What's the best way to brush teeth? Even dentists and dental associations don't agree

Advice on how we should brush our teeth from dental associations and toothpaste companies is 'unacceptably inconsistent', finds new UCL research

Advice on how we should brush our teeth from dental associations and toothpaste companies is 'unacceptably inconsistent', finds new UCL (University College London) research.

The study, published in the British Dental Journal, looked at the brushing advice given by dental associations across ten countries, toothpaste and toothbrush companies and in dental textbooks. They found a wide range of recommendations on what brushing method to use, how often to brush and for how long.

The researchers found no clear consensus between the various sources, and a 'worrying' lack of agreement between advice from dental associations compared with dental textbooks.

"The public needs to have sound information on the best method to brush their teeth," says Aubrey Sheiham, Emeritus Professor of Dental Public Health (UCL Epidemiology & Public Health), senior author of the study. "If people hear one thing from a dental association, another from a toothbrush company and something else from their dentist, no wonder they are confused about how to brush. In this study we found an unacceptably inconsistent array of advice from different sources.

"Dental associations need to be consistent about what method to recommend, based on how effective the method is. Most worryingly, the methods recommended by dental associations are not the same as the best ones mentioned in dental textbooks. There is no evidence to suggest that complicated techniques are any better than a simple gentle scrub."

The most commonly-recommended technique involves gently jiggling the brush back and forth in small motions, with the intention of shaking loose any food particles, plaque and bacteria. However, no large-scale studies have ever shown this method to be any more effective than basic scrubbing.

"Brush gently with a simple horizontal scrubbing motion, with the brush at a forty-five degree angle to get to the dental plaque," Professor Sheiham advises. "To avoid brushing too hard, hold the brush with a pencil grip rather than a fist. This simple method is perfectly effective at keeping your gums healthy.

"There is little point in brushing after eating sweets or sugary drinks to prevent tooth decay. It takes bacteria from food about two minutes to start producing acid, so if you brush your teeth a few minutes after eating sugary foods, the acid will have damaged the enamel."

The conflicting messages given by different organisations highlight the need for research into how effective different brushing methods are. At present, the expert advice in the guidelines, 'The scientific basis of dental health education', recommend a simple scrubbing technique as it is easy to learn and there is no evidence to justify a more complicated method.

"The wide range of recommendations we found is likely due to the lack of strong evidence suggesting that one method is conclusively better than another," says lead author Dr John Wainwright, who carried out the study at UCL and is now a practising dentist. "I advise my patients to focus their brushing on areas where plaque is most likely to collect – the biting surfaces and where the teeth and gums meet – and to use a gentle scrubbing motion. All too frequently I am asked why the method I am describing differs from how previous dentists have taught them in the past.

"What I feel we need is better research into what the easiest to learn, most effective and safest way to brush is. The current situation where not just individual dentists, but different dental organisations worldwide are all issuing different brushing guidelines isn't just confusing – it's undermining faith and trust in the profession as a whole. For something most people do twice a day, you would expect dentists to send a clearer, more unified message to their patients on how to brush their teeth."^

Link between periodontitis and atherosclerosis

Chronic oral infection with the periodontal disease pathogen, Porphyromonas gingivalis, not only causes local inflammation of the gums leading to tooth loss but also is associated with an increased risk of atherosclerosis. A study published on July 10th in PLOS Pathogens now reveals how the pathogen evades the immune system to induce inflammation beyond the oral cavity.

Like other gram-negative bacteria, P. gingivalis has an outer layer that consists of sugars and lipids. The mammalian immune system has evolved to recognize parts of this bacterial coating, which then triggers a multi-pronged immune reaction. As part of the "arms race" between pathogens and their hosts, several types of gram-negative bacteria, including P. gingivalis, employ strategies by which they alter their outer coats to avoid the host immune defense.

