Could your oral health be affecting fertility?

Chronic oral inflammation may impair female fertility by triggering a systemic immune response that affects the ovaries. A new study shows this leads to oxidative damage, reduced egg quality, disrupted follicle development and reduced live birth rate. These findings point to a potential biological link between oral health and unexplained infertility, opening new directions for future treatments.

[Hebrew University of Jerusalem]– A new study led by Prof. Michael Klutstein at the Hebrew University of Jerusalem and Prof. Asaf Wilensky at the Hebrew University-Hadassah Medical center and spearheaded by the students Dr. Paz Kles and Stephen Ameho has uncovered a striking biological link between chronic oral inflammation and female fertility, suggesting that conditions in the mouth may have far-reaching effects on reproductive health.

Published in the Journal of Dental Research, the study shows that persistent inflammation in the oral cavity can impair ovarian function, reduce egg quality, and ultimately lower fertility rates.

Researchers examined in a mouse model inflammation associated with dental implants, a common clinical scenario, and tracked how immune signals spread throughout the body. Their findings reveal that inflammation does not remain confined to the oral cavity but triggers a systemic immune response that reaches the ovaries.

The consequences were significant. Chronic oral inflammation in the animals was linked to increased levels of inflammatory cytokines in the ovaries, along with shifts in immune cell populations. This was accompanied by oxidative damage to ovarian tissue, impaired development of follicles, and reduced quality of oocytes.

These biological changes translated into measurable reproductive outcomes, with markedly reduced birth rates observed under inflammatory conditions in the animals.

The study also identified deeper cellular effects. Oocytes exhibited DNA damage and epigenetic alterations resembling those seen in reproductive aging, pointing to a possible mechanism by which inflammation accelerates the decline in fertility.

“Inflammation is often thought of as a localized response, but our findings show that it can have systemic consequences that extend as far as the reproductive system,” said Prof. Michael Klutstein. “This work suggests that chronic oral inflammation may be an underrecognized factor in female infertility, potentially contributing to cases that currently have no clear explanation.”

The findings add to growing evidence that oral health is closely linked to overall health. Chronic oral inflammatory conditions such as periodontitis are widespread and have already been associated with a range of systemic diseases.

The researchers note that further investigation in clinical settings will be essential to determine how these findings translate to patient care. If confirmed, the work could open new avenues for diagnosis and treatment, including the use of anti-inflammatory or antioxidant approaches to improve fertility outcomes.

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Journal

Journal of Dental Research

DOI

10.1177/00220345251412768 

Why antibiotics fail against a common dental implant disease

 

Dental implants have given tens of millions of people something dentures never could: a full set of fixed and fully functioning teeth. Unfortunately, 10% to 20% of implant patients eventually experience an aggressive jawbone infection called peri-implantitis. 

Antibiotics usually fail to stop the infection for reasons that researchers have never understood – until now.

A new study in PNAS Nexus by researchers with the Rutgers School of Dental Medicine found that bacteria corrode implants, causing them to shed microscopic titanium particles into the surrounding tissue. Those particles hijack the immune cells sent to clear the infection and lock them into a state of inflammation that destroys the jawbone they are supposed to protect.

Working with human tissue samples, cultured human immune cells and a genetically engineered mouse model, the team pinpointed a specific calcium channel in the body’s bacteria-eating macrophages that the titanium particles activate. Switching that channel off in mice prevented the disease. The result is the first credible drug target for a condition that affects up to one in five implant recipients and costs the global health system more than a billion dollars a year.

“For the first time, we show why all the antibiotic treatments that work around teeth do not work around implants,” said Georgios Kotsakis, the study’s senior author and the assistant dean for clinical research at the dental school. “Now that we know the cause, we can start developing therapeutics.”

Peri-implantitis has long been a puzzle because it initially looks like its counterpart in natural teeth, which is called periodontitis and begins with the same oral bacteria. In patients with natural teeth, antibiotics and routine cleaning resolve the infection. In patients with implants, the same drugs against the same bacteria succeed less than half the time, while the bone underneath continues to disappear.

Most research over the past 20 years has focused on the bacteria. Members of Kotsakis’ lab took a different approach and began looking at the implants. Bacteria living on the implant surface produce acidic biofilms that slowly corrode the titanium, releasing billions of particles smaller than a red blood cell. The same shedding can occur during routine cleaning, especially with instruments that dentists typically use on natural teeth.

Inside the gum, those particles get coated with a bacterial toxin called lipopolysaccharide. To the immune system, they suddenly look like enormous, indigestible bacteria. Macrophages, a type of white blood cell that surrounds and kills microorganisms, engulf them but cannot digest metal. The cells become trapped in a hyperinflammatory state, pumping out signaling molecules including interleukin-1 beta, an inflammatory protein also implicated in rheumatoid arthritis and Alzheimer’s disease. 

That inflammation eats away at bone. Worse, the immune cells lose their ability to deal with the original infection. In the lab, macrophages exposed to titanium particles took up less than half as many bacteria as unexposed cells. 

