Researchers have uncovered the complete genetic make-up of the cavity-causing bacterium Bifidobacterium dentium Bd1, revealing the genetic adaptations that allow this microorganism to live and cause decay in the human oral cavity. The study, led by Marco Ventura's Probiogenomics laboratory at the University of Parma, and Prof. Douwe van Sinderen and Dr Paul O'Toole of the Alimentary Pharmabiotic Centre at University College Cork, is published December 24 in the open-access journal PLoS Genetics.
Bifidobacteria, largely known as long-term beneficial gut bacteria, are often included as probiotic components of food to aid digestion and boost the immune system. However, not all species within the genus Bifidobacterium provide beneficial effects to the host's health. In fact, the Bifidobacterium dentium species is an opportunistic pathogen since it has been linked to the development of tooth decay. The genome sequence of B. dentium Bd1 reveals how this microorganism has adapted to the oral environment through specialized nutrient acquisition features, acid tolerance, defences against antimicrobial substances and other gene products that increase fitness and competitiveness within the oral niche.
This report identifies, through various genomic approaches, specific adaptations of a Bifidobacterium taxon to a lifestyle as a tooth decay-causing bacterium. The data in this study indicate that the genome of this opportunistic pathogen has evolved through only a small number of horizontal gene acquisition events, highlighting the narrow boundary that separates bacteria that are long-term residents on or in the human body from opportunistic pathogens.
Saturday, December 26, 2009
Thursday, December 24, 2009
Cracking The Root Of Tooth Strength
After years of biting and chewing, how are human teeth able to remain intact and functional? A team of researchers from The George Washington University and other international scholars have discovered several features in enamel—the outermost tooth tissue—that contribute to the resiliency of human teeth.
A human molar compared to a sea otter molar. (Credit: The George Washington University)
Human enamel is brittle. Like glass, it cracks easily; but unlike glass, enamel is able to contain cracks and remain intact for most individuals’ lifetimes. The research team discovered that the major reason why teeth do not break apart is due to the presence of tufts—small, crack-like defects found deep in the enamel. Tufts arise during tooth development, and all human teeth contain multiple tufts before the tooth has even erupted into the mouth.
Many cracks in teeth do not start at the outer surface of the tooth, as has always been assumed. Instead cracks arise from tufts located deep inside the enamel. From here, cracks can grow towards the outer tooth surface. Once reaching the surface, these cracks can potentially act as sites for dental decay. Acting together like a forest of small flaws, tufts suppress the growth of these cracks by distributing the stress amongst themselves.
“This is the first time that enigmatic developmental features, such as enamel tufts, have been shown to have any significance in tooth function” said GW researcher Paul Constantino. “Crack growth is also hampered by the “basket weave” microstructure of enamel, and by a ‘self-healing’ process whereby organic material fills cracks extended from the tufts, which themselves also become closed by organic matter. This type of infilling bonds the opposing crack walls, which increases the amount of force required to extend the crack later on.”
This research evolved as part of an interdisciplinary collaboration between anthropologists from The George Washington University and physical scientists from the National Institute of Standards and Technology in Gaithersburg, Md. The team studied tooth enamel in humans and also sea otters, mammals with teeth showing remarkable resemblances to those of humans.
A human molar compared to a sea otter molar. (Credit: The George Washington University)
Human enamel is brittle. Like glass, it cracks easily; but unlike glass, enamel is able to contain cracks and remain intact for most individuals’ lifetimes. The research team discovered that the major reason why teeth do not break apart is due to the presence of tufts—small, crack-like defects found deep in the enamel. Tufts arise during tooth development, and all human teeth contain multiple tufts before the tooth has even erupted into the mouth.
Many cracks in teeth do not start at the outer surface of the tooth, as has always been assumed. Instead cracks arise from tufts located deep inside the enamel. From here, cracks can grow towards the outer tooth surface. Once reaching the surface, these cracks can potentially act as sites for dental decay. Acting together like a forest of small flaws, tufts suppress the growth of these cracks by distributing the stress amongst themselves.
“This is the first time that enigmatic developmental features, such as enamel tufts, have been shown to have any significance in tooth function” said GW researcher Paul Constantino. “Crack growth is also hampered by the “basket weave” microstructure of enamel, and by a ‘self-healing’ process whereby organic material fills cracks extended from the tufts, which themselves also become closed by organic matter. This type of infilling bonds the opposing crack walls, which increases the amount of force required to extend the crack later on.”
