Peer-Reviewed Journal of the Academy of General Dentistry
GENERAL DENTISTRY January/February 2012 ~ Volume 60 Number 1
Conscious Sedation n Esthetics Periodontics n Dental Materials Oral Diagnosis n www.agd.org
Contents Departments 6 Editorial De-stress and enjoy life 8 Pharmacology New antiplatelet and anticoagulant drugs 12
Restorative Dentistry Creating an improved environment for restorative dentistry using periodontal surgery and the Broadrick flag occlusal plane analyzer
Oral Diagnosis Diffuse gingival enlargement and Focal gingival hyperpigmentation
77 Answers Oral Diagnosis and Self-Instruction exercises No. 276, 277, and 278
Clinical articles 16 Endodontics Injection of sodium hypochlorite beyond the apical foramen—A case report Marcelo de Almeida Paschoalino, DDS Ainda Assayag Hanan, DDS Andre Augusto Franco Marques, DDS, MSc, PhD Lucas da Fonseca Roberti Garcia, DDS, MSc, PhD Angela Bittencourt Garrido, DDS, MSc, PhD Emilio Carlos Sponchiado Jr., DDS, MSc, PhD
20 Periodontics Potential correlation between periodontitis and coronary heart disease—An overview T.G. Shrihari, BDS, MDS
Cosmetic Dentistry Influence of increment thickness on the similarity of composite shade: A pilot study Lourenco de Moraes Rego Roselino, DDS Lucas da Fonseca Roberti Garcia, DDS, MSc, PhD Ana Beatriz Silva Sousa, DDS Fernanda de Carvalho Panzeri Pires-de-Souza, DDS, MSc, PhD
Conscious Sedation Adult minimal oral sedation in the general practice setting K. David Stillwell, DDS, MAGD
Barbara J. Anderson, DMD
Dental Materials Shear bond strength of seventh generation bonding agents on dentin of primary teeth—An in vitro study Geoffrey Gonzales, DMD Alfred P. Rich, DMD, MDS Matthew D. Finkelman, PhD Catherine DeFuria
51 Orthodontics Effects of modifying the bonding protocol on the shear bond strength of metallic and ceramic orthodontic brackets Thais Maria Freire Fernandes, DDS, MSc, PhD Guilherme Janson, DDS, MSc, PhD Joyce Somensi Arnaldo Pinzan, DDS, MSc, PhD Paulo Afonso Silveira Francisconi, DDS, MSc, PhD Renata Sathler, DDS, MSc, PhD Jose Fernando Castanha Henriques, DDS, MSc, PhD
58 Exodontia Predictive variables for postoperative pain after 520 consecutive dental extraction surgeries Marcelo Carlos Bortoluzzi, DDS, PhD Aline Rosler Grings Manfro Rudy Jose Nodari Jr., PhD Andreia Antoniuk Presta, PhD
Practice Management Basic principles of dental office logistics: Organizing dental supplies and equipment for optimal accessibility John Mamoun, DMD
Oral Medicine, Oral Diagnosis Acute cervicofacial necrotizing fasciitis: Three clinical cases and a review of the current literature Elizabeth Bilodeau, DMD, MD Vijay P. Parashar, DDS, MDSc Allison Yeung, DDS, MD Anitha Potluri, DMD
e1 Periodontics C-reactive protein as a marker of periodontal disease Rosaiah Kanaparthy, MDS Aruna Kanaparthy, MDS Muktishree Mahendra, MDS
Coming Next Issue In the March/April issue of General Dentistry • Esthetic and functional combination of fixed and removable prostheses • Dietary considerations for patients with dry mouth • Physiotherapy as an adjuvant therapy for treatment of temporomandibular joint disorders
Dental Materials Bond strength of two resin cements to titanium after different surface conditioning methods Mutlu Ozcan, DMD, PhD Luiz Felipe Valandro, DDS, MSD, PhD
e13 Removable Prosthodontics A new intraoral device to facilitate preparation of the guide plane for removable dental prostheses Alexandre Luiz Souto Borges, DDS, MS, PhD Alessandra Buhler Borges, DDS, MS, PhD Lucas Hian da Silva, DDS, MS Eduardo Shigueuki Uemura, DDS, MS, PhD Guilherme de Siqueira Ferreira Anzalone Saavedra, DDS, MS, PhD
In the February issue of AGD Impact • Dental implant centers • Website essentials for rookies and beyond
e17 Restorative Dentistry Influence of restorative techniques on marginal adaptation and dye penetration around Class V restorations Adriana de Fatima Vasconcelos Pereira, DDS, MS, PhD Isis Andrea Venturini Pola Poiate, DDS, MS, PhD Edgar Poiate Jr., MS Flavia Pires Rodrigues, DDS, MS, PhD Mirian Lacalle Turbino, DDS, MS, PhD Walter Gomes Miranda Jr., DDS, MS, PhD
e22 Implants A simple, time-saving chairside device for radiographic diagnosis of vertical bone height and soft tissue thickness for implant placement—Clinical report Pankaj Kharade, MDS Tapas Gupta, MDS
Ardhendu Banerjee, MDS
e26 Dental Materials Effect of light source and solvent on the sorption and solubility of two dual-cured cements photocured through ceramic Lawrence Gonzaga Lopes, DDS, MS, PhD Ana Paula Rodrigues Magalhaes Natasha Amorim Brandao, DDS Andreia Assis Carvalho, DDS, MS Francine do Couto Lima Moreira, DDS, MS Joao Batista de Souza, DDS, MS, PhD
