The innovation comes from researchers at the University of Nottingham’s School of Pharmacy and Department of Chemical and Environmental Engineering. Their new material is inspired by the biological processes that form tooth enamel during early childhood. It is designed to repair enamel that has been weakened by mineral loss or worn away by erosion, while also reinforcing enamel that remains healthy.

The findings, published in Nature Communications, could pave the way for a new generation of dental treatments that go beyond protecting existing enamel and actually help restore its structure.

How the New Gel Regrows Tooth Enamel

One of the most promising features of the technology is its simplicity. Dentists could apply the gel directly to teeth using a procedure similar to existing fluoride treatments, making it potentially easy to incorporate into routine dental care.

Unlike conventional fluoride products, however, the new gel contains no fluoride. Instead, it uses a material made from proteins that imitates important characteristics of the natural proteins responsible for guiding enamel formation when teeth first develop.

Once applied, the gel forms a thin but durable coating that penetrates the tooth’s surface and fills microscopic cracks and gaps. This coating then provides a framework for rebuilding the mineral structure of enamel.

The process relies on calcium and phosphate ions, two essential mineral components naturally present in saliva. The gel attracts these minerals and helps organize them into new crystals that grow in an orderly pattern.

Scientists call this process epitaxial mineralization. Essentially, it means that new mineral crystals grow in alignment with the existing enamel, allowing the newly formed material to become structurally integrated with the original tooth surface.

This organization is especially important because enamel gets its exceptional hardness and durability from the precise arrangement of its mineral crystals. Simply depositing minerals on a tooth is not enough to recreate the complex structure that makes natural enamel so effective.

By guiding crystal growth, the new gel can restore both the microscopic architecture and the physical properties of healthy enamel.

A Potential Solution for Tooth Sensitivity and Decay

The researchers also discovered that their material can be used on exposed dentine, commonly called dentin in the United States. Dentin is the layer of tooth tissue beneath the enamel. It is softer than enamel and contains tiny channels that can transmit sensations toward the nerves inside the tooth.

When enamel wears away, or gums recede, exposed dentin can make teeth particularly sensitive to hot, cold, sweet, or acidic foods and drinks.

The new gel can encourage the formation of an enamel-like mineral layer over exposed dentin. This could help reduce tooth sensitivity while also improving the attachment of dental restorations, such as fillings and other treatments used to repair damaged teeth.

The potential benefits are significant. Enamel deterioration is a major factor in tooth decay and contributes to dental problems that affect nearly half of the world’s population. These conditions can cause pain, infections, and eventually tooth loss. Poor oral health is also associated with broader health problems, including diabetes and cardiovascular disease.

One of the greatest challenges in dentistry is that enamel has no living cells capable of rebuilding it after teeth have fully developed. Although saliva can naturally replace some minerals lost during the earliest stages of enamel damage, the body cannot regenerate substantial amounts of enamel that have been worn away.

Existing treatments, including fluoride varnishes and remineralization products, can help protect teeth and repair early mineral loss. However, they cannot fully reconstruct enamel that has already been lost.

The new technology aims to overcome that limitation by encouraging the formation of new mineral tissue with properties resembling those of the original enamel.

Regenerated Enamel Performs Like Natural Tooth Enamel

The research team tested the mechanical strength and durability of the regenerated material under conditions designed to mimic everyday use.

These experiments examined how the newly formed enamel responded to activities and exposures that teeth routinely experience, including brushing, chewing, and contact with acidic foods.

The results were encouraging. According to the researchers, the regenerated enamel displayed mechanical properties comparable to those of healthy natural enamel, suggesting that the material could provide more than a temporary protective coating.

Dr. Abshar Hasan, a postdoctoral fellow and the study’s lead author, explained why recreating enamel’s internal structure is so important.

“Dental enamel has a unique structure, which gives enamel its remarkable properties that protect our teeth throughout life against physical, chemical, and thermal insults. When our material is applied to demineralized or eroded enamel, or exposed dentine, the material promotes the growth of crystals in an integrated and organized manner, recovering the architecture of our natural healthy enamel. We have tested the mechanical properties of these regenerated tissues under conditions simulating ‘real-life situations’ such as tooth brushing, chewing, and exposure to acidic foods, and found that the regenerated enamel behaves just like healthy enamel.”

These findings suggest that the gel could eventually offer a way to restore the strength and protective function of damaged enamel rather than simply slowing further deterioration. However, the laboratory results do not yet establish how well the treatment will perform over extended periods in patients.

