Researchers build a better dental implant

Preclinical study demonstrates a new ‘smart’ implant and minimally invasive surgery to better retain feel and function of natural teeth

Peer-Reviewed Publication

Tufts University

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From left to right: Study co-authors Subhashis Ghosh, Jake Jinkun Chen, and Siddhartha Das in Chen’s lab at Tufts’ Biomedical Research and Public Health Building.

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Credit: Jenna Schad/Tufts University

Each year, millions of people in the U.S. get dental implants as a long-term, natural-looking fix for missing teeth. But traditional implants don’t fully mimic real teeth.

Researchers from Tufts University School of Dental Medicine and Tufts University School of Medicine recently described a new approach to dental implants that that could better replicate how natural teeth feel and function. Their study, published in Scientific Reports, shows early success with both a “smart” implant and a new gentler surgical technique in rodents.  

“Natural teeth connect to the jawbone through soft tissue rich in nerves, which help sense pressure and texture and guide how we chew and speak. Implants lack that sensory feedback,” says Jake Jinkun Chen, DI09, a professor of periodontology and director of the Division of Oral Biology at the School of Dental Medicine and the senior author on the study.

Traditional dental implants use a titanium post that fuses directly to the jawbone to support a ceramic crown, and the surgery often cuts or damages nearby nerves. To tie these inert pieces of metal into the body’s sensory system, the Tufts team developed an implant wrapped in an innovative biodegradable coating. This coating contains stem cells and a special protein that helps them multiply and turn into nerve tissue. As the coating dissolves during the healing process, it releases the stem cells and protein, fueling the growth of new nerve tissue around the implant.

The coating also contains tiny, rubbery particles that act like memory foam. Compressed so that the implant is smaller than the missing tooth when it’s first inserted, these nanofibers gently expand once in place until the implant snugly fits the socket. This allows for a new minimally invasive procedure that preserves existing nerve endings in the tissue around the implant.

“This new implant and minimally invasive technique should help reconnect nerves, allowing the implant to ‘talk’ to the brain much like a real tooth,” explains Chen. “This breakthrough also could transform other types of bone implants, like those used in hip replacements or fracture repair.”

Six weeks after surgery, the implants stayed firmly in place in rats, with no signs of inflammation or rejection. “Imaging revealed a distinct space between the implant and the bone, suggesting that the implant had been integrated through soft tissue rather than the traditional fusion with the bone,” says Chen. This may restore the nerves around it.

The research was conducted by Chen and School of Dental Medicine faculty Qisheng Tu and Zoe Zhu, as well as postdoctoral scholars Siddhartha Das (lead author) and Subhashis Ghosh at Tufts University School of Medicine.

These initial results are promising, but it will take more studies and time—for example, research in larger animal models to look at outcomes, including safety and efficacy—before trials can begin in human volunteers.

The researchers’ next step will be a preclinical study to see if brain activity confirms that the new nerves surrounding the prototype implant indeed relay sensory information.

Citation: Research reported in this article was supported by the National Institutes of Health under award numbers RO1DK131444, R01DE030074, R01DE025681, and R01DE032006. Complete information on authors, funders, methodology, limitations, and conflicts of interest is available in the published paper. 

Disclaimer: The content is solely the responsibility of the authors and does not necessarily represent the official views of the funders.  

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Journal

Scientific Reports

DOI

10.1038/s41598-025-99923-8 

Toothbrush-shaped ultrasound allows for gum monitoring

 

Peer-Reviewed Publication

American Chemical Society

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The toothbrush-shaped ultrasound transducer (left image) features a small head size (right image), allowing easy access to premolars and molars in the back of the mouth.

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Credit: Adapted from ACS Sensors 2025, DOI: 10.1021/acssensors.5c00521

When visiting the dentist, you might remember being poked and prodded by a thin metal instrument to check your teeth and gums. This technique, called periodontal probing, is used to look for signs of gum disease. Now, researchers publishing in ACS Sensors report a toothbrush-shaped ultrasound transducer that can provide a less invasive screening for gum disease. In proof-of-concept demonstrations on animal tissues, the device produced measurements similar to those of a manual probe.

