Oral Hygiene

Treating Common Gum Condition Could Limit Heart Attacks for Some Patients

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There’s an easy adjustment that could be made to aid people with chronic kidney disease. Treating a common gum condition in chronic kidney disease patients could lower their risk of potentially fatal heart disease by a large margin, according to Aston University researchers.

More than 10 percent of the adult population has CKD, which generally results in poor health. The disease gradually inhibits kidney function while raising blood pressure. It can also cause progressive vascular injury and heart disease.

New research indicates that a higher mortality rate in people with CKD stems from inflammatory conditions like gum inflammation, loss of bone that supports teeth and tooth loss. Studies in the past have shown that 85 percent of people with CKD have inflammatory gum problems, which result from poor removal of dental plaque.

Aston University in England is leading many of the studies on these issues. The research could prove to be pivotal for people who suffer from CKD.

The next study will include 80 people, 60 of whom have CKD. Some will also have periodontitis while others will not. There will be a group of 20 people with CKD and periodontitis who will be randomly treated for the gum problem during a one-year period. These people will have their information analyzed at three monthly intervals to look for signs of cardiovascular disease.The project is part of a collaboration between Dr. Irundika Dias and Professor Helen Griffiths of Aston’s School of Health and Life Sciences, Professor Iain Chapple, Head of Periodontology at the University of Birmingham, and Professor Paul Cockwell, Consultant Nephrologist at University Hospitals Birmingham NHS Foundation Trust. This partnership has provided Dias with the ability to secure samples from patients with and without periodontitis in Birmingham hospitals.

Colgate Expands Oral Health Education Program to Boys & Girls Clubs

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After reaching a billion children around the world, Colgate is expanding its Bright Smiles, Bright Futures (BSBF) oral health education program with a new initiative with the Boys & Girls Clubs of America.

Launched in the United States in 1991 and active in more than 80 countries, BSBF is among the most far-reaching, successful children’s oral health initiatives in the world, driving better oral health actions, greater awareness, and increased access to oral care, Colgate says.

The cornerstone of BSBF is an award-winning educational curriculum presented by classroom teachers. Colgate also has created new classroom toolkits for its employees to bring activities and experiments to children in school.

Also, Colgate operates nine mobile dental vans that visit more than 1,000 cities and towns in the United States to provide free dental screenings, oral health education, and treatment referrals to underserved children in schools, Head Start and afterschool programs, and community events. 

“Tooth decay is the most common chronic disease in children around the world, so it’s our hope to reach the next billion children in half the time it took to reach our first billion,” said Dr. Marsha Butler, a dentist and Colgate-Palmolive vice president who has led the program since its inception. 

“The Colgate brand is found in nearly two thirds of homes around the globe, more than any other brand in the world, so we have a special opportunity and responsibility to promote healthy oral care habits among the next generation,” said Butler. 

In the United States, Colgate is expanding its partnership with Boys & Girls Clubs of America with its “Smile-a-bration” competition. Children at participating clubs will use music, dance, art, or some other creative expression to share the importance of health oral care habits. Winning clubs will receive a grant from Colgate.

“This is our fourth year bringing the Bright Smiles program into our Boys & Girls Clubs across the country,” said Jim Clark, president and CEO of Boys & Girls Clubs of America. “We believe it makes an important contribution to the health of our kids. Good brushing habits and a healthy mouth help build a child’s self-esteem and promote academic success. That’s a big part of our mission.”

In Mexico, Colgate BSBF has reached more than 224 million children since 1999. Colgate worked with the Mexico City government in 2017 to support legislation ensuring that 1.2 million children receive oral health education and a toothbrushing kit from Colgate. The company now hopes to extend the program’s reach to additional Mexican municipalities.

In Romania, the Romanian Red Cross is a valued partner in bringing the BSBF program into schools. In the past 25 years, Colgate BSBF has reached 6 million Romanian children.

In South Africa, Colgate has a longstanding relationship with the Department of Health. This partnership includes two mobile vans that reach 100,000 children a year and visits by dentists to schools to educate, screen, and provide treatment to children.

In India, where the focus has been on reaching underserved children in rural areas, Colgate recently added outreach to children in cities, partnering with the Dental Council of India and government agencies. Colgate India has reached 162 million children with dental education and checkups. 