Caroline Attardo Genco, from Boston University School of Medicine, USA, in collaboration with Richard Darveau, at the University of Washington School of Dentistry, USA, and colleagues focused on the role of a specific lipid expressed on the outer surface of P. gingivalis, called lipid A, which is known to interact with a key regulator of the host's immune system called TLR4. P. gingivalis can produce a number of different lipid A versions, and the researchers wanted to clarify how these modify the immune response and contribute to the ability of the pathogen to survive and cause inflammation—both locally, resulting in oral bone loss, and systemically, in distant blood vessels.

They constructed genetically modified strains of P. gingivalis with two distinct lipid A versions. The resulting bacteria produced either lipid A that activated TLR4 (called "agonist") or lipid A that interacted with TLR4 but blocked activation ("antagonist"). Utilizing these strains, they demonstrate that P. gingivalis production of antagonist lipid A renders the pathogen resistant to host bacterial killing responses. This facilitates bacterial survival in macrophages, specific immune cells that normally not only gobble up the bacteria but also "digest" and kill them.

When the researchers infected atherosclerosis-prone mice with the P. gingivalis TLR4 antagonist strain, they found that this exacerbates inflammation in the blood vessels and promotes atherosclerosis. In contrast, the ability of P. gingivalis to induce local inflammatory bone loss was independent of lipid A variations, which demonstrates that there are distinct mechanisms for induction of local versus systemic inflammation.

The researchers conclude, "P. gingivalis modifies its lipid A structure in order to evade host defenses and establish chronic infection leading to persistent systemic low-grade inflammation". They go on to state that "uniquely among gram-negative pathogens, P. gingivalis evasion of TLR4-mediated host immunity results in progression of inflammation at a site that is distant from local infection by gaining access to the vasculature."

Faster Dental Treatment with New Photoactive Molecule

A new dental filling material, developed at the Vienna University of Technology, is easier to harden. It makes dental treatment faster and easier.

In modern dentistry, amalgam fillings have become unpopular. Instead, white composite materials are more commonly used, which at first glance can hardly be distinguished from the tooth. The majority of these composites are based on photoactive materials that harden when they are exposed to light. But as the light does not penetrate very deeply into the material, the patients often have to endure a cumbersome procedure in which the fillings are applied and hardened in several steps. The Vienna University of Technology in collaboration with the company Ivoclar Vivadent have now developed a new generation of photoactive materials based on the element Germanium. Simply put, improved photoreactivity is good news for everyone who wants to spend as little time as possible in the dental chair.

Hardening With Light

Similar to natural tooth enamel, modern dental composites consist of a mixture of different material components. In addition to inorganic fillers they can also contain photoactive organic resins which react to light of a particular wavelength and readily solidify.

Professor Robert Liska and his team at the Vienna University of Technology (TU Vienna) have been working with such photoactive substances for a long time. Similar photoactive substances are used for additional applications including protective coatings and modern 3d-printing.

The penetration depth of the light depends on its wavelength. “Usually, light in the violet and ultraviolet region is used”, says Robert Liska. It is also possible to use light with longer wavelengths, which penetrates deeper into the material, but then the polymerization process is less efficient. If the filling cannot be hardened in one step, the procedure has to be repeated several times. If the cavity is large, this can be rather uncomfortable.

Germanium-based Compound Initiates Chain Reaction

This problem can now be solved with a new Germanium-based molecule. It only makes up 0.04% of the composite material, but it plays a crucial role. The molecule is split into two parts by blue light, creating radicals, which initiate a chain reaction: molecular compounds, which are already present in the filling, assemble into polymers, and the material hardens.

The Germanium-based photo initiator was created at the Vienna University of Technology and then extensively tested by Ivoclar Vivadent. At Graz University of Technology, the physicochemical mechanism was investigated further. Using this new compound, the hardening depth could be increased from 2 mm to 4 mm, which considerably reduces the duration of the medical procedure.

