center from the National Cancer Institute funded the study.