“Colgate people are honored to play a part in helping children to have a healthier and brighter future,” said Butler. “We believe that every child, everywhere in the world, deserves to have a future to smile about.”

The unexpected dangers of gum disease

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Gum disease is common and unpleasant, but, according to a growing body of evidence, it could also play a role in a surprising range of seemingly unrelated health problems. Plaque – a sticky substance that contains bacteria — builds up on teeth. If it is not brushed away, the bacteria can irritate the gums. The gums may then become swollen, sore, or infected; this is referred to as gingivitis.

In general, gum disease can be treated or prevented by maintaining a good oral health regime.

However, if it is left to develop, it can result in periodontitis, which weakens the supporting structures of the teeth.

Gum disease, which is also called periodontal disease, is widespread. According to the Centers for Disease Control and Prevention (CDC), almost half of adults in the United States have some degree of gum disease.

The mechanisms behind periodontal disease are relatively well-understood, and newer research shows that this health problem may play a role in the development of a number of other conditions, including Alzheimer’s disease, cancer, and respiratory disease.

In this Spotlight, we will cover some of the surprising links between gum disease and disparate health issues.

Gums and the brain

Although spatially the gums are near the brain, one wouldn’t normally associate dental complaints with neurological conditions.

However, some studies have found a link between periodontal disease and tooth loss and cognitive function. One study looking at cognitive performance followed 597 men for up to 32 years. The authors conclude:

“Risk of cognitive decline in older men increases as more teeth are lost. Periodontal disease and caries, major reasons for tooth loss, are also related to cognitive decline.”

Researchers have also linked periodontal disease with an increased buildup of beta-amyloid in the brain — the neurological hallmark of Alzheimer’s.

Other experiments have produced evidence that one type of bacteria commonly found in cases of periodontitis — Porphyromonas gingivalis — can be found in the brains of individuals with Alzheimer’s.

Following on from that discovery, in a more recent study, researchers showed that P. gingivalis infection boosts the production of beta-amyloid in the brain.

In this study, the researchers paid particular attention to an enzyme produced by P. gingivalis called gingipain. They found that this protease was toxic to tau, another protein that plays a pivotal role in Alzheimer’s.

It is worth noting that other researchers have concluded that beta-amyloid is produced in response to a pathogen. The way we view Alzheimer’s is slowly changing.

In the future, scientists hope that targeting gingipain enzymes might help stop neurodegeneration in some people with Alzheimer’s disease. They have already designed a gingipain inhibitor, which they are testing in humans.

The researchers hope that it will “slow or prevent further neurodegeneration and accumulation of pathology in [Alzheimer’s disease] patients.”

The heart of the matter

Although not everyone with heart disease has gum disease, and not everyone with gum disease has heart disease, there does appear to be a correlation.

Of course, individuals who smoke or drink large quantities of alcohol are more likely to have both oral and cardiovascular issues, but there appears to be more to the relationship than shared risk factors alone.

Whether gum disease is an independent risk factor for heart disease is still being discussed, but there are some theories as to how the two might be related. Some think that the link could involve inflammation.

Primarily, inflammation is a response to irritants or pathogens; it is a protective mechanism. However, if it continues for an extended period, it can damage tissues and organs.

It is possible that inflammation in the gums sets off a cascade that, ultimately, sparks inflammation in the cardiovascular system.

Alternatively, the link between heart and gum diseases may be due to bacteria.

Bacteria in the gums can enter the blood supply and be propelled to distant destinations, including the heart, where they can cause inflammation and damage.

As evidence that this is possible, researchers have shown that P. gingivalis is the most commonly found bacterial species in the coronary artery.

Cancer risk increase

Once again, gum disease and cancer do not, on the surface, appear to have much in common.

A study published in 2008 investigated tooth loss and cancer in 48,375 men. The authors concluded that there was, indeed, a link between gum disease and cancer. They write:

“Periodontal disease was associated with a small, but significant, increase in overall cancer risk.”

Another, more recent, study involving more than 68,000 adults found a strong association between gum disease and overall cancer risk; the link was also significant between gum disease and pancreatic cancer.

Why might this be the case? A paper published in Nature goes some way toward an explanation.

