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It is known that teeth can protect themselves, to some extent, from attack by bacteria but that inflammation within a tooth can be damaging and, in extreme cases, lead to abscess or death of the tooth. New research published in BioMed Central's open access journal BMC Immunology shows that odontoblast cells are part of the immune system and fight to protect teeth from decay.
Inside a tooth odontoblast cells sit between the enamel and pulp and produce a layer of dentin to protect the pulp from wear and infection. This research shows that, when under attack from bacteria, the odontoblast cells also orchestrate an immune response, producing antimicrobial peptides (β-defensins) to fight the infection directly, protein messengers (chemokines) which recruit white blood cells to the site of infection, and pro-inflammatory signalling proteins (IL-1β, IL-1α, and TNF-α) which, in turn, initiate an inflammatory response.
Dr Orapin Horst also found that the odontoblast layer produced proteins involved in the down-regulation of this inflammatory response, such as toll-interacting protein (TOLLIP), TGF-β, and IL-10, which help protect the underlying pulp from inflammatory damage.
Dr Horst says that "For the first time we now have targets to control irreversible inflammatory damage to teeth."
Monday, January 24, 2011
Tuesday, January 18, 2011
Healthy gums may lead to healthy lungs
Maintaining healthy teeth and gums may reduce risk for pneumonia, chronic obstructive pumonary disease
Maintaining periodontal health may contribute to a healthy respiratory system, according to research published in the Journal of Periodontology. A new study suggests that periodontal disease may increase the risk for respiratory infections, such as chronic obstructive pulmonary disease (COPD) and pneumonia. These infections, which are caused when bacteria from the upper throat are inhaled into the lower respiratory tract, can be severely debilitating and are one of the leading causes of death in the U.S.
The study included 200 participants between the ages of 20 and 60 with at least 20 natural teeth. Half of the participants were hospitalized patients with a respiratory disease such as pneumonia, COPD, or acute bronchitis, and the other half were healthy control subjects with no history of respiratory disease. Each participant underwent a comprehensive oral evaluation to measure periodontal health status.
The study found that patients with respiratory diseases had worse periodontal health than the control group, suggesting a relationship between respiratory disease and periodontal disease. Researchers suspect that the presence of oral pathogens associated with periodontal disease may increase a patient's risk of developing or exacerbating respiratory disease. However, the study authors note that additional studies are needed to more conclusively understand this link.
"Pulmonary diseases can be severely disabling and debilitating," says Donald S. Clem, DDS, President of the American Academy of Periodontology. "By working with your dentist or periodontist, you may actually be able to prevent or diminish the progression of harmful diseases such as pneumonia or COPD. This study provides yet another example of how periodontal health plays a role in keeping other systems of the body healthy."
Periodontal disease is a chronic inflammatory disease that affects the gum tissue and other structures supporting the teeth. Previous research has associated gum disease with other chronic inflammatory diseases such as diabetes, cardiovascular disease, and rheumatoid arthritis.
Dr. Clem stressed the importance of routine oral care in helping to prevent periodontal disease. "Taking good care of your periodontal health involves daily tooth brushing and flossing. You should also expect to get a comprehensive periodontal evaluation every year," he advised. A dental professional, such as a periodontist, a specialist in the diagnosis, treatment and prevention of gum disease, can conduct a comprehensive exam to assess your periodontal disease status.
Maintaining periodontal health may contribute to a healthy respiratory system, according to research published in the Journal of Periodontology. A new study suggests that periodontal disease may increase the risk for respiratory infections, such as chronic obstructive pulmonary disease (COPD) and pneumonia. These infections, which are caused when bacteria from the upper throat are inhaled into the lower respiratory tract, can be severely debilitating and are one of the leading causes of death in the U.S.
The study included 200 participants between the ages of 20 and 60 with at least 20 natural teeth. Half of the participants were hospitalized patients with a respiratory disease such as pneumonia, COPD, or acute bronchitis, and the other half were healthy control subjects with no history of respiratory disease. Each participant underwent a comprehensive oral evaluation to measure periodontal health status.
The study found that patients with respiratory diseases had worse periodontal health than the control group, suggesting a relationship between respiratory disease and periodontal disease. Researchers suspect that the presence of oral pathogens associated with periodontal disease may increase a patient's risk of developing or exacerbating respiratory disease. However, the study authors note that additional studies are needed to more conclusively understand this link.