This research evolved as part of an interdisciplinary collaboration between anthropologists from The George Washington University and physical scientists from the National Institute of Standards and Technology in Gaithersburg, Md. The team studied tooth enamel in humans and also sea otters, mammals with teeth showing remarkable resemblances to those of humans.
Proline Repeats Help Protein Grow Tooth Enamel
A simple amino acid that is repeated in the center of proteins found in tooth enamel makes teeth stronger and more resilient, according to new research at the University of Illinois at Chicago.
Researchers compared proline repeats in amphibian and animal models and discovered that when the repeats are short, such as in frogs, teeth will not have the enamel prisms that are responsible for the strength of human enamel. In contrast, when the proline repeats are long, they contract groups of molecules that help enamel crystals grow.
The findings will be published in the December 21 online version of the Journal PLoS Biology.
"Proline repeats are amazing," said Tom Diekwisch, professor and head of oral biology in the UIC College of Dentistry and lead researcher on the study. "They hold the key to understanding the structure and function of many natural proteins, including mucins, antifreeze proteins, Alzheimer amyloid, and prion proteins.
"We hope that our findings will help many other important areas of scientific research, including the treatment of neurodegenerative diseases."
When tooth enamel is grown it is bathed in bubble-shaped groupings of proteins, Diekwisch said. The size of the protein bubbles varies in different animals, from 5 nanometers in cows to 20 nanometers in mice and 40 nanometers in frogs.
Diekwisch's team discovered that the longer the stretch of proline repeats, the more the protein bubbles contracted. The study also showed that the smaller protein bubbles were associated with longer enamel crystals, he said.
The new discovery, Diekwisch said, will give new clues to engineer tooth enamel.
"We hope that one day these findings will help people replace lost parts of the tooth with a healthy layer of new enamel."
Researchers compared proline repeats in amphibian and animal models and discovered that when the repeats are short, such as in frogs, teeth will not have the enamel prisms that are responsible for the strength of human enamel. In contrast, when the proline repeats are long, they contract groups of molecules that help enamel crystals grow.
The findings will be published in the December 21 online version of the Journal PLoS Biology.
"Proline repeats are amazing," said Tom Diekwisch, professor and head of oral biology in the UIC College of Dentistry and lead researcher on the study. "They hold the key to understanding the structure and function of many natural proteins, including mucins, antifreeze proteins, Alzheimer amyloid, and prion proteins.
"We hope that our findings will help many other important areas of scientific research, including the treatment of neurodegenerative diseases."
When tooth enamel is grown it is bathed in bubble-shaped groupings of proteins, Diekwisch said. The size of the protein bubbles varies in different animals, from 5 nanometers in cows to 20 nanometers in mice and 40 nanometers in frogs.
Diekwisch's team discovered that the longer the stretch of proline repeats, the more the protein bubbles contracted. The study also showed that the smaller protein bubbles were associated with longer enamel crystals, he said.
The new discovery, Diekwisch said, will give new clues to engineer tooth enamel.
"We hope that one day these findings will help people replace lost parts of the tooth with a healthy layer of new enamel."
Monday, December 21, 2009
Adding raisin to cereals = no extra plaque
Elevated dental plaque acid is a risk factor that contributes to cavities in children. But eating bran flakes with raisins containing no added sugar does not promote more acid in dental plaque than bran flakes alone, according to new research at the University of Illinois at Chicago.
Some dentists believe sweet, sticky foods such as raisins cause cavities because they are difficult to clear off the tooth surfaces, said Christine Wu, professor and director of cariology research at UIC and lead investigator of the study.
But studies have shown that raisins are rapidly cleared from the surface of the teeth just like apples, bananas and chocolate, she said.
In the study, published in the journal Pediatric Dentistry, children ages 7 to 11 compared four food groups -- raisins, bran flakes, commercially marketed raisin bran cereal, and a mix of bran flakes with raisins lacking any added sugar.
Sucrose, or table sugar, and sorbitol, a sugar substitute often used in diet foods, were also tested as controls.
Children chewed and swallowed the test foods within two minutes. The acid produced by the plaque bacteria on the surface of their teeth was measured at intervals.
All test foods except the sorbitol solution promoted acid production in dental plaque over 30 minutes, with the largest production between 10 to 15 minutes.
Wu says there is a "well-documented" danger zone of dental plaque acidity that puts a tooth's enamel at risk for mineral loss that may lead to cavities. Achint Utreja, a research scientist and dentist formerly on Wu's team, said plaque acidity did not reach that point after children consumed 10 grams of raisins. Adding unsweetened raisins to bran flakes did not increase plaque acid compared to bran flakes alone.