The researchers found that an enzyme produced by a type of bacteria commonly associated with gum disease — Treponema denticola — commonly appears in certain tumors of the gastrointestinal system.

The enzyme, known as T. denticola chymotrypsin-like proteinase, helps the bacteria invade tissue in gum disease. The researchers found that it also activated other enzymes that promote cancer cells as they advance into healthy tissue.

How a common oral bacteria makes colon cancer more deadly

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Researchers at the Columbia University College of Dental Medicine have determined how F. nucleatum— a common oral bacteria often implicated in tooth decay — accelerates the growth of colon cancer. The study was published online in the journal EMBO Reports.

Why it matters

The findings could make it easier to identify and treat more aggressive colon cancers. It also helps explain why some cases advance far more quickly than others, thanks to the same bacteria found in dental plaque.

Background

Colon cancer is the second leading cause of cancer death in the U.S. Researchers have long known that the disease is caused by genetic mutations that typically accumulate over the course of a decade. “Mutations are just part of the story,” says study leader Yiping W. Han, PhD, professor of microbial sciences at Columbia University’s College of Dental Medicine and Vagelos College of Physicians & Surgeons. “Other factors, including microbes, can also play a role.”

Scientists have also demonstrated that about a third of colorectal cancers are associated with a common oral bacterium called F. nucleatum. Those cases are often the most aggressive, but nobody knew why. In a prior study, Han’s research team discovered that the bacterium makes a molecule called FadA adhesin, triggering a signaling pathway in colon cells that has been implicated in several cancers. They also found that FadA adhesin only stimulates the growth of cancerous cells, not healthy cells. “We needed to find out why F. nucleatum only seemed to interact with the cancerous cells,” says Han.

What the study found

In the current study, the researchers found in cell cultures that noncancerous colon cells lack a protein, called Annexin A1, which stimulates cancer growth. They then confirmed both in vitro and later in mice that disabling Annexin A1 prevented F. nucleatumfrom binding to the cancer cells, slowing their growth.

The researchers also discovered that F. nucleatum increases production of Annexin A1, attracting more of the bacteria. “We identified a positive feedback loop that worsens the cancer’s progression,” says. Han. “We propose a two-hit model, where genetic mutations are the first hit. F. nucleatum serves as the second hit, accelerating the cancer signaling pathway and speeding tumor growth.”

Clinical implications

The researchers then looked at an RNA-sequencing dataset, available through the National Center for Biotechnology Information of 466 patients with primary colon cancer. Patients with increased Annexin A1 expression had a worse prognosis, regardless of the cancer grade and stage, age, or sex.

Next steps

The researchers are currently looking for ways to develop Annexin A1 as a biomarker for more aggressive cancers and as a potential target for developing new treatments for colon and other types of cancer.

Gum bacteria implicated in Alzheimer’s and other diseases

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Researchers are reporting new findings on how bacteria involved in gum disease can travel throughout the body, exuding toxins connected with Alzheimer’s disease, rheumatoid arthritis and aspiration pneumonia. They detected evidence of the bacteria in brain samples from people with Alzheimer’s and used mice to show that the bacterium can find its way from the mouth to the brain.

The bacterium, Porphyromonas gingivalis, is the bad actor involved in periodontitis, the most serious form of gum disease. These new findings underscore the importance of good dental hygiene as scientists seek ways to better control this common bacterial infection.

“Oral hygiene is very important throughout our life, not only for having a beautiful smile but also to decrease the risk of many serious diseases,” said Jan Potempa, PhD, DSc, a professor at the University of Louisville School of Dentistry and head of the department of microbiology at Jagiellonian University in Krakow, Poland. “People with genetic risk factors that make them susceptible to rheumatoid arthritis or Alzheimer’s disease should be extremely concerned with preventing gum disease.”

While previous researchers have noted the presence of P. gingivalis in brain samples from Alzheimer’s patients, Potempa’s team, in collaboration with Cortexyme, Inc., offers the strongest evidence to date that the bacterium may actually contribute to the development of Alzheimer’s disease. Potempa will present the research at the American Association of Anatomists annual meeting during the 2019 Experimental Biology meeting, held April 6-9 in Orlando, Fla.