"Pulmonary diseases can be severely disabling and debilitating," says Donald S. Clem, DDS, President of the American Academy of Periodontology. "By working with your dentist or periodontist, you may actually be able to prevent or diminish the progression of harmful diseases such as pneumonia or COPD. This study provides yet another example of how periodontal health plays a role in keeping other systems of the body healthy."
Periodontal disease is a chronic inflammatory disease that affects the gum tissue and other structures supporting the teeth. Previous research has associated gum disease with other chronic inflammatory diseases such as diabetes, cardiovascular disease, and rheumatoid arthritis.
Dr. Clem stressed the importance of routine oral care in helping to prevent periodontal disease. "Taking good care of your periodontal health involves daily tooth brushing and flossing. You should also expect to get a comprehensive periodontal evaluation every year," he advised. A dental professional, such as a periodontist, a specialist in the diagnosis, treatment and prevention of gum disease, can conduct a comprehensive exam to assess your periodontal disease status.
Monday, January 10, 2011
New device set to combat fear of the dentist's drill
An innovative device which cancels out the noise of the dental drill could spell the end of people's anxiety about trips to the dentist, according to experts at King's College London, Brunel University and London South Bank University, who pioneered the invention.
It is widely known that the sound of the dental drill is the prime cause of anxiety about dental treatment, and some patients avoid trips to the dentist because of it. This new device could help address people's fears and encourage them to seek the oral healthcare treatment they need.
The prototype device works in a similar way to noise-cancelling headphones but is designed to deal with the very high pitch of the dental drill. Patients would simply unplug their headphones, plug the device into their MP3 player or mobile phone, and then plug the headphones into the device, allowing them to listen to their own music while completely blocking out the unpleasant sound of the drill and suction equipment. The patient can still hear the dentist and other members of the dental team speaking to them but other unwanted sounds are filtered out by the device.
Containing a microphone and a chip that analyses the incoming sound wave, the device produces an inverted wave to cancel out unwanted noise. It also uses technology called 'adaptive filtering' where electronic filters lock onto sound waves and removes them, even if the amplitude and frequency change as the drill is being used.
The device was initially the brainchild of Professor Brian Millar at King's College London's Dental Institute who was inspired initially by carmaker Lotus' efforts to develop a system that removed unpleasant road noise, while still allowing drivers to hear emergency sirens. Then with over a decade of collaboration with engineering researchers at Brunel University and London South Bank University, a prototype has been designed, built and successfully evaluated.
Although the product is not yet available to dental practitioners, King's is calling for an investor to help bring it to market. Professor Brian Millar said: "Many people put off going to the dentist because of anxiety associated with the noise of the dentist's drill. But this device has the potential to make fear of the drill a thing of the past.
"The beauty of this gadget is that it would be fairly cost-effective for dentists to buy, and any patient with an MP3 player would be able to benefit from it, at no extra cost. What we need now is an investor to develop the product further, to enable us to bring this device to as many dental surgeries as possible, and help people whose fear of visiting the dentist stops them from seeking the oral healthcare they need."
It is widely known that the sound of the dental drill is the prime cause of anxiety about dental treatment, and some patients avoid trips to the dentist because of it. This new device could help address people's fears and encourage them to seek the oral healthcare treatment they need.
The prototype device works in a similar way to noise-cancelling headphones but is designed to deal with the very high pitch of the dental drill. Patients would simply unplug their headphones, plug the device into their MP3 player or mobile phone, and then plug the headphones into the device, allowing them to listen to their own music while completely blocking out the unpleasant sound of the drill and suction equipment. The patient can still hear the dentist and other members of the dental team speaking to them but other unwanted sounds are filtered out by the device.
Containing a microphone and a chip that analyses the incoming sound wave, the device produces an inverted wave to cancel out unwanted noise. It also uses technology called 'adaptive filtering' where electronic filters lock onto sound waves and removes them, even if the amplitude and frequency change as the drill is being used.
The device was initially the brainchild of Professor Brian Millar at King's College London's Dental Institute who was inspired initially by carmaker Lotus' efforts to develop a system that removed unpleasant road noise, while still allowing drivers to hear emergency sirens. Then with over a decade of collaboration with engineering researchers at Brunel University and London South Bank University, a prototype has been designed, built and successfully evaluated.
Although the product is not yet available to dental practitioners, King's is calling for an investor to help bring it to market. Professor Brian Millar said: "Many people put off going to the dentist because of anxiety associated with the noise of the dentist's drill. But this device has the potential to make fear of the drill a thing of the past.
