There is nothing like a peculiar, bone-jerking reaction to a damaged tooth that is exposed to something cold: a piece of ice cream, or a cold drink, and suddenly, a sharp, nervous feeling like a needle.
Researchers have known for years that this phenomenon results in damage to the protective outer layer of the tooth. But just how this message goes from the outside of your tooth to the veins is difficult to uncover. On Friday, biologists Report in the journal Science Advances That they have identified an unexpected player in this painful sensation: a protein embedded in the surface of cells inside the teeth. The discovery provides a glimpse of the connection between the external world and the inner of a tooth, and may one day help direct the development of the treatment of toothache.
More than a decade ago, Professor at Friedrich-Alexander University in Germany, Drs. Katrina Zimmerman found that cells making a protein called TRPC5 were sensitive to cold. When things became chilly, TRPC5 opened to form a channel, allowing ions to flow across the cell’s membrane.
Dr. Zimmerman stated that ion channels like TRPC5 are pierced throughout our bodies, and they are behind some surprisingly familiar sensations. For example, if your eyes feel cold and dry in the cold air, it is the result of the ion channel being activated in the cornea. He thought that other parts of the body might use a cold receptor such as TRPC5. And it occurred to him that “the most sensitive tissue in the human body can be teeth” when it is a sensation of cold.
Within the protective shell of their enamel, the teeth are made of a hard material called dentin that is threaded along small tunnels. At the center of dentin is the soft pulp of the tooth, where nerve cells and cells called odontoblots, which form the teeth, are interconnected.
The prevailing theory for how teeth get cold was that the change in temperature exerts pressure on the fluid in the tooth tunnels, which somehow provokes a reaction in the hidden veins. But there was little detail about how this could actually happen and bridging the gap between them.
Dr. Zimmerman and his colleagues looked to see if mice still felt toothache due to the lack of the TRPC5 channel as normal mice did. They were anxious to find out that these rats, when their teeth were damaged, did not behave as if anything happened. He observed, in fact, in the same way as if he had been given an anti-inflammatory painkiller, Drs. Zimmerman said.
His coauthor Dr., a pathologist at Massachusetts General Hospital. Jochen Lennerz examined human teeth for ion channel signals and found it in their veins and other cells. It has been suggested that the channel may have a role in a person’s perception of cold.
Over the years, researchers created a way to properly measure the neural signals that exit the mouse’s damaged molar. They tested their ideas with molecules that can block the activity of various channels, including TRPC5.
The picture he slowly collected is that TRPC5 is active in odontoblots. This was a bit surprising, as these supporting cells are known to form and maintain teeth, not aiding perception. Within Odontoblasts, Drs. The TRPC5 pop opens when the signal for freezing falls under dentin tunnels, Lennerz said, and from this the message is sent to the nerves.
As it happens, one substance that keeps TRPC5 in the open is eugenol, the main ingredient in clove oil, a traditional treatment for toothache. Although the Food and Drug Administration in the United States is similar about the effectiveness of eugenol, if it reduces pain for some people, it may be due to its effect on TRPC5.
Perhaps the knowledge that this channel is at the heart of cold-induced pain will lead to better treatment for toothache down the road – better ways to keep that message from getting heavy.