“These particles are little magnets that attract the bacterial toxin, and they hijack the immune system, preventing it from clearing bacteria,” said Kotsakis. “You have a perfect storm that defies antibiotics.”

Team members traced the cascade to a calcium channel (a specialized, pore-forming protein structure within cell membranes) called TRPC1. In mice engineered without it, the immune cells handled the same titanium-plus-bacteria challenge normally: abscesses were dramatically smaller, inflammatory cytokines dropped, and bacterial clearance was restored. 

Funded by the National Institutes of Health, members of Kotsakis’ group are testing drug candidates that target the same pathway in human cells.

For people who already have implants, the most useful finding may be a quieter one. The strongest known protective factor is regular professional cleaning, but the kind of cleaning matters. Until roughly a decade ago, many dentists scraped implants with the metal scalers used on teeth, a method the Rutgers lab and others have shown can itself corrode the implant and accelerate the disease. Nonabrasive techniques are now standard. 

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Journal

PNAS Nexus

DOI

10.1093/pnasnexus/pgag081 

A simpler way to save root-treated front teeth?

 

 New Study Puts Two Restoration Methods Head to Head

Article by Dr. Abed Alhade Kheder | abedalhade2223@gmail.com | Fixed Prosthodontics, Tishreen University, Latakia, Syrian Arab Republic

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The Problem: Restoring Badly Damaged Front Teeth After Root Canal Treatment

When a front tooth has been root-treated and has lost a large portion of its original structure, restoring it is one of dentistry's more demanding challenges. The traditional approach involves inserting a post down into the root canal, building up a core on top of it, and then placing a crown — a technique that works but requires removing further tooth material, sometimes weakening what little remains and raising the risk of a root fracture that cannot be repaired. A newer, less invasive option called an endocrown skips the post altogether, drawing its hold entirely from the pulp chamber — the hollow space left after root canal treatment — and covering the tooth with a single ceramic restoration. To find out how these two approaches compare when it matters most, researchers from Tishreen University in Syria put both techniques to a controlled mechanical test on 20 freshly extracted upper central incisors that had been badly damaged and then root-treated, splitting them into two equal groups of ten.

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What the Study Found: Both Methods Break Roughly the Same Way

Each restored tooth was mounted at a 45-degree angle — mimicking the real-life direction of biting forces on front teeth — and subjected to steadily increasing pressure until failure occurred. The researchers then recorded exactly what broke and where, classifying each failure as either "favorable" (meaning the tooth could potentially be repaired or saved) or "unfavorable" (meaning the damage was beyond repair). The results showed no statistically significant difference between the two groups in how or where failures occurred. In the endocrown group, fractures were more varied in location, with 80% classified as favorable. In the post-and-core group, the restoration itself — rather than the tooth root — was the most common point of failure, with 60% classed as favorable. The quartz fiber posts used in the second group have a stiffness close to that of natural tooth root, which allows them to bend slightly under pressure and redirect stress away from the root, explaining why root-level fractures were rare in that group.

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What This Means for Patients and Dentists

The findings suggest that endocrowns are a clinically sound option for restoring severely damaged, root-treated front teeth — not just back teeth, where they have long been the accepted standard. Because endocrowns require less drilling and do not involve post placement, they preserve more of the patient's natural tooth structure, shorten treatment time, and make any future re-treatment considerably less complicated. The study's authors are careful to note that the results come from a laboratory setting, that the sample size was small, and that real-world factors such as temperature changes and long-term chewing cycles were not replicated. Larger clinical studies with extended follow-up periods are needed before definitive recommendations can be made. The research was led by corresponding author Dr. Abed Alhade Kheder of the Department of Fixed Prosthodontics, Tishreen University, Latakia, Syrian Arab Republic. The full article is freely available in The Open Dentistry Journal (DOI: 10.2174/0118742106440539260407102718).

Read the published article here: https://bit.ly/4dllEuI

JOURNAL

The Open Dentistry Journal

 DOI: 10.2174/0118742106440539260407102718

If you want to publish your article please visit : https://bit.ly/4de0DRi

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Journal

The Open Dentistry Journal

DOI

10.2174/0118742106440539260407102718 

Stem cells at the root of tooth aging

 

Peer-Reviewed Publication

International Society for Stem Cell Research

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image: 

The immunofluorescence image of the chase result in dental pulp of adult Nfatc1-CreER; tdTomato; 2.3kb-Col1 GFP strain, which demonstrated the NFATc1+ DPSCs continuously gave birth of odontogenesis in vivo. This image is reported in the study titled NFATc1 Dysfunction-Triggered MSC Senescence Induces Tooth Aging Amenable to Senolytic Therapy in Stem Cell Reports (Fig. 2L).

