Dental
Episodes
Dr. Rhonda Patrick discusses GLP-1 agonists, alpha-lipoic acid, ubiquinone vs. ubiquinol, calcium needs, and liquid biopsy cancer screening.
Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. Rhonda Patrick discusses GLP-1 agonists, alpha-lipoic acid, ubiquinone vs. ubiquinol, calcium needs, and liquid biopsy cancer screening.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
Topic Pages
News & Publications
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Dental cavities form when bacteria living on teeth repeatedly turn sugar into acid, lowering the local pH and, over time, leading to mineral loss in the tooth. Scientists have long suspected that certain nutrients might help counter this process, but it has been unclear whether they can make dental plaque less harmful without fundamentally changing which bacteria are present.
The study involved ten adults with high cavity activity, each wearing a custom lower-jaw splint that held small glass surfaces with a texture similar to enamel (the protective outer covering of teeth), where plaque could grow for four days. Three times per day, the growing plaque was briefly exposed to sucrose (common table sugar), then treated on one side with the amino acid arginine and on the other side with water as a control. This split-mouth design allowed each person to serve as their own comparison. Once the plaque matured, researchers examined how acidic it became after a sugar challenge, which bacteria were present, and how the plaque's sticky carbohydrate matrix was organized and where its components were located.
- Plaque grown with or without arginine contained similar core bacteria, mainly Streptococcus and Veillonella, which are typically found in young dental plaque.
- After exposure to sucrose, arginine-treated plaque stayed less acidic than untreated plaque, indicating better resistance to acid buildup.
- Arginine reduced matrix material rich in fucose, a sugar that originates from saliva and becomes incorporated into the sticky matrix of dental plaque.
- Galactose-containing parts of the matrix were not reduced overall, but arginine shifted where they were found, with less accumulation near the tooth surface and more in the outer layers of the plaque.
- Overall changes in the bacterial community were modest and varied from person to person. Arginine exposure was linked to lower levels of the mitis–oralis group of streptococci, a group of bacteria known to produce acid, while some bacteria that can use arginine showed a slight, but not statistically reliable, increase.
- People differed widely in how much arginine helped limit acid buildup, and these differences could not be clearly explained by which bacteria were present or by measured features of the plaque's sticky matrix.
Arginine may work through several overlapping processes. Some oral bacteria can break down arginine using the arginine deiminase system, a metabolic pathway that produces ammonia, which helps neutralize acid. At the same time, arginine appears to reshape the plaque matrix, potentially reducing how well acids are trapped near the tooth surface. These effects could make plaque less damaging during periods of sugar exposure.
Taken as a whole, the results point toward a new strategy that focuses on making dental plaque less damaging rather than eliminating it. Future studies will need to test whether these short-term, microscale pH improvements translate into meaningful protection against cavities over longer periods and in everyday oral care settings.
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When a tooth infection spreads to the root, the body's immune response can become overly aggressive, destroying surrounding bone and tissue. Scientists at São Paulo State University tested whether two accessible lifestyle factors, swimming and omega-3 fatty acids, could reduce this damage.
Thirty male rats were divided into three groups: an exercise‑only group, a group that combined exercise with omega-3 supplementation, and a control group without exercise or omega-3 supplementation. The exercising rats swam for an hour a day, five days a week, for six weeks. The combined group also received daily oral omega-3 supplementation (60% EPA and 40% DHA) at a dose of 40 mg per kilogram of body weight. To induce infection, the researchers drilled small holes in the chewing surfaces of a few teeth, exposing the tooth pulp to oral bacteria.
Exercise and omega-3 clearly improved how their bodies handled the infection:
- Inflammation was strongest in control rats, while both intervention groups showed milder immune responses around the tooth root. Fewer immune cells and lower signals of pro-inflammatory molecules were seen: tumor necrosis factor-alpha dropped with exercise alone, while interleukin-17 declined only when omega-3 was added.
- In rats that exercised, bacteria remained more confined in the tooth's root canal, with fewer reaching nearby tissues. When omega-3 was added, no bacteria were detected outside the tooth root.
- Micro–CT scans showed less bone loss in both intervention groups, with the greatest preservation in the combined group, which lost roughly one-quarter less bone than control animals.
- Fewer bone‑resorbing cells called osteoclasts appeared in both exercise groups, especially when omega-3 was included.
- The combined group also showed more immature collagen fibers, a sign of ongoing tissue repair.
Together, these findings suggest that regular moderate exercise helps regulate infection-related inflammation in dental tissue, while omega-3 fatty acids amplify this benefit by further suppressing inflammatory activity, promoting new collagen formation, and potentially exerting antimicrobial effects.
Although the study was conducted in rats, it highlights a simple, low-cost strategy that warrants further investigation as a potential adjunct to both the prevention and treatment of infection-related bone loss in dental care. Learn more about evidence-based strategies to reduce inflammation in this short clip.
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Frequent use of common household chemicals—including fluoride-based anti-caries agents, air fresheners, and disinfectants—increases the risk of cognitive decline in older adults. pubmed.ncbi.nlm.nih.gov
Cognitive decline—especially among older adults with dementia—can profoundly affect a person’s quality of life and increase their dependency on others. Evidence suggests that environmental exposures influence the risk of dementia. A recent study found that certain household chemicals, widely used for personal hygiene, cleaning, and disinfecting, may pose an unexpected risk for cognitive decline** in older adults.