"The beauty of this gadget is that it would be fairly cost-effective for dentists to buy, and any patient with an MP3 player would be able to benefit from it, at no extra cost. What we need now is an investor to develop the product further, to enable us to bring this device to as many dental surgeries as possible, and help people whose fear of visiting the dentist stops them from seeking the oral healthcare they need."
HHS and EPA announce new scientific assessments and actions on fluoride
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Agencies working together to maintain benefits of preventing tooth decay
while preventing excessive exposure
The U.S. Department of Health and Human Services (HHS) and the U.S. Environmental Protection Agency (EPA) today are announcing important steps to ensure that standards and guidelines on fluoride in drinking water continue to provide the maximum protection to the American people to support good dental health, especially in children. HHS is proposing that the recommended level of fluoride in drinking water can be set at the lowest end of the current optimal range to prevent tooth decay, and EPA is initiating review of the maximum amount of fluoride allowed in drinking water.
These actions will maximize the health benefits of water fluoridation, an important tool in the prevention of tooth decay while reducing the possibility of children receiving too much fluoride. The Centers for Disease Control and Prevention named the fluoridation of drinking water one of the ten great public health achievements of the 20th century.
“One of water fluoridation’s biggest advantages is that it benefits all residents of a community—at home, work, school, or play,” said HHS Assistant Secretary for Health Howard K. Koh, MD, MPH. “Today’s announcement is part of our ongoing support of appropriate fluoridation for community water systems, and its effectiveness in preventing tooth decay throughout one’s lifetime.”
“Today both HHS and EPA are making announcements on fluoride based on the most up to date scientific data,” said EPA Assistant Administrator for the Office of Water, Peter Silva. “EPA’s new analysis will help us make sure that people benefit from tooth decay prevention while at the same time avoiding the unwanted health effects from too much fluoride.”
HHS and EPA reached an understanding of the latest science on fluoride and its effect on tooth decay prevention and the development of dental fluorosis that may occur with excess fluoride consumption during the tooth forming years, age 8 and younger. Dental fluorosis in the United States appears mostly in the very mild or mild form – as barely visible lacy white markings or spots on the enamel. The severe form of dental fluorosis, with staining and pitting of the tooth surface, is rare in the United States.
There are several reasons for the changes seen over time, including that Americans have access to more sources of fluoride than they did when water fluoridation was first introduced in the United States in the 1940s. Water is now one of several sources of fluoride. Other common sources include dental products such as toothpaste and mouth rinses, prescription fluoride supplements, and fluoride applied by dental professionals. Water fluoridation and fluoride toothpaste are largely responsible for the significant decline in tooth decay in the U.S. over the past several decades.
HHS’ proposed recommendation of 0.7 milligrams of fluoride per liter of water replaces the current recommended range of 0.7 to 1.2 milligrams. This updated recommendation is based on recent EPA and HHS scientific assessments to balance the benefits of preventing tooth decay while limiting any unwanted health effects. These scientific assessments will also guide EPA in making a determination of whether to lower the maximum amount of fluoride allowed in drinking water, which is set to prevent adverse health effects.
The new EPA assessments of fluoride were undertaken in response to findings of the National Academies of Science (NAS). At EPA’s request, in 2006 NAS reviewed new data on fluoride and issued a report recommending that EPA update its health and exposure assessments to take into account bone and dental effects and to consider all sources of fluoride. In addition to EPA’s new assessments and the NAS report, HHS also considered current levels of tooth decay and dental fluorosis and fluid consumption across the United States.
The notice of the proposed recommendation will be published in the Federal Register soon and HHS will accept comments from the public and stakeholders on the proposed recommendation for 30 days at CWFcomments@cdc.gov. HHS is expecting to publish final guidance for community water fluoridation by spring 2011. You may view a prepublication version of the proposed recommendation at http://www.hhs.gov/news/press/2011pres/01/pre_pub_frn_fluoride.html. Comments regarding the EPA documents, Fluoride: Dose-Response Analysis For Non-cancer Effects and Fluoride: Exposure and Relative Source Contribution Analysis should be sent to EPA at FluorideScience@epa.gov. The documents can be found at http://water.epa.gov/action/advisories/drinking/fluoride_index.cfm
For more information about community water fluoridation, as well as information for health care providers and individuals on how to prevent tooth decay and reduce the chance of children developing dental fluorosis, visit http://www.cdc.gov/fluoridation. For information about the national drinking water regulations for fluoride, visit: http://water.epa.gov/drink/contaminants/basicinformation/fluoride.cfm
Agencies working together to maintain benefits of preventing tooth decay
while preventing excessive exposure
The U.S. Department of Health and Human Services (HHS) and the U.S. Environmental Protection Agency (EPA) today are announcing important steps to ensure that standards and guidelines on fluoride in drinking water continue to provide the maximum protection to the American people to support good dental health, especially in children. HHS is proposing that the recommended level of fluoride in drinking water can be set at the lowest end of the current optimal range to prevent tooth decay, and EPA is initiating review of the maximum amount of fluoride allowed in drinking water.