However, eating commercially marketed raisin bran led to significantly more acid in the plaque, he said, reaching into what Wu identified as the danger zone.
Plaque bacteria on tooth surfaces can ferment various sugars such as glucose, fructose or sucrose and produce acids that may promote decay. But sucrose is also used by bacteria to produce sticky sugar polymers that help the bacteria remain on tooth surfaces, Wu said. Raisins themselves do not contain sucrose.
In a previous study at UIC, researchers identified several natural compounds from raisins that can inhibit the growth of some oral bacteria linked to cavities or gum disease.
Some dentists believe sweet, sticky foods such as raisins cause cavities because they are difficult to clear off the tooth surfaces, said Christine Wu, professor and director of cariology research at UIC and lead investigator of the study.
But studies have shown that raisins are rapidly cleared from the surface of the teeth just like apples, bananas and chocolate, she said.
In the study, published in the journal Pediatric Dentistry, children ages 7 to 11 compared four food groups -- raisins, bran flakes, commercially marketed raisin bran cereal, and a mix of bran flakes with raisins lacking any added sugar.
Sucrose, or table sugar, and sorbitol, a sugar substitute often used in diet foods, were also tested as controls.
Children chewed and swallowed the test foods within two minutes. The acid produced by the plaque bacteria on the surface of their teeth was measured at intervals.
All test foods except the sorbitol solution promoted acid production in dental plaque over 30 minutes, with the largest production between 10 to 15 minutes.
Wu says there is a "well-documented" danger zone of dental plaque acidity that puts a tooth's enamel at risk for mineral loss that may lead to cavities. Achint Utreja, a research scientist and dentist formerly on Wu's team, said plaque acidity did not reach that point after children consumed 10 grams of raisins. Adding unsweetened raisins to bran flakes did not increase plaque acid compared to bran flakes alone.
However, eating commercially marketed raisin bran led to significantly more acid in the plaque, he said, reaching into what Wu identified as the danger zone.
Plaque bacteria on tooth surfaces can ferment various sugars such as glucose, fructose or sucrose and produce acids that may promote decay. But sucrose is also used by bacteria to produce sticky sugar polymers that help the bacteria remain on tooth surfaces, Wu said. Raisins themselves do not contain sucrose.
In a previous study at UIC, researchers identified several natural compounds from raisins that can inhibit the growth of some oral bacteria linked to cavities or gum disease.
Monday, December 14, 2009
90% with Gum Disease Are at Risk for Diabetes
Study Finds Over 90% of People with Gum Disease Are at Risk for Diabetes; Concludes That at Least Half Could Be Screened in Dental Offices
An overwhelming majority of people who have periodontal (gum) disease are also at high risk for diabetes and should be screened for diabetes, a New York University nursing-dental research team has found. The researchers also determined that half of those at risk had seen a dentist in the previous year, concluded that dentists should consider offering diabetes screenings in their offices, and described practical approaches to conducting diabetes screenings in dental offices.
The study, led by Dr. Shiela Strauss, Associate Professor of Nursing and Co-Director of the Statistics and Data Management Core for NYU’s Colleges of Dentistry and Nursing, examined data from 2,923 adult participants in the 2003-2004 National Health and Nutrition Examination Survey who had not been diagnosed with diabetes. The survey, conducted by the National Center for Health Statistics of the Centers for Disease Control and Prevention, was designed to assess the health and nutritional status of adults and children in the United States.
Using guidelines established by the American Diabetes Association, Dr. Strauss determined that 93 percent of subjects who had periodontal disease, compared to 63 percent of those without the disease, were considered to be at high risk for diabetes and should be screened for diabetes. The guidelines recommend diabetes screening for people at least 45 years of age with a body mass index (a comparative measure of weight and height) of 25 or more, as well as for those under 45 years of age with a BMI of 25 or more who also have at least one additional diabetes risk factor. In Dr. Strauss’s study, two of those additional risk factors - high blood pressure and a first-degree relative (a parent or sibling) with diabetes - were reported in a significantly greater number of subjects with periodontal disease than in subjects without the disease. Dr. Strauss’s findings, published today in the online edition of the Journal of Public Health Dentistry, add to a growing body of evidence linking periodontal infections to an increased risk for diabetes.
