Injectable progesterone contraceptives may be associated with poor periodontal health, according to research in the Journal of Periodontology. The study found that women who are currently taking depotmedroxyprogesterone acetate (DMPA) injectable contraceptive, or have taken DMPA in the past, are more likely to have indicators of poor periodontal health, including gingivitis and periodontitis, than women who have never taken the injectable contraceptive. DMPA is a long-lasting progestin-only injectable contraceptive administered intermuscularly every three months.
Periodontal disease is a chronic inflammatory disease that affects the gum tissue and bone that supports the teeth. Gingivitis, the mildest form of gum disease, causes the gums to become red, swollen, and bleed easily. Periodontitis is the most severe form of gum disease and can lead to tooth loss. Additionally, research has associated gum disease with other chronic inflammatory diseases such as diabetes, cardiovascular disease, and rheumatoid arthritis.
The data for this study were obtained from the NHANES 1999-2004 public use datasets. The participants chosen were non-pregnant, premenopausal women aged 15-44 who had provided complete DMPA usage data, indicating current usage of DMPA, past usage of DMPA, or no usage of DMPA at all. All participants received a dental examination that noted clinical attachment (CA) loss, periodontal pocket assessment at two or three sites per tooth, and presence of gingival bleeding.
After adjusting for age, race, education, poverty income level, and smoking status, the study found that current and past DMPA users had significantly increased periodontal pockets, gingival bleeding, and CA loss than women who have never used DMPA. Current DMPA users were more likely to have gingivitis, while past DMPA users were more likely to have periodontitis.
According to Dr. Pamela McClain, President of the American Academy of Periodontology (AAP) and a practicing periodontist in Aurora, Colorado, women currently taking DMPA or that have used DMPA in the past should pay careful attention to their teeth and gums. "Hormones can play a role in woman's periodontal health. These findings suggest that women that use, or have used, a hormone-based injectable contraception such as DMPA may have increased odds of poor periodontal health. I would encourage women that use or previously used this form of contraception to maintain excellent oral care, and to be sure to see a dental professional for a comprehensive periodontal evaluation on an annual basis."
Monday, February 6, 2012
Friday, January 27, 2012
Study Pinpoints Genetic Variation that Raises Risk of Serious Complication Linked to Osteoporosis Drugs
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Researchers at the Columbia University College of Dental Medicine have identified a genetic variation that raises the risk of developing serious necrotic jaw bone lesions in patients who take bisphosphonates, a common class of osteoclastic inhibitors. The discovery paves the way for a genetic screening test to determine who can safely take these drugs. The study appears in the online version of the journal The Oncologist.
Oral bisphosphonates are currently taken by some 3 million women in the United States for the prevention or treatment of osteoporosis. In addition, intravenous bisphosphonates are given to thousands of cancer patients each year to control the spread of bone cancer and prevent excess calcium (hypercalcemia) from accumulating in the blood. Bisphosphonates work by binding to calcium in the bone and inhibiting osteoclasts, bone cells that break down the bone’s mineral structure.
“These drugs have been widely used for years and are generally considered safe and effective,” said study leader Athanasios I. Zavras, DMD, MS, DMSc, associate professor of Dentistry and Epidemiology and Director of the Division of Oral Epidemiology & Biostatistics at the Columbia University College of Dental Medicine. “But the popular literature and blogs are filled with stories of patients on prolonged bisphosphonate therapy who were trying to control osteoporosis or hypercalcemia only to develop osteonecrosis of the jaw.”
Osteonecrosis of the jaw, or ONJ, often leads to painful and hard-to-treat bone lesions, which can eventually lead to loss of the entire jaw. Among people taking bisphosphonates, ONJ tends to occur in those with dental disease or those who undergo invasive dental procedures.
There are no reliable figures on the incidence of ONJ in patients taking oral bisphosphonates. Estimates range from 1 in 1,000 to 1 in 100,000 patients for each year of exposure to the medication, according to the American College of Rheumatology. ONJ is more common among cancer patients taking the intravenous form of the drug, affecting about 5 to 10 percent of these individuals, noted Dr. Zavras.