The researchers compared brain samples from deceased people with and without Alzheimer’s disease who were roughly the same age when they died. They found P. gingivalis was more common in samples from Alzheimer’s patients, evidenced by the bacterium’s DNA fingerprint and the presence of its key toxins, known as gingipains.

In studies using mice, they showed P. gingivalis can move from the mouth to the brain and that this migration can be blocked by chemicals that interact with gingipains. An experimental drug that blocks gingipains, known as COR388, is currently in phase 1 clinical trials for Alzheimer’s disease. Cortexyme, Inc. and Potempa’s team are working on other compounds that block enzymes important to P. gingivalis and other gum bacteria in hopes of interrupting their role in advancing Alzheimer’s and other diseases.

The researchers also report evidence on the bacterium’s role in the autoimmune disease rheumatoid arthritis, as well as aspiration pneumonia, a lung infection caused by inhaling food or saliva.

P. gingivalis‘s main toxins, the enzymes the bacterium need to exert its devilish tasks, are good targets for potential new medical interventions to counteract a variety of diseases,” said Potempa. “The beauty of such approaches in comparison to antibiotics is that such interventions are aimed only at key pathogens, leaving alone good, commensal bacteria, which we need.”

P. gingivalis commonly begins to infiltrate the gums during the teenage years. About one in five people under age 30 have low levels of the bacterium in their gums. While it is not harmful in most people, if it grows to large numbers the bacteria provoke the body’s immune system to create inflammation, leading to redness, swelling, bleeding and the erosion of gum tissue.

Making matters worse, P. gingivalis even causes benign bacteria in the mouth to change their activities and further increase the immune response. Bacteria can travel from the mouth into the bloodstream through the simple act of chewing or brushing teeth.

The best way to prevent P. gingivalis from growing out of control is by brushing and flossing regularly and visiting a dental hygienist at least once a year, Potempa said. Smokers and older people are at increased risk for infection. Genetic factors are also thought to play a role, but they are not well understood.

Teeth whitening products can harm protein-rich tooth layer

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Americans spend more than a billion dollars on teeth whitening products each year. Although these products can make smiles brighter, new research shows that they might also be causing tooth damage.

In three new studies, researchers found that hydrogen peroxide, the active ingredient in over-the-counter whitening strips, can damage the protein-rich dentin tissue found beneath the tooth’s protective enamel.

Undergraduates working in the laboratory of Kelly Keenan, PhD, associate professor of chemistry at Stockton University in New Jersey, will present this research at the American Society for Biochemistry and Molecular Biology annual meeting during the 2019 Experimental Biology meeting to be held April 6-9 in Orlando, Fla.

The tooth is made of three layers: the outer tooth enamel, an underlying dentin layer and connective tissue that binds the roots to the gum. Most studies of whitening strips have focused on tooth enamel, which contains very little protein. Kennan’s research team focuses on dentin, which makes up most of the tooth and has high levels of protein, most of which is collagen.

It is well established that hydrogen peroxide can penetrate the enamel and dentin. Previous work by the researchers showed that collagen in the dentin layer decreased when teeth were treated with whitening strips.

“We sought to further characterize what the hydrogen peroxide was doing to collagen,” said Keenan. “We used entire teeth for the studies and focused on the impact hydrogen peroxide has on the proteins.”

In the new work, the researchers demonstrated that the major protein in the dentin is converted to smaller fragments when treated with hydrogen peroxide. In additional experiments, they treated pure collagen with hydrogen peroxide and then analyzed the protein using a gel electrophoresis laboratory technique that allows the protein to be visualized.

“Our results showed that treatment with hydrogen peroxide concentrations similar to those found in whitening strips is enough to make the original collagen protein disappear, which is presumably due to the formation of many smaller fragments,” said Keenan.

The researchers point out that their experiments did not address whether collagen and other proteins in the teeth can be regenerated, so it is unknown if the tooth damage is permanent. Next, they plan to further characterize the protein fragments released when collagen is treated with hydrogen peroxide and determine if hydrogen peroxide has the same impact on other proteins in the teeth.

Orthodontics no guarantee of long-term oral health

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A commonly held belief among the general public is orthodontic treatment will prevent future tooth decay. Research undertaken at the University of Adelaide has found that this is not the case.

