We’ve all had a moment when we cursed at our teeth nerves for being so damn sensitive and painful. But if you’ve ever bitten down too hard and recoiled before anything truly terrible happened, your nerves may have saved your tooth.

For decades, the nerves inside our teeth were cast in a singular role: to deliver pain so sharp it sends us straight to the dentist. But a new study, published in Cell Reports by scientists at the University of Michigan, turns that view on its head. These nerves don’t just scream in agony, they also act as guardians, detecting threats and activating a protective jaw-opening reflex before your brain even knows what’s happened.

“We suspected there was a more fundamental role for tooth nerves,” said Joshua Emrick, senior author of the study and assistant professor at the U-M School of Dentistry. “When we consider regenerating a tooth pulp, we need to bring back the nerves.”

Teeth and Pain

Inside the tooth lies a specialized network of sensory cells known as intradental neurons. Specifically, the study focuses on a subset of these called high-threshold mechano-nociceptors—HTMRs for short. Until now, they were mostly blamed for dental pain. But using a suite of state-of-the-art techniques (live calcium imaging, behavioral analysis powered by AI, and more), Emrick’s team discovered these neurons serve a second role that’s just as important (or even more so).

These HTMRs are embedded deep in the inner dentin and pulp, areas that normally remain insulated unless the tooth suffers trauma or decay. When researchers simulated such damage in mice by removing enamel or applying pressure, HTMRs lit up like alarm bells. But they didn’t just send pain signals. Within just 5 to 15 milliseconds, they triggered a reflexive opening of the jaw, preventing further damage.

“Our study challenges the prior assumption that nerves inside the tooth primarily function to elicit pain and force us straight to the dentist for help,” Emrick said. “If you’ve ever accidentally bitten down on your fork, you’ve probably experienced a startling jolt, but also stopped short of fracturing your teeth. You may thank these intradental HTMRs for that.”

The reflex appears to be evolutionarily conserved in mammals with permanent teeth, like humans and mice, who can’t replace damaged molars. This rapid jaw-opening response is likely a critical adaptation to prevent catastrophic damage during mastication.

An Evolutionary Shield

The discovery opens the door to a deeper understanding of dental pain—and potentially, new ways to manage it.

“We think protection of the teeth through this jaw-opening reflex is highly conserved among mammals that haven’t developed the ability to replace teeth—like humans or in the molar teeth of mice,” Emrick said. Our work reports an ability to use these neurons to also elicit pain which will open up possibilities for developing new methods for relieving toothache at the dentist’s office.

Interestingly, these pain and reflex signals persisted even when two well-known molecular players (Piezo2 and Nav1.8) were genetically disabled. That suggests that HTMRs may be operating through previously unidentified mechanosensitive channels.

Elizabeth Ronan, postdoctoral fellow at the School of Dentistry and lead author of the work, said the findings are the start of a deeper understanding of how this system works.

“While we typically think of sensation as giving rise to our perceived external experience of the world, sensory neurons are equally essential in protecting and maintaining our tissues throughout life,” she said. “Much remains to be discovered regarding how sensory neurons function within individual tissues, especially internal ones such as the teeth.”

The findings could turn out to be impactful. “This hints at the existence of an unknown high-threshold mechanical receptor,” said Dr. Arash Ravanbakhsh, who was not involved in the study. “Identifying that could be a game changer for next-generation dental anesthetics.”

What We Still Don’t Know

Despite its breakthroughs, the study leaves several intriguing questions on the table.

First, the research focused mainly on a particular type of nerve—large, fast-conducting fibers called myelinated neurons. These are the HTMRs that trigger rapid reflexes and pain. But there’s another kind of nerve fiber, known as C-fibers, which are thinner, slower, and unmyelinated. These have been found deep in the tooth pulp and are often associated with the lingering, dull ache of chronic tooth pain. This study didn’t explore their role, so it’s still unclear how they might fit into the larger picture of dental sensation and protection.

Another open question involves cells called odontoblasts. These are specialized cells that form the inner lining of the tooth and help maintain dentin, the tissue just beneath the enamel. Some previous lab studies have suggested that odontoblasts might be able to sense changes in temperature or pressure, possibly even communicating with nearby nerves. But in this study, the researchers did not examine whether odontoblasts actually send signals to the neurons in living animals.

So while the study has redrawn the map of how teeth feel and protect themselves, it has also pointed to vast unexplored territory.

Teeth, it seems, may be even more sensitive—and more sophisticated—than we ever imagined.

Elizabeth A. Ronan et al, Intradental mechano-nociceptors serve as sentinels that prevent tooth damage, Cell Reports (2025). DOI: 10.1016/j.celrep.2025.116017