These actions will maximize the health benefits of water fluoridation, an important tool in the prevention of tooth decay while reducing the possibility of children receiving too much fluoride. The Centers for Disease Control and Prevention named the fluoridation of drinking water one of the ten great public health achievements of the 20th century.
“One of water fluoridation’s biggest advantages is that it benefits all residents of a community—at home, work, school, or play,” said HHS Assistant Secretary for Health Howard K. Koh, MD, MPH. “Today’s announcement is part of our ongoing support of appropriate fluoridation for community water systems, and its effectiveness in preventing tooth decay throughout one’s lifetime.”
“Today both HHS and EPA are making announcements on fluoride based on the most up to date scientific data,” said EPA Assistant Administrator for the Office of Water, Peter Silva. “EPA’s new analysis will help us make sure that people benefit from tooth decay prevention while at the same time avoiding the unwanted health effects from too much fluoride.”
HHS and EPA reached an understanding of the latest science on fluoride and its effect on tooth decay prevention and the development of dental fluorosis that may occur with excess fluoride consumption during the tooth forming years, age 8 and younger. Dental fluorosis in the United States appears mostly in the very mild or mild form – as barely visible lacy white markings or spots on the enamel. The severe form of dental fluorosis, with staining and pitting of the tooth surface, is rare in the United States.
There are several reasons for the changes seen over time, including that Americans have access to more sources of fluoride than they did when water fluoridation was first introduced in the United States in the 1940s. Water is now one of several sources of fluoride. Other common sources include dental products such as toothpaste and mouth rinses, prescription fluoride supplements, and fluoride applied by dental professionals. Water fluoridation and fluoride toothpaste are largely responsible for the significant decline in tooth decay in the U.S. over the past several decades.
HHS’ proposed recommendation of 0.7 milligrams of fluoride per liter of water replaces the current recommended range of 0.7 to 1.2 milligrams. This updated recommendation is based on recent EPA and HHS scientific assessments to balance the benefits of preventing tooth decay while limiting any unwanted health effects. These scientific assessments will also guide EPA in making a determination of whether to lower the maximum amount of fluoride allowed in drinking water, which is set to prevent adverse health effects.
The new EPA assessments of fluoride were undertaken in response to findings of the National Academies of Science (NAS). At EPA’s request, in 2006 NAS reviewed new data on fluoride and issued a report recommending that EPA update its health and exposure assessments to take into account bone and dental effects and to consider all sources of fluoride. In addition to EPA’s new assessments and the NAS report, HHS also considered current levels of tooth decay and dental fluorosis and fluid consumption across the United States.
The notice of the proposed recommendation will be published in the Federal Register soon and HHS will accept comments from the public and stakeholders on the proposed recommendation for 30 days at CWFcomments@cdc.gov. HHS is expecting to publish final guidance for community water fluoridation by spring 2011. You may view a prepublication version of the proposed recommendation at http://www.hhs.gov/news/press/2011pres/01/pre_pub_frn_fluoride.html. Comments regarding the EPA documents, Fluoride: Dose-Response Analysis For Non-cancer Effects and Fluoride: Exposure and Relative Source Contribution Analysis should be sent to EPA at FluorideScience@epa.gov. The documents can be found at http://water.epa.gov/action/advisories/drinking/fluoride_index.cfm
For more information about community water fluoridation, as well as information for health care providers and individuals on how to prevent tooth decay and reduce the chance of children developing dental fluorosis, visit http://www.cdc.gov/fluoridation. For information about the national drinking water regulations for fluoride, visit: http://water.epa.gov/drink/contaminants/basicinformation/fluoride.cfm
Tuesday, January 4, 2011
Porphyromonas gingivalis accelerates inflammatory atherosclerosis
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Atherosclerosis is the leading cause of death in the developed world. While a number of risk factors for atherosclerosis have been defined, scientists continue to study other possible risk factors for this disease. Recent epidemiological and experimental studies link infectious agents with the development of inflammatory atherosclerosis. A hallmark of chronic infection with the oral pathogen Porphyromonas gingivalis is the induction of a chronic inflammatory response. P. gingivalis induces a local inflammatory response that results in oral bone destruction, which is manifested as periodontal disease, an inflammatory disease that affects approximately 100 million people in the US. In addition to chronic inflammation at the initial site of infection, mounting evidence has accumulated supporting a role for P. gingivalis-mediated periodontal disease as a risk factor for systemic diseases including, diabetes, pre-term birth, stroke, and atherosclerotic cardiovascular disease.