Researchers analyzed data from a large cohort study of adults over 65. They evaluated how frequently the participants used eight common household chemicals, including insecticides, air fresheners, and disinfectants, and then examined whether these products were linked to declines in cognitive function.
They found that frequent use of anti-caries agents raised the likelihood of developing cognitive decline by 68%, while frequent use of air fresheners increased it by 148%, and disinfectants raised it by 40%. In general, more frequent chemical use was linked with worsening cognitive function.
Anti-caries agents prevent or reduce the development of dental caries, also known as cavities or tooth decay. Common anti-caries agents include fluoride mouth rinses, toothpaste formulations, and dental varnishes or sealants. Air fresheners contain various indoor pollutants, including phthalates and benzene. When these substances react with ozone, they create harmful byproducts that can harm the central nervous system. Sulforaphane, a bioactive compound derived from broccoli, boosts the excretion of pollutants like benzene. Learn more in this clip featuring Dr. Jed Fahey.
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Vitamin D promotes tooth remineralization, reducing the risk of cavities. www.ncbi.nlm.nih.gov
Tooth decay – a risk factor for cavities and tooth loss – often begins as white spots on the enamel, an early sign of demineralization. Strategies that promote tooth remineralization can reduce the need for invasive dental procedures. A 2022 study found that vitamin D promotes tooth remineralization, potentially reducing the risk of cavities.
Researchers gave 40 healthy adults vitamin D supplements (1,000 IU) for six weeks. They collected saliva samples from the participants at the beginning of the intervention and again at the third and sixth weeks. They exposed healthy, extracted teeth to an acidic solution to mimic the changes in pH that normally occur in the mouth in response to foods and beverages, causing demineralization. Then, they exposed the teeth to the saliva samples for 12 hours and assessed their mineral content, a measure of hardness.
They found that the amount of calcium and phosphorus in the teeth decreased considerably after exposure to the acidic solution – an indicator of demineralization. However, both minerals increased in the teeth after exposure to saliva collected from participants taking vitamin D.
These findings suggest that vitamin D promotes tooth remineralization, potentially reducing the risk of cavities. They also align with other findings showing that vitamin D helps treat gingivitis (gum disease), a major cause of tooth loss.
Vitamin D is a fat-soluble vitamin and hormone that participates in many physiological processes, including calcium balance, blood pressure regulation, immune function, and cell growth. Poor vitamin D status drives the pathogenesis of many acute and chronic diseases, including rickets, osteoporosis, multiple sclerosis, and cancer. Learn more about vitamin D in our comprehensive overview article.
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Poor oral health may triple Alzheimer's disease risk. www.brainandlife.org
Oral health is intricately linked to overall well-being, with emerging research identifying associations between poor oral health and an increased risk of many chronic diseases, including cardiovascular disease, diabetes, and cancer. A recent study found that oral diseases associated with tooth loss more than tripled the risk of developing Alzheimer’s disease.
Researchers assessed Alzheimer’s disease risk among more than 32 million people. They categorized the participants as having normal or poor oral health and assessed serum biomarkers associated with Alzheimer’s, including blood glucose, lipids, and C-reactive protein (a marker of inflammation).
They found that more than 1.2 million participants had poor oral health, while the remainder had normal oral health. Those with poor oral health were more than twice as likely to develop Alzheimer’s disease than those with normal oral health, regardless of age, gender, or serum biomarkers. Those with oral conditions associated with tooth loss were more than three times more likely to develop Alzheimer’s.
The findings from this large epidemiological study suggest that poor oral health markedly increases a person’s risk for developing Alzheimer’s disease. In vitro research further supports these findings, demonstrating that oral bacteria colonize the brain and release toxins that disrupt the blood-brain barrier, impairing its function and increasing the risk of Alzheimer’s. And research in mice shows that oral bacteria over-stimulate microglia, impairing their ability to eliminate amyloid-beta, a harmful protein linked to Alzheimer’s.
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Microglia's Alzheimer's defense impaired by oral bacteria, study reveals. www.sciencedaily.com
Microglia, the brain’s resident immune cells, play a vital role in managing brain inflammation and neurodegenerative diseases by eliminating amyloid-beta, a harmful protein linked to Alzheimer’s disease, and forming barriers around insoluble amyloid-beta deposits. A new study in mice shows that oral bacteria over-stimulate microglia, impairing their anti-amyloid properties.
Researchers induced periodontal disease in mice by placing ligatures around their teeth, creating an environment conducive to bacterial growth. Then they examined the effects of the disease on the animals' gums, bones, and microglial cells. They found that the gum infections caused progressive periodontal disease and bone loss in the mice. In addition, the severity of periodontal disease correlated with increased microglial cell activation in the brain. Then, the researchers exposed microglial cells to bacteria from the animals' infected gums. They found that this exposure increased inflammation and changes in the cells' ability to interact with amyloid-beta.
These findings suggest that periodontal disease influences the brain’s immune response via changes in microglial activation and their interactions with amyloid-beta. This link between gum and brain health underscores the potential importance of oral hygiene in preventing or managing neuroinflammatory conditions like Alzheimer’s disease.
Related studies have found that oral bacteria colonize the brain and release toxins that disrupt the blood-brain barrier, impairing its function and increasing the risk of Alzheimer’s disease. Learn more about the role of blood-brain barrier dysfunction in Alzheimer’s disease in this episode featuring Dr. Axel Montagne.