Studies have suggested that genetic factors play a major role in predisposing patients to ONJ.
Delving deeper into this question, Dr. Zavras and his colleagues performed genome-wide analyses of 30 patients who were taking bisphosphonates and had developed ONJ and compared them with several bisphosphonate users who were disease free.
The researchers found that patients who had a small variation in the RBMS3 gene were 5.8 times more likely to develop ONJ than those without the variation. The study also identified small variations in two other genes, IGFBP7 and ABCC4, that may contribute to ONJ risk.
“Our ultimate goal is to develop a pharmacogenetic test that personalizes risk assessment for ONJ, a test that you could give to people before they start to use bisphosphonates,” said Dr. Zavras. “Those who are positive for this genetic variation would select some other treatment, while those who are negative could take these medications with little fear of developing ONJ.”
“At the moment, many women discontinue or avoid treatment for serious osteoporosis because they are afraid of losing their jaw bones,” added Dr. Zavras. “There even are reports of dentists who have refused to perform certain invasive procedures in patients taking bisphosphonates. So there is a great need for a pharmacogenetic screening test to determine which patients are really at risk for ONJ.”
The current study looked only at Caucasians. Further studies are needed to determine whether the RBMS3 gene variation is seen in other racial groups, according to the researchers.
The paper is entitled, “Genome-wide pharmacogenetics of bisphosphonate-induced osteonecrosis of the jaw: the role of RBMS3.”
Researchers at the Columbia University College of Dental Medicine have identified a genetic variation that raises the risk of developing serious necrotic jaw bone lesions in patients who take bisphosphonates, a common class of osteoclastic inhibitors. The discovery paves the way for a genetic screening test to determine who can safely take these drugs. The study appears in the online version of the journal The Oncologist.
Oral bisphosphonates are currently taken by some 3 million women in the United States for the prevention or treatment of osteoporosis. In addition, intravenous bisphosphonates are given to thousands of cancer patients each year to control the spread of bone cancer and prevent excess calcium (hypercalcemia) from accumulating in the blood. Bisphosphonates work by binding to calcium in the bone and inhibiting osteoclasts, bone cells that break down the bone’s mineral structure.
“These drugs have been widely used for years and are generally considered safe and effective,” said study leader Athanasios I. Zavras, DMD, MS, DMSc, associate professor of Dentistry and Epidemiology and Director of the Division of Oral Epidemiology & Biostatistics at the Columbia University College of Dental Medicine. “But the popular literature and blogs are filled with stories of patients on prolonged bisphosphonate therapy who were trying to control osteoporosis or hypercalcemia only to develop osteonecrosis of the jaw.”
Osteonecrosis of the jaw, or ONJ, often leads to painful and hard-to-treat bone lesions, which can eventually lead to loss of the entire jaw. Among people taking bisphosphonates, ONJ tends to occur in those with dental disease or those who undergo invasive dental procedures.
There are no reliable figures on the incidence of ONJ in patients taking oral bisphosphonates. Estimates range from 1 in 1,000 to 1 in 100,000 patients for each year of exposure to the medication, according to the American College of Rheumatology. ONJ is more common among cancer patients taking the intravenous form of the drug, affecting about 5 to 10 percent of these individuals, noted Dr. Zavras.
Studies have suggested that genetic factors play a major role in predisposing patients to ONJ.
Delving deeper into this question, Dr. Zavras and his colleagues performed genome-wide analyses of 30 patients who were taking bisphosphonates and had developed ONJ and compared them with several bisphosphonate users who were disease free.
The researchers found that patients who had a small variation in the RBMS3 gene were 5.8 times more likely to develop ONJ than those without the variation. The study also identified small variations in two other genes, IGFBP7 and ABCC4, that may contribute to ONJ risk.