Based on these excellent results, the Vienna University of Technology and Ivoclar Vivadent have made additional strides to further extend their collective research insterests in dental materials. Already in 2012, the Institute for Applied Synthetic Chemistry together with the Institute for Materials Science and Technology with collective funding from Ivoclar Vivadent and the Christian Doppler Research Association put into place a Laboratory for “Photopolymers in digital and restorative dentistry”. Since its inception the laboratory has Goals for the laboratory include the development of improved photosensitive substances for dentistry with additional research efforts placed on 3D-printing of ceramic implants. 

Genetic signature reveals new way to classify gum disease

Researchers at Columbia University Medical Center (CUMC) have devised a new system for classifying periodontal disease based on the genetic signature of affected tissue, rather than on clinical signs and symptoms. The new classification system, the first of its kind, may allow for earlier detection and more individualized treatment of severe periodontitis, before loss of teeth and supportive bone occurs. The findings were published recently in the online edition of the Journal of Dental Research.
Currently, periodontal disease is classified as either "chronic" or "aggressive," based on clinical signs and symptoms, such as severity of gum swelling and extent of bone loss. "However, there is much overlap between the two classes," said study leader Panos N. Papapanou, DDS, PhD, professor and chair of oral and diagnostic sciences at the College of Dental Medicine at CUMC. "Many patients with severe symptoms can be effectively treated, while others with seemingly less severe infection may continue to lose support around their teeth even after therapy. Basically, we don't know whether a periodontal infection is truly aggressive until severe, irreversible damage has occurred."

Looking for a better way to classify periodontitis, Dr. Papapanou turned to cancer as a model. In recent years, cancer biologists have found that, in some cancers, clues to a tumor's aggressiveness and responsiveness to treatment can be found in its genetic signature. To determine if similar patterns could be found in periodontal disease, the CUMC team performed genome-wide expression analyses of diseased gingival (gum) tissue taken from 120 patients with either chronic or aggressive periodontitis. The test group included both males and females ranging in age from 11 to 76 years.

The researchers found that, based on their gene expression signatures, the patients fell into two distinct clusters. "The clusters did not align with the currently accepted periodontitis classification," said Dr. Papapanou. However, the two clusters did differ with respect to the extent and severity of periodontitis, with significantly more serious disease in Cluster 2. The study also found higher levels of infection by known oral pathogens, as well as a higher percentage of males, in Cluster 2 than in Cluster 1, in keeping with the well-established observation that severe periodontitis is more common in men than in women.

"Our data suggest that molecular profiling of gingival tissues can indeed form the basis for the development of an alternative, pathobiology-based classification of periodontitis that correlates well with the clinical presentation of the disease," said Dr. Papapanou.

The researchers' next goal is to conduct a prospective study to validate the new classification system's ability to predict disease outcome. The team also hopes to find simple surrogate biomarkers for the two clusters, as it would be impractical to perform genome-wide testing on every patient.

The new system could offer huge advantages for classifying people with different types of periodontitis. "If a patient is found to be highly susceptible to severe periodontitis, we would be justified in using aggressive therapies, even though that person may have subclinical disease," said Dr. Papapanou. "Now, we wait years to make this determination, and by then, significant damage to the tooth-supporting structures may have occurred.

Genetic techniques have role in future of dental care

A visit to the dentist could one day require a detailed look at how genes in a patient's body are being switched on or off, as well as examining their pearly whites, according to researchers at the University of Adelaide.

In a new paper published in the Australian Dental Journal, researchers from the University of Adelaide's School of Dentistry have written about the current and future use of the field of epigenetics as it relates to oral health.

Co-author Associate Professor Toby Hughes says epigenetics has much to offer in the future treatment and prevention of dental disease.

"Our genetic code, or DNA, is like an orchestra - it contains all of the elements we need to function - but the epigenetic code is essentially the conductor, telling which instruments to play or stay silent, or how to respond at any given moment," Associate Professor Hughes says.