Gum disease is a common condition affecting tissue that surrounds and supports teeth. If left untreated, it causes the gums to pull away from the teeth, creating pockets where harmful bacteria can grow. Currently, manual periodontal probing is the standard way to check for gum disease, but the technique is uncomfortable and can miss early stages. So, Jesse Jokerst and colleagues developed a small, non-invasive ultrasound method capable of imaging teeth and gums — even hard-to-reach molars and premolars at the back of the mouth.

Ultrasounds work by sending sound waves into the body. When the sound waves encounter a structure, like gum tissue or a tooth, they are reflected and detected by a transducer. The transducer then converts the reflected sound waves into an image. Currently, most ultrasound transducers have large heads that are about the same size as a wireless earbuds case. Although they work for larger parts of the body, these transducers cannot access smaller spaces like those in the mouth. Smaller transducers that are about half the length and width of traditional devices are available, but current models have limited image resolution because they are only able to produce and detect low frequencies. To overcome these limitations, the researchers created an even smaller toothbrush-shaped transducer that operates at a higher frequency and can produce high-quality images of teeth and gums.

To test the transducer’s accuracy, the researchers used the new instrument to measure the gum thickness and gum height of pig teeth. Then the researchers repeated the measurements using a manual metal periodontal probe. After analyzing the correlation between the two sets of measurements, the team found that the ultrasound measurements were statistically similar to those of the manual technique. The results support the reliability of the toothbrush-shaped transducer as a less invasive technique for monitoring gum health.

“We designed this tool to meet the realities of clinical dentistry — it is miniaturized, accurate and easy to use. Future work will use this device with patients to image below the gumline, where we will monitor treatments and diagnose earlier to reduce dental pain and help patients keep a healthy smile," says Jokerst.

Study predicts national fluoride ban would substantially increase children’s tooth decay and dental costs

 

• Mass General Brigham researchers developed a model to estimate the impact on children’s dental health and its cost if fluoride were no longer added to U.S. public drinking water.
• The model estimated that a fluoride ban would result in a 7.5 percentage point increase in tooth decay and cost an additional $9.8 billion over 5 years.
• This translates to tooth decay in 25.4 million more teeth, the equivalent of a decayed tooth for one out of every three children.

Fluoride has been added to public water systems in the United States since 1945 to strengthen tooth enamel and fight off bacteria, ultimately reducing tooth decay. Mass General Brigham researchers developed a model to estimate dental health outcomes for children if the United States were to ban fluoridation of public water. The new study, published in JAMA Health Forum, found that banning fluoride would substantially increase dental decay and costs particularly for publicly insured and uninsured children.

“Fluoride replaces weaker ions within tooth enamel, making it stronger and less susceptible to tooth decay caused by bacteria,” said senior author Lisa Simon MD, DMD, Division of General Internal Medicine at Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system. “There’s strong evidence from other countries and cities, such as Calgary in Canada, showing that when fluoride is eliminated, dental disease increases. Our study offers a window into what would happen in the United States if water fluoridation ceased.”

Simon and the research team focused on children for the study, because fluoride strengthens teeth during development, and more robust data links fluoridated water to oral health in this age group.

The study used detailed oral health and water fluoridation data collected from 8,484 children (ages 0-19, 49% girls) in the nationally representative National Health and Nutrition Examination Survey (NHANES). Using this dataset, the researchers developed a microsimulation model to see how banning fluoride from drinking water would impact oral health, quality of life and dental care costs.

The researchers simulated two scenarios over 5- and 10-year periods, which align with policy planning horizons. First, maintaining current fluoride levels, and second, eliminating the addition of fluoride to public water.