Dr. Strauss also examined how often those with gum disease and a risk for diabetes visit a dentist, finding that three in five reported a dental visit in the past two years; half in the past year; and a third in the past six months.
“In light of these findings, the dental visit could be a useful opportunity to conduct an initial diabetes screening — an important first step in identifying those patients who need follow-up testing to diagnose the disease.”
“It’s been estimated that 5.7 million Americans with diabetes were undiagnosed in 2007,” Dr. Strauss added, “with the number expected to increase dramatically in coming years. The issue of undiagnosed diabetes is especially critical because early treatment and secondary prevention efforts may help to prevent or delay the long-term complications of diabetes that are responsible for reduced quality of life and increased levels of mortality among these patients. Thus, there is a critical need to increase opportunities for diabetes screening and early diabetes detection.”
Dr. Strauss said that dentists could screen patients for diabetes by evaluating them for risk factors such as being overweight; belonging to a high-risk ethnic group (African-American, Latino, Native American, Asian-American, or Pacific Islander); having high cholesterol; high blood pressure; a first-degree relative with diabetes; or gestational diabetes mellitus; or having given birth to a baby weighing more than nine pounds.
Alternatively, dentists could use a glucometer — a diagnostic instrument for measuring blood glucose — to analyze finger-stick blood samples, or use the glucometer to evaluate blood samples taken from pockets of inflammation in the gums.
“The oral blood sample would arguably be more acceptable to dentists because providers and patients anticipate oral intervention in the dental office,” Dr. Strauss noted. In an earlier study involving 46 subjects with periodontal disease published in June 2009 by the Journal of Periodontology, an NYU nursing-dental research team led by Dr. Strauss determined that the glucometer can provide reliable glucose-level readings for blood samples drawn from deep pockets of gum inflammation, and that those readings were highly correlated with glucometer readings for finger-stick blood samples.
An overwhelming majority of people who have periodontal (gum) disease are also at high risk for diabetes and should be screened for diabetes, a New York University nursing-dental research team has found. The researchers also determined that half of those at risk had seen a dentist in the previous year, concluded that dentists should consider offering diabetes screenings in their offices, and described practical approaches to conducting diabetes screenings in dental offices.
The study, led by Dr. Shiela Strauss, Associate Professor of Nursing and Co-Director of the Statistics and Data Management Core for NYU’s Colleges of Dentistry and Nursing, examined data from 2,923 adult participants in the 2003-2004 National Health and Nutrition Examination Survey who had not been diagnosed with diabetes. The survey, conducted by the National Center for Health Statistics of the Centers for Disease Control and Prevention, was designed to assess the health and nutritional status of adults and children in the United States.
Using guidelines established by the American Diabetes Association, Dr. Strauss determined that 93 percent of subjects who had periodontal disease, compared to 63 percent of those without the disease, were considered to be at high risk for diabetes and should be screened for diabetes. The guidelines recommend diabetes screening for people at least 45 years of age with a body mass index (a comparative measure of weight and height) of 25 or more, as well as for those under 45 years of age with a BMI of 25 or more who also have at least one additional diabetes risk factor. In Dr. Strauss’s study, two of those additional risk factors - high blood pressure and a first-degree relative (a parent or sibling) with diabetes - were reported in a significantly greater number of subjects with periodontal disease than in subjects without the disease. Dr. Strauss’s findings, published today in the online edition of the Journal of Public Health Dentistry, add to a growing body of evidence linking periodontal infections to an increased risk for diabetes.
Dr. Strauss also examined how often those with gum disease and a risk for diabetes visit a dentist, finding that three in five reported a dental visit in the past two years; half in the past year; and a third in the past six months.
“In light of these findings, the dental visit could be a useful opportunity to conduct an initial diabetes screening — an important first step in identifying those patients who need follow-up testing to diagnose the disease.”
“It’s been estimated that 5.7 million Americans with diabetes were undiagnosed in 2007,” Dr. Strauss added, “with the number expected to increase dramatically in coming years. The issue of undiagnosed diabetes is especially critical because early treatment and secondary prevention efforts may help to prevent or delay the long-term complications of diabetes that are responsible for reduced quality of life and increased levels of mortality among these patients. Thus, there is a critical need to increase opportunities for diabetes screening and early diabetes detection.”
Dr. Strauss said that dentists could screen patients for diabetes by evaluating them for risk factors such as being overweight; belonging to a high-risk ethnic group (African-American, Latino, Native American, Asian-American, or Pacific Islander); having high cholesterol; high blood pressure; a first-degree relative with diabetes; or gestational diabetes mellitus; or having given birth to a baby weighing more than nine pounds.