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Credit: Fanyuan Yu & colleagues

With age, teeth get increasingly brittle and susceptible to damage from tooth decay, which can eventually lead to tooth loss. Teeth have an intrinsic capability to regenerate, a process which is driven by dental pulp stem cells (DPSCs) which replenish the dental pulp including the dentin-producing cells called odontoblasts. DPSCs stops working in aging teeth, divide less, and generate less odontoblasts, a process which is called senescence or the biological process of aging through gradual deterioration. DPSC senescence is thought to be a cause for the declining tooth health with age. 

A research team led by Fanyuan Yu from Sichuan University, China, has now discovered one of the mechanisms of DPSC senescence and identified a potential strategy to counter it. In their work published today in the journal Stem Cell Reports, the researchers first compared the regenerative capacity of young and old human molars affected by severe tooth decay. While most of the young teeth could be preserved, more than half of the aged teeth eventually died off, suggesting that tooth aging impairs dental pulp regeneration.  

To explain this phenomenon, Yu’s team used genetically engineered mouse models to identify a distinct subset of DPSCs responsible for generating new dental pulp cells and odontoblasts in young teeth. These stem cells were nearly absent in the teeth of old mice. Further, when these stem cells were eliminated from the teeth of young mice, the dental pulp underwent senescence and contained significantly less odontoblasts, further underscoring the essential role of this DPSC subset in tooth regeneration.  

A unique feature of these stem cells was the expression of a protein called NFATC1, which was abundant in young DPSCs but significantly reduced in old cells in both mouse and human teeth. NFATC1 was essential for the proper function of the mouse DPSCs, as its deletion halted odontoblast generation, induced senescence in young teeth, and reduced the tooth’s ability to regenerate after injury. Encouragingly, tooth regeneration could be stimulated in NFATC1 deficient mice by a combination of “senolytic” drugs which act by eliminating senescent cells.  

This study shows that a specific type of NFATC1+ DPSCs is essential for tooth regeneration and to prevent senescence. Follow-up studies will be required to show if preserving these stem cells can counteract tooth aging. 

About Stem Cell Reports
Stem Cell Reports is the open access, peer-reviewed journal of the International Society for Stem Cell Research (ISSCR) for communicating basic discoveries in stem cell research, in addition to translational and clinical studies. Stem Cell Reports focuses on original research with conceptual or practical advances that are of broad interest to stem cell biologists and clinicians. Stem Cell Reports is a Cell Press partner journal. Find the journal on X: @StemCellReports.

About ISSCR
Across more than 80 countries, the International Society for Stem Cell Research (@ISSCR) is the preeminent global, cross-disciplinary, science-based organization dedicated to advancing stem cell research and its translation to medicine.

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Journal

Stem Cell Reports

DOI

10.1016/j.stemcr.2026.102925 

Don't rush into braces with disc displacement:

 experts reveal the science of sequential therapy

Peer-Reviewed Publication

KeAi Communications Co., Ltd.

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image: 

This illustration was drafted by Prof. Yang himself and finished by his students. It depicts the sequential strategy for combined joint–mandible–occlusion diagnosis and treatment. Before and after the disc reduction surgery, preoperative orthodontics, postoperative jaw position adjustment and stabilization, and postoperative comprehensive orthodontic treatment are performed.

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Credit: Guo Bai and Qianyang Xie

A new study published in Dental Research reveals that while proper orthodontics can help a healthy jaw joint, incorrect treatment can worsen disc displacement and even cause bone loss. The authors, from Shanghai Ninth People's Hospital, created a "Joint-Mandible-Occlusion" sequential model: first surgically reposition the disc, then address teeth alignment. This approach aims to fix the joint first to ensure stable, long-term results for both bite and facial appearance.

"The aim is to promote balanced bilateral joint growth in growing patients and maintain joint stability in adults," says co-corresponding author Chu Yang. "This idea underpins a pioneering approach to treating temporomandibular joint (TMJ) disc displacement, a common yet often misunderstood condition."

The authors noted that teenagers with receding chins or crooked teeth are usually told their issues were purely dental. "But the real cause is often the jaw joint itself: when the articular disc— a cartilage shock absorber—slips, it can erode the jawbone's condyle over time, leading to facial asymmetry, receding chins and misaligned bites," adds Yang. "This changes treatment entirely."

"Notably, traditional orthodontics alone often relapses, as the joint problem remains unaddressed. For adolescents, this unlocks balanced jaw growth; for adults, it stops bone erosion and restores joint stability," says Yang. "Many patients feel no pain, unknowingly suffering silent bone loss. Screening joint health before orthodontics is key—this root-cause approach delivers stable, long-term results, improving bite, facial harmony and jaw health."

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Contact the author: Please contact Guo Bai and Qianyang Xie from Department of Oral Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University via surgeonb@163.com and Xieqianyang86@126.com.

The publisher KeAi was established by Elsevier and China Science Publishing & Media Ltd to unfold quality research globally. In 2013, our focus shifted to open access publishing. We now proudly publish more than 200 world-class, open access, English language journals, spanning all scientific disciplines. Many of these are titles we publish in partnership with prestigious societies and academic institutions, such as the National Natural Science Foundation of China (NSFC).

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DOI

10.1016/j.dtrs.2025.100001