Published in the journal Community Dentistry and Oral Epidemiology the study, conducted by Dr Esma J Dogramaci and co-author Professor David Brennan from the University’s Adelaide Dental School, assessed the long-term dental health of 448 people from South Australia.

“The study found that people who had orthodontic treatment did not have better dental health later in life,” says Dr Dogramaci.

“Patients often complain about their crooked teeth and want braces to make their teeth straight so they can avoid problems, like decay, in the future.”

The study, which followed people from the age of 13 until they were 30, recorded patients’ dental health behaviours and the number of decayed, missing or filled teeth.

“By the age of 30 over a third of participants had received orthodontic treatment,” says Dr Dogramaci.

“There is a misconception amongst patients that orthodontic treatment prevents tooth decay, but this is not the case.”

The cost of orthodontic treatment, in which crooked teeth are realigned using braces worn over several years, varies from approximately AUS$3000 to $13,000 according to the severity of the problems. Braces are becoming increasingly popular, with one in five patients being adults. The global orthodontics market is predicted to be worth more than US$6 billion by 2023.

“Evidence from the research clearly shows that people cannot avoid regularly brushing their teeth, good oral hygiene and regular dental check-ups to prevent decay in later life,” says Dr Dogramaci.

“Having your teeth straightened does not prevent tooth decay in later life.”

The research was carried out by the Adelaide Dental School, and the Australian Research Centre for Population Oral Health (ARCOPH), the University of Adelaide.

Irish Famine victims’ heavy smoking led to dental decay, new research reveals

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Irish Famine victims were heavy smokers which caused badly rotten teeth, researchers from the University of Otago and Queen’s University Belfast, in Ireland, have discovered. The research was carried out on on the teeth of 363 adult victims of the Great Irish Famine, who died in the Kilkenny Union Workhouse between 1847 and 1851. Their remains were discovered in an unmarked mass burial ground by archaeologists in 2005.

The findings show poor oral health among most of the famine victims, with 80 per cent of the adult remains showing evidence of tooth decay, and over half missing teeth. There were also revealing signs of pipe smoking marks on their teeth.

This is the first study that explores the relationship between smoking and oral health in an archaeological sample of a historical population.

Professor Eileen Murphy, from the School of Natural and Built Environment at Queen’s University Belfast explains this research is important as the current clinical understanding of how smoking affects oral health is not fully understood, and this study adds to that discourse.

“As well as this, the study also gives us a unique insight into the living conditions of the working classes in Victorian Irish society at the time of the Great Famine,” Professor Murphy says.

“Smoking was evidently an important part of life for these people, a habit that they could enjoy amongst deprived social conditions and a very harsh and difficult life, but it may have contributed to their ill health,” she says.

“Despite a vast amount of historical records surviving from the nineteenth century, very little is known about the experienced living conditions of the poor and labouring classes.”

Dr Jonny Geber, from the Department of Anatomy at the University of Otago says: “We believe the bad condition of the teeth studied was because of widespread pipe smoking in both men and women, rather than their diet of potatoes and milk, as a comparative study of the 20th century population on the same diet didn’t have the same evidence of poor oral health.”

“Our study shows that it is not only diet that affects your oral health, but many other factors — and we believe that smoking was a major contributing factor in the Kilkenny population sample,” Dr Geber says.

“The high frequency of clay pipe facets or marks from clenching a pipe between the teeth in many of the skeletons was evidence of smoking in both males and females.

“The current study adds to the growing body of evidence that demonstrates that smoking is not only bad for your health; it is also bad for your teeth.”

Oral bacteria in pancreas linked to more aggressive tumors

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The presence of oral bacteria in so-called cystic pancreatic tumours is associated with the severity of the tumour, a study by researchers at Karolinska Institutet in Sweden published in the journal Gutreports. It is hoped that the results can help to improve diagnosis and treatment of pancreatic cancer.

Pancreatic cancer is one of the most lethal cancers in the west. The disease is often discovered late, which means that in most cases the prognosis is poor. But not all pancreatic tumours are cancerous. For instance there are so-called cystic pancreatic tumours (pancreatic cysts), many of which are benign. A few can, however, become cancerous.

It is currently difficult to differentiate between these tumours. To rule out cancer, many patients therefore undergo surgery, which puts a strain both on the patient and on the healthcare services. Now, however, researchers at Karolinska Institutet have found that the presence of bacteria inside the cystic tumours is linked to how severe the tumour is.