Alternatively, dentists could use a glucometer — a diagnostic instrument for measuring blood glucose — to analyze finger-stick blood samples, or use the glucometer to evaluate blood samples taken from pockets of inflammation in the gums.
“The oral blood sample would arguably be more acceptable to dentists because providers and patients anticipate oral intervention in the dental office,” Dr. Strauss noted. In an earlier study involving 46 subjects with periodontal disease published in June 2009 by the Journal of Periodontology, an NYU nursing-dental research team led by Dr. Strauss determined that the glucometer can provide reliable glucose-level readings for blood samples drawn from deep pockets of gum inflammation, and that those readings were highly correlated with glucometer readings for finger-stick blood samples.
Wednesday, December 9, 2009
Older mercury-based fillings unlikely to be toxic
A new study, "The Chemical Forms of Mercury in Aged and Fresh Dental Amalgam Surfaces," on the surface chemistry of silver-colored, mercury-based dental fillings suggests that the surface forms of mercury may be less toxic than previously thought. It appears online in ACS' journal Chemical Research in Toxicology.
In the study, Graham George and colleagues note that mercury-based fillings, also called amalgams, have been used by dentists to repair teeth for well-over a century. In recent decades their use has become controversial because of concerns about exposure to potentially toxic mercury. However, mercury can potentially exist in several different chemical forms, each with a different toxicity. Prior to this report, little was known about how the chemical forms of mercury in dental amalgam might change over time.
Using a special X-ray technique, the scientists analyzed the surface of freshly prepared metal fillings and compared these with the surface of aged fillings (about 20 years old) from a dental clinic. Fresh fillings contained metallic mercury, which can be toxic. Aged fillings, however, typically contain a form of mercury, called beta-mercuric sulfide or metacinnabar, which is unlikely to be toxic in the body. The scientists found that the surfaces of metal fillings seem to lose up to 95 percent of their mercury over time. Loss of potentially toxic mercury from amalgam may be due to evaporation, exposure to some kinds of dental hygiene products, exposure to certain foods, or other factors. The scientists caution that "human exposure to mercury lost from fillings is still of concern."
In the study, Graham George and colleagues note that mercury-based fillings, also called amalgams, have been used by dentists to repair teeth for well-over a century. In recent decades their use has become controversial because of concerns about exposure to potentially toxic mercury. However, mercury can potentially exist in several different chemical forms, each with a different toxicity. Prior to this report, little was known about how the chemical forms of mercury in dental amalgam might change over time.
Using a special X-ray technique, the scientists analyzed the surface of freshly prepared metal fillings and compared these with the surface of aged fillings (about 20 years old) from a dental clinic. Fresh fillings contained metallic mercury, which can be toxic. Aged fillings, however, typically contain a form of mercury, called beta-mercuric sulfide or metacinnabar, which is unlikely to be toxic in the body. The scientists found that the surfaces of metal fillings seem to lose up to 95 percent of their mercury over time. Loss of potentially toxic mercury from amalgam may be due to evaporation, exposure to some kinds of dental hygiene products, exposure to certain foods, or other factors. The scientists caution that "human exposure to mercury lost from fillings is still of concern."
Tuesday, December 8, 2009
The state of pediatric oral health in US
Special issue of Academic Pediatrics reports on state of pediatric oral health in US
Oral disease, primarily dental caries, is the most common pediatric disease and can lead to physical and psychological disabilities as well as significant morbidity in adulthood. In May 2000, Dr David Satcher's landmark report, Oral Health in America: A Report of the Surgeon General, highlighted the state of oral health for children and adults in the United States and offered strategies to improve oral health outcomes. The November/December issue of Academic Pediatrics, devoted entirely to children's oral health, represents a ''midterm examination'' of how far the US has come since the 2000 Surgeon General's report in meeting Healthy People 2010 oral health objectives and other key recommendations.
Bringing together 19 contributions from experts in dentistry, medicine, nursing, and public policy, guest editors Wendy E. Mouradian and Rebecca L. Slayton have assembled an impressive summary of the state of children's oral health in the US and urge healthcare professionals to make oral health a pediatric priority. A number of papers were presented at the landmark American Academy of Pediatrics' (AAP) National Summit on Children's Oral Health: A New Era of Collaboration, held November 7-8, 2008 in Chicago.