“Our ultimate goal is to develop a pharmacogenetic test that personalizes risk assessment for ONJ, a test that you could give to people before they start to use bisphosphonates,” said Dr. Zavras. “Those who are positive for this genetic variation would select some other treatment, while those who are negative could take these medications with little fear of developing ONJ.”
“At the moment, many women discontinue or avoid treatment for serious osteoporosis because they are afraid of losing their jaw bones,” added Dr. Zavras. “There even are reports of dentists who have refused to perform certain invasive procedures in patients taking bisphosphonates. So there is a great need for a pharmacogenetic screening test to determine which patients are really at risk for ONJ.”
The current study looked only at Caucasians. Further studies are needed to determine whether the RBMS3 gene variation is seen in other racial groups, according to the researchers.
The paper is entitled, “Genome-wide pharmacogenetics of bisphosphonate-induced osteonecrosis of the jaw: the role of RBMS3.”
Wednesday, January 4, 2012
Dried licorice root fights the bacteria that cause tooth decay and gum disease
Scientists are reporting identification of two substances in licorice — used extensively in Chinese traditional medicine — that kill the major bacteria responsible for tooth decay and gum disease, the leading causes of tooth loss in children and adults. In a study in ACS' Journal of Natural Products, they say that these substances could have a role in treating and preventing tooth decay and gum disease.
Stefan Gafner and colleagues explain that the dried root of the licorice plant is a common treatment in Chinese traditional medicine, especially as a way to enhance the activity of other herbal ingredients or as a flavoring. Despite the popularity of licorice candy in the U.S., licorice root has been replaced in domestic candy with anise oil, which has a similar flavor. Traditional medical practitioners use dried licorice root to treat various ailments, such as respiratory and digestive problems, but few modern scientific studies address whether licorice really works. (Consumers should check with their health care provider before taking licorice root because it can have undesirable effects and interactions with prescription drugs.) To test whether the sweet root could combat the bacteria that cause gum disease and cavities, the researchers took a closer look at various substances in licorice.
They found that two of the licorice compounds, licoricidin and licorisoflavan A, were the most effective antibacterial substances. These substances killed two of the major bacteria responsible for dental cavities and two of the bacteria that promote gum disease. One of the compounds — licoricidin — also killed a third gum disease bacterium. The researchers say that these substances could treat or even prevent oral infections.
Stefan Gafner and colleagues explain that the dried root of the licorice plant is a common treatment in Chinese traditional medicine, especially as a way to enhance the activity of other herbal ingredients or as a flavoring. Despite the popularity of licorice candy in the U.S., licorice root has been replaced in domestic candy with anise oil, which has a similar flavor. Traditional medical practitioners use dried licorice root to treat various ailments, such as respiratory and digestive problems, but few modern scientific studies address whether licorice really works. (Consumers should check with their health care provider before taking licorice root because it can have undesirable effects and interactions with prescription drugs.) To test whether the sweet root could combat the bacteria that cause gum disease and cavities, the researchers took a closer look at various substances in licorice.
They found that two of the licorice compounds, licoricidin and licorisoflavan A, were the most effective antibacterial substances. These substances killed two of the major bacteria responsible for dental cavities and two of the bacteria that promote gum disease. One of the compounds — licoricidin — also killed a third gum disease bacterium. The researchers say that these substances could treat or even prevent oral infections.
Tuesday, December 27, 2011
How Bacteria Fight Fluoride in Toothpaste and in Nature
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Yale researchers have uncovered the molecular tricks used by bacteria to fight the effects of fluoride, which is commonly used in toothpaste and mouthwash to combat tooth decay.
In the Dec. 22 online issue of the journal Science Express, the researchers report that sections of RNA messages called riboswitches -- which control the expression of genes -- detect the build-up of fluoride and activate the defenses of bacteria, including those that contribute to tooth decay.
"These riboswitches are detectors made specifically to see fluoride," said Ronald Breaker, the Henry Ford II Professor and chair of the Department of Molecular, Cellular and Developmental Biology and senior author of the study.