“We find most bacteria at the stage where the cysts are starting to show signs of cancer,” says corresponding author Margaret Sällberg Chen, docent and senior lecturer at the Department of Dental Medicine, Karolinska Institutet. “What we hope is that this can be used as a biomarker for the early identification of the cancerous cysts that need to be surgically removed to cure cancer, this will in turn also reduce the amount of unnecessary surgery of benignant tumours. But first, studies will be needed to corroborate our findings.”

The researchers examined the presence of bacterial DNA in fluid from pancreatic cysts in 105 patients and compared the type and severity of the tumours. Doing this they found that the fluid from the cysts with high-grade dysplasia and cancer contained much more bacterial DNA than that from benign cysts.

To identify the bacteria, the researchers sequenced the DNA of 35 of the samples that had high amounts of bacterial DNA. They found large variations in the bacterial composition between different individuals, but also a greater presence of certain oral bacteria in fluid and tissue from cysts with high-grade dysplasia and cancer.

“We were surprised to find oral bacteria in the pancreas, but it wasn’t totally unexpected,” says Dr Sällberg Chen. “The bacteria we identified has already been shown in an earlier, smaller study to be higher in the saliva of patients with pancreatic cancer.”

The results can help to reappraise the role of bacteria in the development of pancreatic cysts, she notes. If further studies show that the bacteria actually affects the pathological process it could lead to new therapeutic strategies using antibacterial agents.

The researchers also studied different factors that could conceivably affect the amount of bacterial DNA in the tumour fluid. They found that the presence of bacterial DNA was higher in patients who had undergone invasive pancreas endoscopy, a procedure that involves the insertion of a flexible tube into the mouth to examine and treat pancreatic conditions thus the possible transfer of oral bacteria into the pancreas.

“The results were not completely unequivocal, so the endoscopy can’t be the whole answer to why the bacteria is there,” she continues. “But maybe we can reduce the risk of transferring oral bacteria to the pancreas by rinsing the mouth with an antibacterial agent and ensuring good oral hygiene prior to examination. That would be an interesting clinical study.”

The study was conducted in collaboration with researchers at the Department of Clinical Science, Intervention and Technology, the Department of Laboratory Medicine at Karolinska Institutet and Science for Life Laboratory. It was financed by the Swedish Cancer Society, Stockholm County Council (ALF funding), Styrgruppen KI/SLL för Odontologisk Forskning (the KI/SLL steering group for dental research, SOF), KI KID-funding, and the Ruth and Richard Julin Foundation.

New technique could help regrow tissue lost to periodontal disease

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According to the U.S. Centers for Disease Control and Prevention, about half of all Americans will have periodontal disease at some point in their lives. Characterized by inflamed gums and bone loss around teeth, the condition can cause bad breath, toothache, tender gums and, in severe cases, tooth loss. Now, in ACS Nano, researchers report development of a membrane that helps periodontal tissue regenerate when implanted into the gums of rats.

To regrow lost gum tissue and bone, scientists have tried implanting pieces of polymers that form a protected niche near the root of a tooth, recruiting nearby stem cells and helping them differentiate into new gum and bone cells. However, a second surgery is usually required to remove the polymeric membrane, which can get in the way of the healing process. Although researchers have developed biodegradable membranes, these materials don’t tend to work as well for re-growing periodontal tissue. Alireza Moshaverinia, Paul Weiss and colleagues wanted to develop a membrane that would enhance periodontal tissue regeneration and then be absorbed by the body when healing was complete.

The researchers made nanofibrous membranes of poly(ε-caprolactone), a biocompatible polymer already approved for medical applications. They then coated the membrane with polydopamine (PDA), a synthetic polymer that mimics the sticky protein that mussels use to attach to wet surfaces. In the lab, dental-derived stem cells adhered to the membrane and differentiated. The PDA coating also attracted calcium and phosphate ions, leading to early bone mineralization. When the researchers implanted the membranes into the gums of rats with periodontal defects, bone at the defect sites regenerated to normal levels within eight weeks. By this time, the membranes had degraded and were absorbed by the rats. Now, the researchers are working on adding other components to the membrane that aid healing and prevent infection.

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