In his commentary, Editor-in-Chief Peter G. Szilagyi, University of Rochester Medical Center, asks the question, "Why should Academic Pediatrics devote an entire issue to children's oral health now?" His answers: "First, oral health is health, and children's oral health is part of pediatrics...Second, we are far from achieving our Healthy People 2010 oral health objectives in reducing the prevalence of caries in children...Third, substantial disparities exist in children's oral health and access to care...Fourth, oral health represents an excellent paradigm in which the traditional pediatric community needs to work more closely with other health professionals—in this case dental professionals—to advance the health of children."
Szilagyi continues, "I look forward to the day when a future issue of Academic Pediatrics or a future Surgeon General's report proclaims victory on the plight of dental caries and declares that children's mouths are largely absent of dental or oral disease."
Wendy E. Mouradian and her co-authors then present an overview of the papers and comment on progress made in meeting Surgeon General David Satcher's goals set in 2000, calling for "dentists, physicians, and other health professionals who work with children to embrace a shared responsibility for children's oral health and work to overcome the historic separation between dentistry and medicine...." Dr. Satcher himself follows with a renewed call to arms to improve children's oral health.
Rebecca L. Slayton and Harold C. Slavkin address how scientific and technological advances in sequencing of the human genome, tissue engineering and saliva diagnostics may have significant potential to impact oral health.
Paul S. Casamassimo relates the medical history of a young man with special-needs, to illustrate how oral health may be mishandled by both community dentists and physicians in a health care system with too many gaps, in "A Life Without Teeth."
The Science and Surveillance section includes articles that discuss tooth decay, especially in younger children, and the lack of improvement in reducing this disease. Children's diets, a subject of recent concern for obesity, can also increase dental caries.
Three articles dealing with Access and Barriers to Care are included. These review current measures of access to dental care for children, including those with special health care needs, and the ethical and policy issues in the care of children with craniofacial conditions including quality of life, costs of care, and prenatal diagnosis of craniofacial defects,
The Oral Health Workforce, including dental and medical education issues, is covered in six articles. Authors review the state of the oral health workforce, including new models of mid-level dental practitioners, and stress the need to better educate both dentists (especially general and pediatric dentists) and primary care medical providers (pediatricians, family physicians, nurse practitioners, physicians' assistants) to promote children's oral health and ensure they have adequate access to dental care.
Finally, two articles on Policy Achievements and Challenges discuss how government actions and policy decisions have affected children's oral health. Burton Edelstein writes about congressional action to reauthorize CHIP (Child's Health Insurance Program) and to include funding for oral care. James J. Crall discusses how the Surgeon General's Report on Oral Health drove Congress and State Legislatures, Federal and State Agencies, the Federal Courts, and various professional societies and associations to adopt policies and procedures to enhance children's oral health, and reflects on the work remaining to fully address children's oral health needs.
Oral disease, primarily dental caries, is the most common pediatric disease and can lead to physical and psychological disabilities as well as significant morbidity in adulthood. In May 2000, Dr David Satcher's landmark report, Oral Health in America: A Report of the Surgeon General, highlighted the state of oral health for children and adults in the United States and offered strategies to improve oral health outcomes. The November/December issue of Academic Pediatrics, devoted entirely to children's oral health, represents a ''midterm examination'' of how far the US has come since the 2000 Surgeon General's report in meeting Healthy People 2010 oral health objectives and other key recommendations.
Bringing together 19 contributions from experts in dentistry, medicine, nursing, and public policy, guest editors Wendy E. Mouradian and Rebecca L. Slayton have assembled an impressive summary of the state of children's oral health in the US and urge healthcare professionals to make oral health a pediatric priority. A number of papers were presented at the landmark American Academy of Pediatrics' (AAP) National Summit on Children's Oral Health: A New Era of Collaboration, held November 7-8, 2008 in Chicago.
In his commentary, Editor-in-Chief Peter G. Szilagyi, University of Rochester Medical Center, asks the question, "Why should Academic Pediatrics devote an entire issue to children's oral health now?" His answers: "First, oral health is health, and children's oral health is part of pediatrics...Second, we are far from achieving our Healthy People 2010 oral health objectives in reducing the prevalence of caries in children...Third, substantial disparities exist in children's oral health and access to care...Fourth, oral health represents an excellent paradigm in which the traditional pediatric community needs to work more closely with other health professionals—in this case dental professionals—to advance the health of children."