A New Era of Tooth Enamel Repair?

Beyond its ability to regenerate enamel, the researchers emphasize that the technology was developed with practical dental applications in mind.

The gel is designed to be safe, simple to apply, and suitable for manufacturing on a larger scale. Its versatility could also allow it to be incorporated into several types of dental products, potentially benefiting patients of different ages with enamel erosion, tooth sensitivity, or other problems involving exposed dentin.

Professor Alvaro Mata, Chair in Biomedical Engineering & Biomaterials at the University of Nottingham, led the study and highlighted the potential for translating the discovery into products that dentists can use.

“We are very excited because the technology has been designed with the clinician and patient in mind. It is safe, can be easily and rapidly applied, and it is scalable. Also, the technology is versatile, which opens the opportunity to be translated into multiple types of products to help patients of all ages suffering from a variety of dental problems associated with loss of enamel and exposed dentine. We have started this process with our start-up company Mintech-Bio and hope to have a first product out by next year; this innovation could soon be helping patients worldwide.”

The researchers have already begun working toward commercialization through their company, Mintech-Bio, with the goal of introducing an initial product as early as the year following the announcement.

Although further development and clinical validation will be important before the technology becomes an established dental treatment, its ability to recreate the structure and strength of natural enamel represents a promising advance.

If the approach proves successful in patients, it could fundamentally change how dentists address enamel loss, opening the possibility of rebuilding tooth surfaces that previously could only be protected or restored using conventional dental materials.

Now, scientists in Japan have identified a promising molecule that could help protect the body’s natural muscle repair system and potentially make it more effective. In laboratory experiments, the compound strengthened an important biological signal involved in muscle regeneration, increasing its ability to connect with a key cellular receptor by more than twofold.

The discovery comes from a team led by Professor Ryuichi Tatsumi at Kyushu University’s Faculty of Agriculture. Their findings, published in Scientific Reports, suggest a possible new approach to addressing the cellular changes that make aging muscles increasingly difficult to repair.

How Aging Disrupts the Body’s Muscle Repair System

Skeletal muscles are the muscles attached to bones that allow us to walk, lift objects, maintain posture, and perform other voluntary movements. Although these muscles experience wear and tear throughout life, they also have a remarkable ability to repair themselves.

Much of that repair depends on specialized stem cells known as satellite cells. These cells normally remain inactive, positioned alongside muscle fibers until they receive a signal that repair or regeneration is needed. Once activated, they can multiply and develop into muscle cells that help restore damaged tissue.

An essential part of this process involves a protein called hepatocyte growth factor, or HGF. Despite its name, HGF plays important roles beyond the liver, including helping activate the stem cells responsible for muscle regeneration.

Under normal conditions, HGF is stored within the supportive material surrounding muscle fibers. When muscles experience an injury or mechanical stimulation, such as physical movement or stretching, the protein can be released.

HGF then attaches to a receptor called c-met on the surface of satellite cells. Receptors are specialized proteins that receive molecular signals and trigger responses inside cells. In this case, the interaction helps awaken dormant satellite cells, allowing them to multiply, mature, and participate in repairing muscle fibers.

But this carefully coordinated system becomes less reliable with age.

A Hidden Chemical Change May Weaken Aging Muscles

The researchers’ previous work revealed that HGF can undergo a chemical modification known as nitration. This process attaches a chemical group called a nitro group to particular locations on a protein, potentially changing its structure and interfering with its normal activity.

For HGF, the researchers identified two especially important locations, Y198 and Y250. Both lie within the region involved in attaching to the c-met receptor.

When these sites undergo nitration, HGF becomes less capable of connecting with its receptor. The result is similar to a key that has become damaged and can no longer operate its intended lock.

This disruption could have important consequences for aging muscles. Even if the body continues producing HGF, chemical changes may prevent the protein from properly activating the stem cells needed for tissue repair. The researchers believe this mechanism may contribute to age-related muscle wasting and declining regenerative capacity.

“HGF is not necessarily missing as we age,” explains Tatsumi. “Rather, it can be chemically altered after it is made. That led us to wonder whether a compound with strong antioxidant capacity might protect HGF, either by preventing nitration or by compensating for the functional loss it causes.”

Scientists Test Two Powerful Sulfur Compounds

To investigate that possibility, the team studied two compounds with strong antioxidant properties: glutathione trisulfide (GSSSG) and lipoic acid trisulfide (LASSS).