Fluoride in over-the-counter and prescription toothpastes is widely credited with the large reduction in dental cavities seen since these products were made available beginning in the 1950s. This effect is largely caused by fluoride bonding to the enamel of our teeth, which hardens them against the acids produced by bacteria in our mouths. However, it has been known for many decades that fluoride at high concentrations also is toxic to bacteria, causing some researchers to propose that this antibacterial activity also may help prevent cavities.
The riboswitches work to counteract fluoride's effect on bacteria. "If fluoride builds up to toxic levels in the cell, a fluoride riboswitch grabs the fluoride and then turns on genes that can overcome its effects," said Breaker.
Since both fluoride and some RNA sensor molecules are negatively charged, they should not be able to bind, he notes.
"We were stunned when we uncovered fluoride-sensing riboswitches" said Breaker. "Scientists would argue that RNA is the worst molecule to use as a sensor for fluoride, and yet we have found more than 2000 of these strange RNAs in many organisms."
By tracking fluoride riboswitches in numerous species, the research team concluded that these RNAs are ancient -- meaning many organisms have had to overcome toxic levels of fluoride throughout their history. Organisms from at least two branches of the tree of life are using fluoride riboswitches, and the proteins used to combat fluoride toxicity are present in many species from all three branches.
"Cells have had to contend with fluoride toxicity for billions of years, and so they have evolved precise sensors and defense mechanisms to do battle with this ion," said Breaker, who is also an investigator with the Howard Hughes Medical Institute. Now that these sensors and defense mechanisms are known, Breaker said, it may be possible to manipulate these mechanisms and make fluoride even more toxic to bacteria. Fluoride riboswitches and proteins common in bacteria are lacking in humans, and so these fluoride defense systems could be targeted by drugs. For example, the Yale team discovered protein channels that flush fluoride out of cells. Blocking these channels with another molecule would cause fluoride to accumulate in bacteria, making it more effective as a cavity fighter.
Fluoride is the 13th most common element in Earth's crust, and it is naturally present in high concentrations throughout the United States and elsewhere. Its use in toothpaste and its addition to city water supplies across the United States sparked a controversy 60 years ago, and the dispute continues to this day. In the United Kingdom, and in other European Union countries, fluoride is used to a much lesser extent due to fierce public opposition.
The new findings from Yale only reveal how microbes overcome fluoride toxicity. The means by which humans contend with high fluoride levels remains unknown, Breaker notes. He adds that the use of fluoride has had clear benefits for dental health and that these new findings do not indicate that fluoride is unsafe as currently used.
Yale researchers have uncovered the molecular tricks used by bacteria to fight the effects of fluoride, which is commonly used in toothpaste and mouthwash to combat tooth decay.
In the Dec. 22 online issue of the journal Science Express, the researchers report that sections of RNA messages called riboswitches -- which control the expression of genes -- detect the build-up of fluoride and activate the defenses of bacteria, including those that contribute to tooth decay.
"These riboswitches are detectors made specifically to see fluoride," said Ronald Breaker, the Henry Ford II Professor and chair of the Department of Molecular, Cellular and Developmental Biology and senior author of the study.
Fluoride in over-the-counter and prescription toothpastes is widely credited with the large reduction in dental cavities seen since these products were made available beginning in the 1950s. This effect is largely caused by fluoride bonding to the enamel of our teeth, which hardens them against the acids produced by bacteria in our mouths. However, it has been known for many decades that fluoride at high concentrations also is toxic to bacteria, causing some researchers to propose that this antibacterial activity also may help prevent cavities.
The riboswitches work to counteract fluoride's effect on bacteria. "If fluoride builds up to toxic levels in the cell, a fluoride riboswitch grabs the fluoride and then turns on genes that can overcome its effects," said Breaker.
Since both fluoride and some RNA sensor molecules are negatively charged, they should not be able to bind, he notes.
"We were stunned when we uncovered fluoride-sensing riboswitches" said Breaker. "Scientists would argue that RNA is the worst molecule to use as a sensor for fluoride, and yet we have found more than 2000 of these strange RNAs in many organisms."