"This is important because, in the case of oral health, epigenetic factors may help to orchestrate healthy and unhealthy states in our mouths. They respond to the current local environment, such as the type and level of our oral microbes, regulating which of our genes are active. This means we could use them to determine an individual's state of health, or even influence how their genes behave. We can't change the underlying genetic code, but we may be able to change when genes are switched on and off," he says.

Associate Professor Hughes is part of a team of researchers at the University of Adelaide that has been studying the underlying genetic and environmental influences on dental development and oral health.

He says that since the completion of the Human Genome Project in 2007, epigenetics has had an increasing role in biological and medical research.

"Dentistry can also greatly benefit from new research in this area," he says. "It could open up a range of opportunities for diagnosis, treatment and prevention.

"We know that our genome plays a key role in our dental development, and in a range of oral diseases; we know that the oral microbiota also play a key role in the state of our oral health; we now have the potential to develop an epigenetic profile of a patient, and use all three of these factors to provide a more personalized level of care.

"Other potential oral health targets for the study of epigenetics include the inflammation and immune responses that lead to periodontitis, which can cause tooth loss; and the development and progression of oral cancers.

"What's most exciting is the possibility of screening for many of these potential oral health problems from an early age so that we can prevent them or reduce their impact."

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The full paper can be found at the Australian Dental Journal's website.

Pulling problem teeth before heart surgery to prevent infection may be catch-22

Patients with dental extractions before cardiac surgery still at risk for poor outcomes, study finds

To pull or not to pull? That is a common question when patients have the potentially dangerous combination of abscessed or infected teeth and the need for heart surgery. In such cases, problem teeth often are removed before surgery, to reduce the risk of infections including endocarditis, an infection of the inner lining of the heart that can prove deadly. But Mayo Clinic research suggests it may not be as simple as pulling teeth: The study found that roughly 1 in 10 heart surgery patients who had troublesome teeth extracted before surgery died or had adverse outcomes such as a stroke or kidney failure.

The findings are published in The Annals of Thoracic Surgery.

Prosthetic heart valve-related endocarditis accounts for up to one-fourth of infective endocarditis cases and proves fatal for up to 38 percent of patients who develop it. In light of that high mortality rate, physicians try to address risk factors such as poor dental health before cardiac surgery. Removing diseased teeth at some point before surgery as a preventive measure is common, but research on whether that helps has been limited. Medical guidelines acknowledge a lack of conclusive evidence, the Mayo researchers noted.

The new study shows that the risk for patients who do have teeth removed before heart surgery "may be higher than we thought," says senior author Kendra Grim, M.D., a Mayo Clinic anesthesiologist.

"We are always concerned with improving safety, and pulling infected teeth before heart surgery seemed to be the safer intervention. But we became interested in studying this complex patient group, as many patients that come to the operating room for dental surgery just before heart surgery are quite ill," Dr. Grim says.

The study is believed to be the largest so far evaluating adverse outcomes after pre-cardiac surgery dental extractions. The researchers studied outcomes in 205 adult Mayo patients who had teeth pulled before cardiovascular surgery. The study covered January 1, 2003, through Feb. 28, 2013; 80 percent of the patients were men, the median age at the time of tooth extraction was 62, and the median time lapse between dental extraction and heart surgery was seven days. The research found:

Six patients, or 3 percent, died in the period between their tooth extraction and the planned cardiac procedure.

Another six died after heart surgery, all while still hospitalized.

Ten patients, or roughly 5 percent, had other major adverse outcomes after heart surgery, such as bleeding, stroke, kidney failure requiring dialysis, acute coronary syndrome or stroke-like transient ischemic attacks.

Due to unexpected complications or findings from dental surgery, at least 14 patients, or 7 percent, had to have heart surgery delayed.

More information is needed to understand why patients died or had other major adverse outcomes, the researchers say. In addition to the stress placed on the body by dental extraction and heart surgery themselves, potential factors include the severity of individual patients' heart disease, other serious health problems they may have had, and how they reacted to anesthesia.

