Puzzle of the chalk teeth solved? – Local immigration of the “wrong” protein blocks the mineralization of the tooth enamel – scinexx.de

Blocked crystals: Researchers could have clarified how the enigmatic chalk teeth are formed in children – brownish discolored, insufficiently hardened areas in the tooth enamel. Accordingly, the problem does not lie in the enamel-producing cells, but in the enamel itself. In chalk teeth, the wrong protein is deposited there, which then hinders the growth of the minerals. As a result, the enamel does not harden properly.

The so-called chalk teeth have increased dramatically: in the meantime, every fifth child suffers from the brownish discoloration and damage to the tooth enamel, and one in three children of twelve-year-olds is affected. Because the mineral storage in the tooth enamel is disturbed, this hard protective layer of the teeth remains soft. At the same time, the tooth surface is rough and brittle, which means that tooth decay can develop particularly quickly.

But what is the reason for this? So far there have been several “suspects”, but no comprehensive explanation for the phenomenon of chalk teeth. In some cases, genetic factors seem to play a role that disrupt mineralization during tooth development. But environmental factors such as the plastic additive bisphenol A or antibiotics are also suspected. Infections in early childhood are also discussed as possible risk factors.

Excess protein in the enamel

Now there is another lead. In search of the cause of the chalk teeth, Michael Hubbard from the University of Melbourne and his colleagues took a closer look at tooth enamel formation. First of all, the protein amelogenin is produced by the enamel-forming cells and binds to the still small mineral crystals in the enamel. When the enamel hardens, an enzyme breaks down the amelogenin and enables the mineral crystals to grow.

But this is different with chalk teeth: the soft, discolored areas contain three to 15 times more protein than normal, hardened tooth enamel, as the researchers found. Apparently the protein was not broken down when the enamel was mineralized. As a result, the excess proteins blocked the growth of the mineral crystals and thus the hardening of the tooth enamel.

If albumin gets into immature tooth enamel instead of the normal enamel protein amelogenin, enzymes (red) cannot break down the protein. As a result, the proteins block the growth of the mineral crystals (black). © Hubbard et al./ Frontiers in Physiology, CC-by-sa 4.0

Serum protein blocks mineralization

But why aren’t the proteins removed? To find out, Hubbard and his team carried out a protein analysis of the defective enamel sites – with astonishing results: “Surprisingly, we could only find small traces of amelogenin in them,” they report. Instead, the soft enamel areas contained an increased amount of the serum protein albumin – a molecule that is not found in intact tooth enamel.

This has consequences for tooth enamel: “The albumin mimics amelogenin by attaching itself to the immature enamel crystals,” the researchers explain. Because the albumin cannot be broken down again by the enzymes in the enamel, it remains in place. “The result is a blockage of the mineralization that is limited to local areas,” explains Hubbard. This explains why only some parts of the teeth are affected.

Indicative of early childhood triggers

If this is confirmed, then it sheds new light on the deeper causes of the chalk teeth. Contrary to popular belief, the problem is not in the enamel-producing cells of the tooth, but in the enamel itself. “Our discovery corrects 40 years of dental dogma that blamed these cells,” says Hubbard.

At the same time, the presence of the serum protein albumin in the pathologically altered tooth enamel suggests that the trigger must lie in early childhood – at the time when immature teeth are hardening. This could be an indication that early childhood infections play a role: “Epidemiology has already provided evidence of a link with previous diseases, but the specific mechanisms were missing,” said Hubbard and his colleagues.

The now identified immigration of serum albumin and the resulting blockage of mineralization could provide this missing link. “Building on this, we can now look for a strategy to avoid this global problem,” says Hubbard. (Frontiers of Physiology, 2021; doi: 10.3389/fphys.2021.802833)

Quelle: Science in Public


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