Diabetes May Induce Tooth Weakness and Decay: Study
A new study conducted by Rutgers University has found that mice that became diabetic had the enamel and dentin on their teeth become softer and less durable, giving a possible answer for why human diabetic patients are often more prone to tooth decay.“We’ve long seen elevated rates of cavity formation and tooth loss in patients with diabetes, and we’ve long known that treatments such as fillings do not last as long in such patients, but we did not know exactly why,” said lead researcher Mohammad Ali Saghiri on May 31. To study the reason behind prevalent tooth decay and oral health problems, researchers induced Type 1 diabetes by killing insulin-producing beta cells in 35 healthy mice and compared the hardness of the teeth to normal mice over 28 weeks. While enamel and dentin are expected to last over a lifetime under due care, the team observed that microhardness in teeth increased in the normal group, and microhardness decreased for the diabetic group over time. Enamel hardness between the normal and the diabetic group was observed to be comparable within the first 12 weeks, however a significant difference of around 26 units was observed at the week 12 interval, and the gap widened over the entire 28 weeks of the study. By week 28, significant decreases in dentin microhardness—the hard structure that lies underneath enamel and makes up the structure of the teeth—were also observed. The team also found magnesium and strontium—minerals that form structural components of the teeth—were significantly lower compared to the normal group, further confirming the relationship between diabetes and an induced weakness in tooth. Previous studies have also shown that the hyperglycemic–high blood sugar concentration–properties of diabetics can hinder the work of cells responsible for developing teeth as well as cells that sense caries-related bacteria and irritations, leading to poor tooth formation. A 2014 study has also suggested that crucial bone-forming minerals such as calcium and phosphorous may be reduced in diabetic individuals due to the swapping of less crucial minerals such as strontium for calcium in the structure of the teeth, leading to a dismantling of the original mineral structure. The authors speculate that the reason behind overall teeth deterioration may be due to a reduction in the thickness of enamel and dentin as well as inhibitory effects of hyperglycemia on the mineralization of enamel and dentine. However, as the study mimicked Type 1 diabetes in mice by killing insulin-producing cells rather than inducing insulin insensitivity, the authors caution that their findings are limited and can only serve as a “foundation for future studies,” and therefore may not be applicable for Type 2 diabetes due to differences in mechanism. “The population of people with diabetes continues to grow rapidly,” said Saghiri. “There is a great need for treatments that will allow patients to keep their teeth health.”
A new study conducted by Rutgers University has found that mice that became diabetic had the enamel and dentin on their teeth become softer and less durable, giving a possible answer for why human diabetic patients are often more prone to tooth decay.
“We’ve long seen elevated rates of cavity formation and tooth loss in patients with diabetes, and we’ve long known that treatments such as fillings do not last as long in such patients, but we did not know exactly why,” said lead researcher Mohammad Ali Saghiri on May 31.
To study the reason behind prevalent tooth decay and oral health problems, researchers induced Type 1 diabetes by killing insulin-producing beta cells in 35 healthy mice and compared the hardness of the teeth to normal mice over 28 weeks.
While enamel and dentin are expected to last over a lifetime under due care, the team observed that microhardness in teeth increased in the normal group, and microhardness decreased for the diabetic group over time.
Enamel hardness between the normal and the diabetic group was observed to be comparable within the first 12 weeks, however a significant difference of around 26 units was observed at the week 12 interval, and the gap widened over the entire 28 weeks of the study.
By week 28, significant decreases in dentin microhardness—the hard structure that lies underneath enamel and makes up the structure of the teeth—were also observed.
The team also found magnesium and strontium—minerals that form structural components of the teeth—were significantly lower compared to the normal group, further confirming the relationship between diabetes and an induced weakness in tooth.
Previous studies have also shown that the hyperglycemic–high blood sugar concentration–properties of diabetics can hinder the work of cells responsible for developing teeth as well as cells that sense caries-related bacteria and irritations, leading to poor tooth formation.
A 2014 study has also suggested that crucial bone-forming minerals such as calcium and phosphorous may be reduced in diabetic individuals due to the swapping of less crucial minerals such as strontium for calcium in the structure of the teeth, leading to a dismantling of the original mineral structure.
The authors speculate that the reason behind overall teeth deterioration may be due to a reduction in the thickness of enamel and dentin as well as inhibitory effects of hyperglycemia on the mineralization of enamel and dentine.
However, as the study mimicked Type 1 diabetes in mice by killing insulin-producing cells rather than inducing insulin insensitivity, the authors caution that their findings are limited and can only serve as a “foundation for future studies,” and therefore may not be applicable for Type 2 diabetes due to differences in mechanism.
“The population of people with diabetes continues to grow rapidly,” said Saghiri. “There is a great need for treatments that will allow patients to keep their teeth health.”