In new studies Dr. Caroline Genco together with Dr. James Hamilton at Boston University School of Medicine have begun to define the precise mechanisms contributing to the link between infection with P. gingivalis and atherosclerotic disease. In elegant studies recently published (Atherosclerosis-12-22-10 online publication date) these investigators report on in-vivo high-resolution magnetic resonance imaging (MRI) to document P. gingivalis mediated inflammation and atherosclerosis in a mouse model. MRI is a novel modality that allows for detailed studies of atherosclerosis progression in the same animal that can depict the narrowing of the arterial lumen and small vessel wall areas. Genco and collogues demonstrate that P. gingivalis infection accelerates inflammation and atherosclerosis in the innominate artery, an artery that has a high degree of lesion progression. Lesions in the innominate artery express features characteristic of clinical disease in humans including vessel narrowing characterized by atrophic media and perivascular inflammation and plaque disruption. Plaque rupture is the basis for the coronary thrombosis in acute ischemia. In humans, plaques with extensive macrophage accumulation and inflammation have a greater likelihood of disruption at their luminal surface, and formation of a life-threatening thrombus. Genco's studies are the first to demonstrate progression of plaque in the innominate arteries by in-vivo MRI, and lipid and immunohistochemical analysis following exposure to an infectious agent, and to document protection from plaque progression via immunization. An important question is whether P. gingivalis accelerates atherosclerotic plaque formation in the innominate artery leading to increased numbers of vulnerable plaques, and possibly enhanced plaque rupture. Future studies will explore this possibility as well as the testing of new therapeutic strategies to prevent infection induced atherosclerotic disease.
Atherosclerosis is the leading cause of death in the developed world. While a number of risk factors for atherosclerosis have been defined, scientists continue to study other possible risk factors for this disease. Recent epidemiological and experimental studies link infectious agents with the development of inflammatory atherosclerosis. A hallmark of chronic infection with the oral pathogen Porphyromonas gingivalis is the induction of a chronic inflammatory response. P. gingivalis induces a local inflammatory response that results in oral bone destruction, which is manifested as periodontal disease, an inflammatory disease that affects approximately 100 million people in the US. In addition to chronic inflammation at the initial site of infection, mounting evidence has accumulated supporting a role for P. gingivalis-mediated periodontal disease as a risk factor for systemic diseases including, diabetes, pre-term birth, stroke, and atherosclerotic cardiovascular disease.
In new studies Dr. Caroline Genco together with Dr. James Hamilton at Boston University School of Medicine have begun to define the precise mechanisms contributing to the link between infection with P. gingivalis and atherosclerotic disease. In elegant studies recently published (Atherosclerosis-12-22-10 online publication date) these investigators report on in-vivo high-resolution magnetic resonance imaging (MRI) to document P. gingivalis mediated inflammation and atherosclerosis in a mouse model. MRI is a novel modality that allows for detailed studies of atherosclerosis progression in the same animal that can depict the narrowing of the arterial lumen and small vessel wall areas. Genco and collogues demonstrate that P. gingivalis infection accelerates inflammation and atherosclerosis in the innominate artery, an artery that has a high degree of lesion progression. Lesions in the innominate artery express features characteristic of clinical disease in humans including vessel narrowing characterized by atrophic media and perivascular inflammation and plaque disruption. Plaque rupture is the basis for the coronary thrombosis in acute ischemia. In humans, plaques with extensive macrophage accumulation and inflammation have a greater likelihood of disruption at their luminal surface, and formation of a life-threatening thrombus. Genco's studies are the first to demonstrate progression of plaque in the innominate arteries by in-vivo MRI, and lipid and immunohistochemical analysis following exposure to an infectious agent, and to document protection from plaque progression via immunization. An important question is whether P. gingivalis accelerates atherosclerotic plaque formation in the innominate artery leading to increased numbers of vulnerable plaques, and possibly enhanced plaque rupture. Future studies will explore this possibility as well as the testing of new therapeutic strategies to prevent infection induced atherosclerotic disease.
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