Szilagyi continues, "I look forward to the day when a future issue of Academic Pediatrics or a future Surgeon General's report proclaims victory on the plight of dental caries and declares that children's mouths are largely absent of dental or oral disease."
Wendy E. Mouradian and her co-authors then present an overview of the papers and comment on progress made in meeting Surgeon General David Satcher's goals set in 2000, calling for "dentists, physicians, and other health professionals who work with children to embrace a shared responsibility for children's oral health and work to overcome the historic separation between dentistry and medicine...." Dr. Satcher himself follows with a renewed call to arms to improve children's oral health.
Rebecca L. Slayton and Harold C. Slavkin address how scientific and technological advances in sequencing of the human genome, tissue engineering and saliva diagnostics may have significant potential to impact oral health.
Paul S. Casamassimo relates the medical history of a young man with special-needs, to illustrate how oral health may be mishandled by both community dentists and physicians in a health care system with too many gaps, in "A Life Without Teeth."
The Science and Surveillance section includes articles that discuss tooth decay, especially in younger children, and the lack of improvement in reducing this disease. Children's diets, a subject of recent concern for obesity, can also increase dental caries.
Three articles dealing with Access and Barriers to Care are included. These review current measures of access to dental care for children, including those with special health care needs, and the ethical and policy issues in the care of children with craniofacial conditions including quality of life, costs of care, and prenatal diagnosis of craniofacial defects,
The Oral Health Workforce, including dental and medical education issues, is covered in six articles. Authors review the state of the oral health workforce, including new models of mid-level dental practitioners, and stress the need to better educate both dentists (especially general and pediatric dentists) and primary care medical providers (pediatricians, family physicians, nurse practitioners, physicians' assistants) to promote children's oral health and ensure they have adequate access to dental care.
Finally, two articles on Policy Achievements and Challenges discuss how government actions and policy decisions have affected children's oral health. Burton Edelstein writes about congressional action to reauthorize CHIP (Child's Health Insurance Program) and to include funding for oral care. James J. Crall discusses how the Surgeon General's Report on Oral Health drove Congress and State Legislatures, Federal and State Agencies, the Federal Courts, and various professional societies and associations to adopt policies and procedures to enhance children's oral health, and reflects on the work remaining to fully address children's oral health needs.
Monday, December 7, 2009
Nearly 1/3 of human genome is involved in gingivitis
Gingivitis, which may affect more than one-half of the U.S. adult population, is a condition commonly attributed to lapses in simple oral hygiene habits. However, a new study shows that development and reversal of gingivitis at the molecular level is apparently much more complicated than its causes might indicate.
Research conducted jointly by the University of North Carolina at Chapel Hill and Procter & Gamble (P&G) Oral Care has found that more than 9,000 genes – nearly 30 percent of the genes found in the human body – are expressed differently during the onset and healing process associated with gingivitis. Biological pathways associated with activation of the immune system were found to be the major pathways being activated and critical to controlling the body's reaction to plaque build-up on the teeth. Additionally, other gene expression pathways activated during plaque overgrowth include those involved in wound healing, neural processes and skin turnover.
Results of the study are published today in the December 2009 edition of the Journal of Periodontology. This study is the first to successfully identify gene expression and biological pathways involved with the onset and healing process of gingivitis.
Gingivitis is characterized by gums that are red, swollen and tender and that bleed easily during brushing and flossing. If untreated, gingivitis can lead to periodontal disease, which has been studied extensively for its possible relation to heart disease, diabetes and pre-term birth. Researchers said that understanding how gingivitis develops and resolves on a molecular level can possibly provide critical insights into gum disease prevention, as well as new treatments.
"The study's findings demonstrate that clinical symptoms of gingivitis reflect complicated changes in cellular and molecular processes within the body," said Steven Offenbacher, D.D.S., Ph.D., the study's lead author and director of the UNC School of Dentistry-based Center for Oral and Systemic Diseases. "Understanding the thousands of individual genes and multiple systems involved in gingivitis will help explain exactly what is occurring in a person's body at the onset of the disease and how it relates to their overall health."
The build-up of plaque formed during the onset of gingivitis represents the overgrowth of bacteria as a biofilm on the teeth above and below the gum line. Biofilms can form in other parts of the body and are known to be involved with health conditions, such as urinary tract infections, ear infections and chronic sinusitis. Researchers believe learning about how the body interacts with bacteria overgrowth during gingivitis could provide insight into a variety of bio-film-associated diseases.