By tracking fluoride riboswitches in numerous species, the research team concluded that these RNAs are ancient -- meaning many organisms have had to overcome toxic levels of fluoride throughout their history. Organisms from at least two branches of the tree of life are using fluoride riboswitches, and the proteins used to combat fluoride toxicity are present in many species from all three branches.
"Cells have had to contend with fluoride toxicity for billions of years, and so they have evolved precise sensors and defense mechanisms to do battle with this ion," said Breaker, who is also an investigator with the Howard Hughes Medical Institute. Now that these sensors and defense mechanisms are known, Breaker said, it may be possible to manipulate these mechanisms and make fluoride even more toxic to bacteria. Fluoride riboswitches and proteins common in bacteria are lacking in humans, and so these fluoride defense systems could be targeted by drugs. For example, the Yale team discovered protein channels that flush fluoride out of cells. Blocking these channels with another molecule would cause fluoride to accumulate in bacteria, making it more effective as a cavity fighter.
Fluoride is the 13th most common element in Earth's crust, and it is naturally present in high concentrations throughout the United States and elsewhere. Its use in toothpaste and its addition to city water supplies across the United States sparked a controversy 60 years ago, and the dispute continues to this day. In the United Kingdom, and in other European Union countries, fluoride is used to a much lesser extent due to fierce public opposition.
The new findings from Yale only reveal how microbes overcome fluoride toxicity. The means by which humans contend with high fluoride levels remains unknown, Breaker notes. He adds that the use of fluoride has had clear benefits for dental health and that these new findings do not indicate that fluoride is unsafe as currently used.
Saturday, December 17, 2011
Addition of Mannitol Increases Effectiveness of Dental Nerve Block Anesthesia
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Allowing a patient to be comfortable and pain-free during surgical and restorative dental procedures is an essential part of the process. The most commonly used local anesthetic injection for lower teeth is the inferior alveolar nerve (IAN) block. However, failure rates ranging from 10 to 39 percent have been reported.
Allowing a patient to be comfortable and pain-free during surgical and restorative dental procedures is an essential part of the process. The most commonly used local anesthetic injection for lower teeth is the inferior alveolar nerve (IAN) block. However, failure rates ranging from 10 to 39 percent have been reported.
The current issue of the journal Anesthesia Progress presents a study testing the efficacy of adding a solution of mannitol to the anesthetic typically used in IAN blocks. Forty adult subjects participated in the study, receiving an IAN block at each of three separate appointments at least one week apart.
The study compared the effectiveness of the standard anesthetic, lidocaine with epinephrine, to the effectiveness of two different volumes of lidocaine with epinephrine plus 0.5 M mannitol. Mannitol is a sugar alcohol that occurs naturally in fruits and vegetables. It is rapidly excreted by the kidneys.
Though its impact is short-lived, mannitol has the positive effect of opening the perineurial membrane. It is believed that, in cases of IAN block failure, the perineurial barrier around the nerve does not allow complete diffusion of the anesthetic into the nerve trunk. The addition of mannitol apparently allows enhanced permeability, increasing the success of an IAN block when administered concurrently.
After injections of the IAN block solutions, subjects’ pain levels were measured by an electric pulp test of their mandibular teeth at 4-minute intervals for 60 minutes. The study concluded that the addition of mannitol to lidocaine with epinephrine significantly increased the effectiveness of the anesthesia.
About Anesthesia Progress
Anesthesia Progress is the official publication of the American Dental Society of Anesthesiology (ADSA). The quarterly journal is dedicated to providing a better understanding of the advances being made in the science of pain and anxiety control in dentistry. The journal invites submissions of review articles, reports on clinical techniques, case reports, and conference summaries. To learn more about the ADSA, visit:
Oral Bacteria Enables Breaking Bond On Blood Vessels to Allow Invaders in
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A common oral bacteria, Fusobacterium nucleatum, acts like a key to open a door in human blood vessels and leads the way for it and other bacteria like Escherichia coli to invade the body through the blood and make people sick, according to dental researchers at Case Western Reserve University.