"Using a simulation model to track the progression of diseases in current populations, we estimated the impact of removing fluoride on the risk of tooth decay and the related dental care costs, including treatment for decay and complications from delayed treatment. We ran the simulation 1,000 times to see how different factors could affect the results. This approach helps ensure that our predictions are more reliable and reflective of real-world variability,” said first author Sung Eun Choi, PhD, assistant professor of Oral Health Policy & Epidemiology at Harvard School of Dental Medicine.

The researchers found that eliminating fluoride increased the total number of decayed teeth by 7.5 percentage points, or 25.4 million more teeth with tooth decay over five years (equivalent to a tooth for one out of every three American children). The number of fluorosis cases—a discoloring of tooth enamel due to excessive fluoride intake—decreased by 0.2 million. They also estimated a cost of $9.8 billion in additional dental care costs over five years, which rose to $19.4 billion after 10 years.

“Most of the increased cost could be attributed to publicly insured children, meaning it would be a direct public health cost,” said Simon.

The study did not model cognitive effects from fluoride exposure as current levels of fluoride in public water are not associated with worse neurobehavioral outcomes. The researchers note that their model demonstrates meaningful, ongoing benefit from fluoride at safe levels currently recommended by the Environmental Protection Agency, the National Toxicity Program, and the Centers for Disease Control and Prevention.

“We know fluoride works. We’re able to show just how much it works for most communities and how much people stand to lose if we get rid of it,” said Simon.

 

Dental flosser for at-home stress monitoring

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This dental floss pick has a sensor that can assess your stress level.

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Credit: Atul Sharma

Over time, stress and anxiety can build to a point where life’s challenges become overwhelming and cause physical effects. Now, in ACS Applied Materials & Interfaces, researchers report a dental floss pick with a built-in sensor that could monitor stress as part of a daily routine. The device, which accurately senses levels of the stress hormone cortisol in minutes, could help users recognize when it’s time to get help.

Unchecked chronic stress can lead to health conditions such as heart disease and mental disorders. Catching rising stress levels early is important, but daily blood tests at a doctor’s office aren’t feasible for most people, and self-reported questionnaires are subjective. That’s why researchers are developing point-of-care tests that measure cortisol levels in saliva, which mirror the hormone’s concentrations in blood. Although the saliva tests are promising, many of them require people to remember to perform the complicated analyses or use a bulky mouthguard. In addition, the anxiety of performing a test can cause stress levels to spike. So, Sameer Sonkusale and colleagues took a completely different approach by integrating a cortisol sensor into a dental floss pick — something many people use every day.

The team’s dental pick features floss that collects saliva. The floss is connected to a microfluidic thread that transports saliva to a flexible electrochemical sensor embedded in the handle of the pick. The sensor is made of an electrode with an electropolymerized molecularly imprinted polymer (eMIP) on it. The researchers made the eMIP by embossing cortisol molecules into an electrically conductive film and then removing them — similar to a shoe leaving an impression in wet cement. During tests, salivary cortisol binds in the impressions, decreasing the electrical current flowing through the sensor, which produces a signal that is wirelessly transmitted to a mobile device. The strength of the signal corresponds to the amount of cortisol in the saliva. Finally, the analyzed saliva moves to an adsorbent waste pad next to the sensor and the pick can be discarded.

The device takes around 10 minutes to report a result. In tests with cortisol-spiked artificial saliva, the dental pick was sensitive enough to detect small increases in cortisol that could be early indicators of stress. In tests with real human saliva samples, the dental flosser performed just as well as the commonly used ELISA saliva test for measuring levels of cortisol.

Overall, the researchers say that this device is one of the best-performing cortisol sensors reported so far, and it could someday be modified to detect other clinically important salivary molecules.

Anti-inflammatory drug reverses periodontal damage via cellular cleanup

Peer-Reviewed Publication

West China Hospital of Sichuan University

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Schematic diagram for the beneficial effects of dimethyl fumarate against periodontitis through the regulation of TUFM dependent Mitophagy.

