About half of children with celiac disease have damaged enamel: Common milk protein causes an immune reaction

A damaged enamel makes the tooth more porous, and more prone to caries and cavities. For some, enamel defects lead to major dental health problems. 

A recent Norwegian study has tried to look at the causes of why so many Norwegian children get enamel defects.

An international research group have now shown that about half of childen with celiac disease have enamel damage. 

“This is the first time it is shown that enamel damage can be caused by an autoimmune disease, autoimmune amelogenesis imperfect,” Eystein Husebye says.

He is a professor at the University of Bergen's Department of Clinical Science.

Autoimmune reaction to a common protein in milk

In celiac patients, the research team found a link between autoantibodies to the milk protein kappa-casein and enamel damage.

“It may seem that in the same way as celiac patients react to gluten in their diet and get intestinal damage, they react to kappa-casein in cow’s milk and get tooth damage,” Husebye says.

Enables earlier diagnosis

The other condition with autoimmune enamel damage that was studied is the very rare and hereditary disease autoimmune polyendocrine syndrome type I (APS-I) that affects children. 

It was the widespread enamel damage in this disease that put the research team onto the idea that autoimmunity was the cause.

“The new findings will help us to diagnose celiac disease at an earlier stage and thus prevent enamel damage,” Huesbye says. 

It also makes it possible to find a 'cure' for these damages in children.

“If possible, removing kappa-casein from your diet can prevent enamel damage. In addition, the findings make it possible to consider whether there are similar mechanisms for enamel damage in other diseases,” he concludes. 

Reference:

Dobeš et al. Extrathymic expression of Aire controls the induction of effective TH17 cell-mediated immune response to Candida albicans, Nature Immunology, 2022. DOI: 10.1038/s41590-022-01247-6

About the study

This was a collaborative study between the University of Bergen, Norway, The Qeizmann Institute of Science, Israel, and other international partners. 

The research team in Bergen was led by Anette Wolff and Eystein Husebye. 

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