Yiping Han, professor of periodontics at the Case Western Reserve School of Dental Medicine, made the discovery in her continued work with the Fusobacterium nucleatum bacterium, one of the most prevalent of the more than 700 bacteria in the mouth.
She found the gram-negative anaerobe has a novel adhesin or bonding agent she's named FadA that triggers a cascade of signals that break the junctures in an interlocking sheath of endothelial cells on blood vessel's surface just enough to allow F. nucleatum and other bacteria into the blood.
A description of bond-breaking process was described in the Molecular Microbiology article, "Fusobacterium nucleatum adhesin FadA binds vascular endothelial cadherin and alters endothelial integrity."
The microbiologist at the dental school has studied the oral bacteria over the past decade and was the first to find direct evidence that linked it to preterm labor and fetal death. But its presence is found in other infections and abscesses in the brain, lungs, liver, spleen and joints.
After finding and genetically matching the oral bacteria in the fetal death, she began to unravel the mystery of how an oral bacterium can be found throughout the body and jumps the blood-brain and placental barriers that usually block disease-causing agents.
Through years of lab work, her research led to the vascular endothelial (VE)-cadherin, cell-cell junctures that link the endothelial vascular cells together on the blood vessels.
These junctures are like a hook and loop connection, but for some unknown reason when F. nucleatum invades the body through breaks in the mucous membranes of the mouth, due to injuries or periodontal disease, this particular bacterium triggers a cascade of signals that causes the hook to recede back into the endothelial cell. The oral bacterium leads the way with any other harmful invaders following along.
This "deceding" was observed by confocal microscopy when Han used cells from human umbilical cord. The researchers introduced F. nucleatum and demonstrated the VE-cadherins break on bonds on the endothelial cells and creating enough space in the endothelium for the invaders to move in.
Lab tests included introducing F. nucleatum with and without other bacteria. When E. coli alone was introduced, the bond did not break. But when F. nucleatum was introduced first, the bond broke, and the E. coli bacteria were able to move through the otherwise intact cell layers.
"This cascade knocks out the guard on duty and allows the bacteria to enter the blood and travel like a bus loaded with riders throughout the system. Whenever the F. nucleatum wants to get off the bus at the liver, brain, spleen, or another place, it does," Han said.
When it disembarks from its ride through the blood, it begins to colonize. The colony of bacteria induces an inflammatory reaction that has a range of consequences from necrosis of tissue to fetal death.
A common oral bacteria, Fusobacterium nucleatum, acts like a key to open a door in human blood vessels and leads the way for it and other bacteria like Escherichia coli to invade the body through the blood and make people sick, according to dental researchers at Case Western Reserve University.
Yiping Han, professor of periodontics at the Case Western Reserve School of Dental Medicine, made the discovery in her continued work with the Fusobacterium nucleatum bacterium, one of the most prevalent of the more than 700 bacteria in the mouth.
She found the gram-negative anaerobe has a novel adhesin or bonding agent she's named FadA that triggers a cascade of signals that break the junctures in an interlocking sheath of endothelial cells on blood vessel's surface just enough to allow F. nucleatum and other bacteria into the blood.
A description of bond-breaking process was described in the Molecular Microbiology article, "Fusobacterium nucleatum adhesin FadA binds vascular endothelial cadherin and alters endothelial integrity."
The microbiologist at the dental school has studied the oral bacteria over the past decade and was the first to find direct evidence that linked it to preterm labor and fetal death. But its presence is found in other infections and abscesses in the brain, lungs, liver, spleen and joints.
After finding and genetically matching the oral bacteria in the fetal death, she began to unravel the mystery of how an oral bacterium can be found throughout the body and jumps the blood-brain and placental barriers that usually block disease-causing agents.
Through years of lab work, her research led to the vascular endothelial (VE)-cadherin, cell-cell junctures that link the endothelial vascular cells together on the blood vessels.