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Credit: International Journal of Oral Science

A recent study reveals that dimethyl fumarate (DMF), a compound already approved for other inflammatory diseases, can prevent and alleviate periodontal tissue damage. The research demonstrates that DMF significantly shifts immune cell behavior, promoting anti-inflammatory macrophages and restoring mitochondrial health by enhancing mitophagy—a cellular process that removes damaged mitochondria. The drug achieves this through regulation of Tu translation elongation factor (TUFM), a protein critical to mitochondrial function. This breakthrough suggests a new therapeutic approach for periodontitis by targeting mitochondrial quality control and immune modulation rather than relying solely on traditional plaque-removal strategies.

Periodontitis is a chronic inflammatory condition and one of the leading causes of tooth loss in adults worldwide. Traditional treatments mainly focus on plaque removal and antimicrobial strategies but often fall short in halting disease progression. Recent advances indicate that immune imbalance—specifically the skewed polarization of macrophages toward a pro-inflammatory state—plays a critical role in disease severity. Additionally, mitochondrial dysfunction and oxidative stress have been shown to hinder the transition of macrophages from inflammatory (M1) to reparative (M2) types, aggravating tissue destruction. Due to these challenges, new research has focused on modulating mitochondrial health and immune responses to combat periodontal disease.

A research team from Wenzhou Medical University and collaborating institutions has published a study (DOI: 10.1038/s41368-025-00360-0) on April 17, 2025, in the International Journal of Oral Science, revealing a novel therapeutic mechanism for treating periodontitis. The team demonstrated that dimethyl fumarate (DMF) protects gum tissue by improving mitochondrial function and altering macrophage polarization. Their findings identify Tu translation elongation factor (TUFM)-mediated mitophagy as a key pathway regulated by DMF, offering a promising strategy to combat this prevalent oral health issue through immune and mitochondrial modulation.

The study employed both in vivo and in vitro models to explore the role of DMF in periodontal disease. Mice with ligature-induced periodontitis were treated with DMF, resulting in significantly reduced bone loss and inflammation. Immunofluorescence and micro-CT scans confirmed improved alveolar bone density and suppressed osteoclast formation. At the cellular level, DMF treatment in RAW 264.7 macrophages decreased M1 markers (iNOS, IL-1β) and elevated M2 markers (Arg1, CD206). Additionally, DMF reduced oxidative stress by restoring mitochondrial membrane potential, ATP levels, and reactive oxygen species (ROS) balance.

Central to this mechanism is TUFM—a mitochondrial elongation factor. DMF preserved TUFM levels by inhibiting its ubiquitin-proteasome-mediated degradation. This preservation promoted mitophagy, thereby maintaining mitochondrial homeostasis. When TUFM was silenced using siRNA, DMF lost its protective effects, confirming TUFM’s crucial role. Notably, DMF also outperformed a known mitochondrial antioxidant, MitoQ, in restoring cellular function and macrophage balance. Collectively, these findings highlight DMF as a potent immunometabolic regulator capable of reprogramming macrophage responses and safeguarding periodontal tissues.

＂Dimethyl fumarate’s ability to fine-tune macrophage polarization through mitophagy is a game-changer in periodontal therapy,＂ said Dr. Shengbin Huang, the study’s corresponding author. ＂By targeting the mitochondrial protein TUFM, we uncovered a molecular switch that controls the inflammatory response in gum tissue. These insights could redefine how we treat chronic inflammatory conditions beyond the oral cavity.＂ The research opens the door for developing new localized therapies using DMF or similar compounds, especially in formulations designed to minimize systemic side effects.

This study paves the way for innovative treatments that go beyond traditional antimicrobial and mechanical approaches. By targeting TUFM-mediated mitophagy, DMF offers a method to restore mitochondrial health, reduce oxidative damage, and rebalance immune responses in periodontal tissue. Given DMF's existing approval for other diseases, its clinical translation could be accelerated. Future development may include hydrogel-based topical delivery systems to concentrate its effects in the gum region and minimize systemic exposure. These findings also open avenues for treating other inflammation-related diseases involving mitochondrial dysfunction and immune dysregulation.