The bottom line for patients and physicians, the researchers conclude: Rather than following a rule of thumb, physicians should evaluate each patient individually to weigh the possible benefit of tooth extraction before heart surgery against the risk of death and other major adverse events.

"We hope this study sparks future discussion and research," Dr. Grim says. "In the meantime, we recommend an individualized approach for these patients, to weigh their particular risk and benefit of a dental procedure before cardiac surgery with the information we have currently available."

Two bacteria prevalent in gum disease incite the growth of deadly Kaposi's sarcoma-related (KS) lesions and tumors in the mouth

Researchers from Case Western Reserve University have discovered how byproducts in the form of small fatty acids from two bacteria prevalent in gum disease incite the growth of deadly Kaposi's sarcoma-related (KS) lesions and tumors in the mouth.

The discovery could lead to early saliva testing for the bacteria, which, if found, could be treated and monitored for signs of cancer and before it develops into a malignancy, researchers say.

"These new findings provide one of the first looks at how the periodontal bacteria create a unique microenvironment in the oral cavity that contributes to the replication the Kaposi's sarcoma Herpesvirus (KSHV) and development of KS," said Fengchun Ye, the study's lead investigator from Case Western Reserve School of Dental Medicine's Department of Biological Sciences.

The discovery is described in The Journal of Virology article, "Short Chain Fatty Acids from Periodontal Pathogens Suppress HDACs, EZH2, and SUV39H1 to Promote Kaposi's Sarcoma-Associated Herpesvirus Replication."

The research focuses on how the bacteria, Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn), which are associated with gum disease, contribute to cancer formation.

Ye said high levels of these bacteria are found in the saliva of people with periodontal disease, and at lower levels in those with good oral health -- further evidence of the link between oral and overall physical health.

KS impacts a significant number of people with HIV, whose immune systems lack the ability to fight off the herpesvirus and other infections, he said.

"These individual are susceptible to the cancer," Ye said.

KS first appears as lesions on the surface of the mouth that, if not removed, can grow into malignant tumors. Survival rates are higher when detected and treated early in the lesion state than when a malignancy develops.

Also at risk are people with compromised immune systems: people on medications to suppress rejection of transplants, cancer patients on chemotherapies and the elderly population whose immune systems naturally weaken with age.

The researchers wanted to learn why most people never develop this form of cancer and what it is that protects them.

The researchers recruited 21 patients, dividing them into two groups. All participants were given standard gum-disease tests.

The first group of 11 participants had an average age of 50 and had severe chronic gum disease. The second group of 10 participants, whose average age was about 26, had healthy gums, practiced good oral health and showed no signs of bleeding or tooth loss from periodontal disease.

The researchers also studied a saliva sample from each. Part of the saliva sample was separated into its components using a spinning centrifuge. The remaining saliva was used for DNA testing to track and identify bacteria present, and at what levels.

The researchers were interested in Pg's and Fn's byproducts of lipopolysaccharide, fimbriae, proteinases and at least five different short-chain fatty acids (SCFA): butyric acid, isobutryic acid, isovaleric acid, propionic acid and acetic acid.

After initially testing the byproducts, the researchers suspected that the fatty acids were involved in replicating KSHV. The researchers cleansed the fatty acids and then introduced them to cells with quiescent KSHV virus in a petri dish for monitoring the virus' reaction.

After introducing SCFA, the virus began to replicate. But the researchers saw that, while the fatty acids allowed the virus to multiple, the process also set in motion a cascade of actions that also inhibited molecules in the body's immune system from stopping the growth of KSHV.

"The most important thing to come out of this study is that we believe periodontal disease is a risk factor for Kaposi sarcoma tumor in HIV patients," Ye said.

With that knowledge, Ye said those with HIV must be informed about the importance of good oral health and the possible consequences of overlooking that area.