These junctures are like a hook and loop connection, but for some unknown reason when F. nucleatum invades the body through breaks in the mucous membranes of the mouth, due to injuries or periodontal disease, this particular bacterium triggers a cascade of signals that causes the hook to recede back into the endothelial cell. The oral bacterium leads the way with any other harmful invaders following along.
This "deceding" was observed by confocal microscopy when Han used cells from human umbilical cord. The researchers introduced F. nucleatum and demonstrated the VE-cadherins break on bonds on the endothelial cells and creating enough space in the endothelium for the invaders to move in.
Lab tests included introducing F. nucleatum with and without other bacteria. When E. coli alone was introduced, the bond did not break. But when F. nucleatum was introduced first, the bond broke, and the E. coli bacteria were able to move through the otherwise intact cell layers.
"This cascade knocks out the guard on duty and allows the bacteria to enter the blood and travel like a bus loaded with riders throughout the system. Whenever the F. nucleatum wants to get off the bus at the liver, brain, spleen, or another place, it does," Han said.
When it disembarks from its ride through the blood, it begins to colonize. The colony of bacteria induces an inflammatory reaction that has a range of consequences from necrosis of tissue to fetal death.
Wednesday, December 14, 2011
Oral Surgery Protocol to Control Bleeding for Heart Patients Shows Positive Results
Cardiac patients that take anticoagulant medications and need a tooth extraction face an increased risk of bleeding that must be addressed by the treating clinician. Therefore, a protocol for heart patients is needed that will avoid significant bleeding after dental extractions without suspending anticoagulant therapy.
A study reported in the current issue of the Journal of Oral Implantology evaluated the use of leukocyte- and platelet-rich fibrin biomaterial. This material is commonly used in dentistry to improve healing and tissue regeneration. It was tested as a safe filling and hemostatic material after dental extractions in 50 heart patients undergoing oral anticoagulant therapy.
These heart patients had mechanical valve substitutions, and then were placed on anticoagulant oral therapy with warfarin. It is not recommended that the anticoagulant be suspended and replaced with heparin before a minor surgery, although this substitution may control the risk of postoperative bleeding.
One method of controlling bleeding without suspending the anticoagulant is the use of platelet-rich plasma gel placed in postextraction tooth sockets. Although this protocol has been successful, there are barriers to its daily use. The platelet concentrates are expensive and take a long time to prepare.
Platelet-rich fibrin offers an alternative biomaterial that is simple and inexpensive to prepare. Blood is collected in tubes without anticoagulant and centrifuged. It divides into three layers, creating a strong platelet-rich fibrin clot in the middle layer. Platelet-rich fibrin has proved useful in daily dental practice as filling material for regeneration in order to place implants.
In this study, 50 heart patients following an anticoagulant therapy were treated with leukocyte- and platelet-rich fibrin clots placed into postextraction sockets. Complications of bleeding were reported in only two of these patients, and 10 had mild bleeding. All complications were resolved within a few hours after the oral surgery.
Additionally, the study reported no painful events, quick healing of soft tissue, and complete wound closure within one week after oral surgery. Leukocyte- and platelet-rich fibrin offers an excellent option for use in heart patients on an anticoagulant regimen.
Full text of the article, “Prevention of Hemorrhagic Complications After Dental Extractions Into Open Heart Surgery Patients Under Anticoagulant Therapy: The Use of Leukocyte- and Platelet-Rich Fibrin ,” Journal of Oral Implantology, Vol. 37, No. 6, 2011, is available at http://www.joionline.org/ .
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About Journal of Oral Implantology
The Journal of Oral Implantology is the official publication of the American Academy of Implant Dentistry and of the American Academy of Implant Prosthodontics. It is dedicated to providing valuable information to general dentists, oral surgeons, prosthodontists, periodontists, scientists, clinicians, laboratory owners and technicians, manufacturers, and educators. The JOI distinguishes itself as the first and oldest journal in the world devoted exclusively to implant dentistry. For more information about the journal or society, please visit: http://www.aaid-implant.org/index.html
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