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References

DOI

10.1038/s41368-025-00360-0

Original Source URL

https://doi.org/10.1038/s41368-025-00360-0

Unlocking faster orthodontic treatments: the role of atf6 in bone remodeling

 

Peer-Reviewed Publication

West China Hospital of Sichuan University

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This diagram illustrates the role of macrophage ATF6 in orthodontic tooth movement. When corticotomy is applied, monocytes are recruited to the bone, where they differentiate into pro-inflammatory macrophages. These macrophages activate ATF6, which then enhances the transcription of TNFα by binding to its promoter. This process accelerates osteoclast activity, promoting bone resorption and speeding up tooth movement. The diagram highlights key molecular interactions, including the activation of ATF6 and its interaction with the TNFα promoter.

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Credit: International Journal of Oral Science

Orthodontic treatments often take years, but a breakthrough discovery could drastically shorten this period. Researchers have uncovered that ATF6, a protein activated in macrophages during corticotomy, accelerates tooth movement by promoting inflammation and boosting the production of TNFα, a key factor in bone remodeling. This finding paves the way for faster, more efficient orthodontic procedures, minimizing both treatment time and patient discomfort. The study highlights the potential for non-invasive therapies that could reshape the future of orthodontic care.

Corticotomy, a surgical procedure aimed at accelerating tooth movement, induces bone remodeling through a phenomenon known as the regional acceleratory phenomenon (RAP). While this technique is effective, the molecular mechanisms behind RAP are not yet fully understood. Macrophages, crucial players in immune responses and bone remodeling, have been identified as key participants in this process. However, the precise role of molecules like ATF6, which controls stress responses in cells, remains elusive. Based on these knowledge gaps, there’s a clear need for more focused research to understand how ATF6 influences bone remodeling in corticotomy.

This research (DOI: 10.1038/s41368-025-00359-7), led by Zhichun Jin, Hao Xu, Weiye Zhao, and their team from the Department of Orthodontics at Nanjing Medical University, was published on April 1, 2025, in the International Journal of Oral Science. The study highlights the crucial role of macrophage ATF6 in accelerating orthodontic tooth movement during corticotomy. The researchers discovered that activation of ATF6 in macrophages increases the production of TNFα, a cytokine key to bone resorption. This process accelerates bone remodeling, facilitating faster tooth movement. The study suggests that ATF6 could be a potential target for future non-invasive orthodontic treatments, providing a path for more efficient orthodontic care.

The study used advanced murine models to explore the relationship between macrophage ATF6 and orthodontic tooth movement. Researchers found that corticotomy-induced activation of ATF6 in macrophages triggered a pro-inflammatory response, significantly accelerating the movement of teeth. The presence of pro-inflammatory macrophages in periodontal tissue indicated enhanced bone remodeling. When ATF6 was genetically knocked out in macrophages, the acceleration of tooth movement was reduced. Conversely, overexpressing ATF6 intensified the process. Further analysis revealed that ATF6 directly interacts with the Tnfα promoter, enhancing the transcription of this crucial cytokine. This discovery opens new avenues for targeted treatments that could improve the speed and effectiveness of orthodontic procedures.

"Macrophage ATF6 has proven to be a key regulator in orthodontic bone remodeling," said Prof. Bin Yan, a leading researcher involved in the study. "This protein not only accelerates tooth movement by influencing inflammation but also provides us with a new therapeutic target that could revolutionize orthodontic treatments, making them quicker and less invasive."

This research holds significant promise for the future of orthodontics. By targeting the ATF6-TNFα pathway, new therapies could be developed to accelerate tooth movement without the need for surgery. Such advancements could make orthodontic procedures faster, less painful, and more accessible. Beyond orthodontics, this study could have broader applications in bone healing and treatment for diseases involving bone loss. With further research, these findings could lead to the development of non-invasive, more effective treatments for bone-related conditions, ultimately transforming patient care across multiple fields.

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References

DOI

10.1038/s41368-025-00359-7

Original Source URL

https://doi.org/10.1038/s41368-025-00359-7