"Data generated by the study will be crucial in developing new approaches to treating gingivitis," said Leslie Winston, D.D.S., Ph.D., co-author of the study and Director of Professional and Scientific Relations at P&G Oral Care (makers of Crest and Oral-B). "We plan to conduct additional research to identify biomarkers of gum disease in at risk individuals and hope that this will lead to new and more advanced treatment options and preventative measures."
About the Study
The objective of this study was to understand gingivitis on a molecular level by identifying changes in gene expression taking place in the mouth during gingivitis onset and the healing process. Fourteen healthy individuals with mild gingivitis participated in the study. After baseline tooth cleanings, gingivitis was induced in each study participant, followed by the participants adhering to an oral hygiene regimen of twice-daily brushing and regular flossing. Gum tissue was collected at baseline, four weeks after the induction of gingivitis and one week after resuming the oral hygiene regimen of brushing and flossing.
Gene expression data was analyzed using gene chip technology that enabled the investigators to detect changes in the expression of more than 30,000 genes. By applying advanced genomics bioinformatics tools, the investigators were able to identify the biological pathways and gene expression patterns associated with gingivitis.
As part of the study findings, researchers identified several biological pathways triggered by the onset and healing of gingivitis, including those associated with immune response, energy metabolism, neural processes, vasculature, chemotaxis, wound healing and steroid metabolism.
Research conducted jointly by the University of North Carolina at Chapel Hill and Procter & Gamble (P&G) Oral Care has found that more than 9,000 genes – nearly 30 percent of the genes found in the human body – are expressed differently during the onset and healing process associated with gingivitis. Biological pathways associated with activation of the immune system were found to be the major pathways being activated and critical to controlling the body's reaction to plaque build-up on the teeth. Additionally, other gene expression pathways activated during plaque overgrowth include those involved in wound healing, neural processes and skin turnover.
Results of the study are published today in the December 2009 edition of the Journal of Periodontology. This study is the first to successfully identify gene expression and biological pathways involved with the onset and healing process of gingivitis.
Gingivitis is characterized by gums that are red, swollen and tender and that bleed easily during brushing and flossing. If untreated, gingivitis can lead to periodontal disease, which has been studied extensively for its possible relation to heart disease, diabetes and pre-term birth. Researchers said that understanding how gingivitis develops and resolves on a molecular level can possibly provide critical insights into gum disease prevention, as well as new treatments.
"The study's findings demonstrate that clinical symptoms of gingivitis reflect complicated changes in cellular and molecular processes within the body," said Steven Offenbacher, D.D.S., Ph.D., the study's lead author and director of the UNC School of Dentistry-based Center for Oral and Systemic Diseases. "Understanding the thousands of individual genes and multiple systems involved in gingivitis will help explain exactly what is occurring in a person's body at the onset of the disease and how it relates to their overall health."
The build-up of plaque formed during the onset of gingivitis represents the overgrowth of bacteria as a biofilm on the teeth above and below the gum line. Biofilms can form in other parts of the body and are known to be involved with health conditions, such as urinary tract infections, ear infections and chronic sinusitis. Researchers believe learning about how the body interacts with bacteria overgrowth during gingivitis could provide insight into a variety of bio-film-associated diseases.
"Data generated by the study will be crucial in developing new approaches to treating gingivitis," said Leslie Winston, D.D.S., Ph.D., co-author of the study and Director of Professional and Scientific Relations at P&G Oral Care (makers of Crest and Oral-B). "We plan to conduct additional research to identify biomarkers of gum disease in at risk individuals and hope that this will lead to new and more advanced treatment options and preventative measures."
About the Study
The objective of this study was to understand gingivitis on a molecular level by identifying changes in gene expression taking place in the mouth during gingivitis onset and the healing process. Fourteen healthy individuals with mild gingivitis participated in the study. After baseline tooth cleanings, gingivitis was induced in each study participant, followed by the participants adhering to an oral hygiene regimen of twice-daily brushing and regular flossing. Gum tissue was collected at baseline, four weeks after the induction of gingivitis and one week after resuming the oral hygiene regimen of brushing and flossing.
Gene expression data was analyzed using gene chip technology that enabled the investigators to detect changes in the expression of more than 30,000 genes. By applying advanced genomics bioinformatics tools, the investigators were able to identify the biological pathways and gene expression patterns associated with gingivitis.
As part of the study findings, researchers identified several biological pathways triggered by the onset and healing of gingivitis, including those associated with immune response, energy metabolism, neural processes, vasculature, chemotaxis, wound healing and steroid metabolism.
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