Antioxidants can help limit certain types of chemical damage caused by reactive molecules. Such damage can interfere with proteins and other essential components of cells, particularly when the body’s normal protective systems become less effective.

The two compounds belong to a chemical family called trisulfides. Their defining feature is a chain of three sulfur atoms connected to one another. This arrangement gives them unusual chemical properties, including an ability to participate in reactions involving the transfer of electrons, known as redox reactions.

Because these reactions play important roles in cellular chemistry, trisulfides have attracted growing interest as potential ingredients in new medicines.

In the first set of experiments, both compounds reduced nitration at the two vulnerable sites on HGF. However, preventing this chemical modification did not completely restore the protein’s ability to attach to c-met.

The scientists therefore increased the amount of trisulfide used relative to HGF. They changed the molar ratio, which compares the number of molecules of each substance, from 1:4000 to 1:8000.

That adjustment produced an unexpected result.

An Unexpected Discovery Creates “Super HGF”

At the higher concentration, LASSS did much more than protect HGF from chemical damage. It also dramatically improved the protein’s ability to bind to its receptor.

Compared with untreated HGF, the protein exposed to LASSS showed more than twice the binding affinity for c-met. In other words, it could attach to its target receptor much more strongly, potentially enhancing a critical step in the muscle repair process.

The treatment also made HGF more resistant to the loss of function caused by nitration, particularly at the Y198 site.

Notably, the effect was specific to LASSS. Although GSSSG had also reduced nitration in the earlier experiments, it did not produce the same improvement in receptor binding.

“This exceeded our expectations,” comments Tatsumi. “We knew trisulfides had diverse biological functions, but we never expected that simply mixing HGF with LASSS would produce such a striking effect.

“What this tells us is that LASSS does more than simply neutralize reactive molecules. It may interact directly with HGF and induce a subtle structural change, creating an enhanced ‘Super HGF’ form that binds c-met more strongly and resists nitration.”

The researchers suspect that LASSS interacts with HGF in a way that slightly alters the protein’s three-dimensional shape. Because a protein’s shape helps determine how well it interacts with other molecules, even a small structural adjustment could substantially change its activity.

The result is what the team describes as “Super HGF,” a potentially enhanced form of the body’s existing muscle repair signal.

Importantly, stronger receptor binding does not automatically establish that muscle regeneration itself has improved. Additional experiments will be needed to determine whether this molecular enhancement translates into better muscle healing and strength.

Mouse Experiments Reveal Promising Protection

After observing the effects in laboratory experiments, the researchers wanted to determine whether LASSS could also protect HGF inside living muscle tissue.

They used mice subjected to tail suspension, an established experimental method for studying muscle atrophy. By reducing normal weight bearing and muscle use, this technique produces some of the changes associated with prolonged inactivity, including muscle deterioration.

Mice that received LASSS before the experiment showed significantly less HGF nitration than untreated animals. This suggested that the compound’s ability to protect the muscle repair protein was not limited to controlled laboratory conditions.

Once again, GSSSG failed to produce the same protective result.

These findings provide early evidence that LASSS can influence the chemical processes affecting HGF within living animals. However, the mouse experiments demonstrated protection against nitration, not that LASSS restored lost muscle mass or improved physical strength.

The researchers emphasize that studies involving aging animals are still necessary to establish the compound’s effectiveness and safety in vivo, meaning within a living organism.

A Potential New Strategy Against Age-Related Muscle Loss

The discovery could eventually contribute to treatments aimed at maintaining muscle function during aging or extended periods of inactivity.

Muscle deterioration is not limited to older adults. It can also occur during prolonged bed rest or other situations in which muscles are used less frequently. When muscle repair mechanisms become impaired, recovering lost strength and function can become especially challenging.

Rather than replacing the body’s natural repair machinery, the approach explored in this study seeks to protect and enhance an existing biological signal. If the benefits can be confirmed in future studies, strengthening HGF activity could become one strategy for supporting muscle regeneration.

The scientists also believe that the underlying effects of LASSS on HGF may extend across species. That raises the possibility of applications not only in human medicine but also in veterinary care, particularly for aging companion animals such as dogs and cats.

For now, the findings represent an early step toward understanding how a naturally occurring muscle repair pathway might be strengthened. Whether LASSS can safely and effectively preserve muscle function during aging remains an open question.

Still, the unexpected discovery that a sulfur-based compound can both protect and enhance a critical repair protein offers a promising direction for future research, with the long-term goal of helping people maintain mobility, independence, and a better quality of life as they grow older.