Suvarna Patil, MDS
e39 Anesthesia and Pain Control Anesthetic efficacy of articaine for inferior alveolar nerve blocks in patients with symptomatic versus asymptomatic irreversible pulpitis Liliana Argueta-Figueroa, DDS Hugo Mendieta-Zeron, PhD
Continuing Dental Education (CDE) Opportunities Earn two hours of CDE credit by signing up for and completing these exercises based on various subjects. 25 Self-Instruction Exercise No. 297 Periodontics 44 Self-Instruction Exercise No. 298 Conscious Sedation 56 Self-Instruction Exercise No. 299 Orthodontics
e32 Multidisciplinary Topics Forced orthodontic extrusion and use of CAD/CAM technique for reconstruction of maxillary central incisor with a severely damaged crown: Rehabilitation with a multidisciplinary approach Rahul Kumar, BDS
self CDE 2 HOURS instruction
Instructions for Authors For an electronic copy of General Dentistry’s Instructions for Authors, please visit the journal’s website at www.agd.org/ publications/GD/AuthorInfo.
Gabriel Arzate-Sosa, DDS
e44 Oral Medicine, Oral Diagnosis Difficulty in diagnosing oral paracoccidioidomycosis after topical nystatin usage Felipe Fornias Sperandio, DDS, MSc Fernanda Salgueiredo Giudice, DDS, MSc Ana Patricia Carneiro Goncalves Bezerra Coelho, DDS, MSc Suzana Cantanhede Orsini Machado de Sousa, DDS, MSc, PhD Marilia Triervelier Martins, DDS, PhD
Editor Roger D. Winland, DDS, MS, MAGD
Email: [email protected]
Associate Editor William J. Hartel, DMD, FAGD
Back Issues and Change of Address Members, call 888.AGD.DENT (toll-free) and ask for a Member Services representative. Nonmembers, call Cassie Vanderbeek (ext. 4962).
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General Dentistry (ISSN 0363-6771) is published bimonthly (every other month) by the AGD, 211 E. Chicago Ave., Suite 900, Chicago, IL 60611-1999. AGD members receive General Dentistry as part of membership. The nonmember individual subscription rate for General Dentistry is $100 for the print version, $100 for the online version, and $175 for print and online versions; the nonmember institution rate is $300 (add $20 for Canada and $50 for outside the U.S. and Canada). Single copies of General Dentistry are available to nonmember individuals for $15 and nonmember institutions for $18 (add $3 for orders outside the U.S.). Academy of General Dentistry Corporate Sponsors
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Advisory Board Dental Materials
Oral and Maxillofacial Pathology
is in general practice in Bellevue, Washington. He is a visiting faculty member of the Pankey Institute and the Pride Institute and is a Diplomate of the American Board of Dental Sleep Medicine.
certified oral and maxillofacial pathologist at Virginia Commonwealth University in Richmond. He currently is a professor of oral and maxillofacial pathology and maintains a private practice in oral medicine and oral pathology.
University School of Dentistry and a professor in the Department of Orthodontics at LSUSD.
Dental Public Health
Oral and Maxillofacial Radiology
Steve Carstensen, DDS, FAGD,
Larry Williams, DDS, ABGD, MAGD, is a Captain in the United States Navy Dental Corps, currently stationed at the Great Lakes Naval Training Center as a member of the Great Lakes Naval Health Clinic. Dr. Williams is the Public Health Emergency Officer for the 16 states of the Navy Region MidWest and for the Naval Health Clinic. He also serves as the co-chair of the Navy’s Tobacco Cessation Action Team and as a member of the Department of Defense Alcohol and Tobacco Advisory Council. Dr. Williams teaches for the Dental Hygiene program at the College of Lake County and as an assistant clinical professor for the Rosalind Franklin University for Medicine and Science.
Wynn H. Okuda, DMD, is Past National President (2002–03) and a board-accredited member of the American Academy of Cosmetic Dentistry (AACD). He also is on the Advisory Board of Best Dentists in America and on the Executive Council of the International Federation of Esthetic Dentistry (IFED). He practices cosmetic, implant, and restorative dentistry at the Dental Day Spa of Hawaii in Honolulu.
John Svirsky, DDS, MEd, is a board-
Kavas Thunthy, BDS, MS, MEd,
has been a professor of oral and maxillofacial radiology in the Department of Oral Diagnosis, Medicine, Radiology, at the Louisiana State University School of Dentistry in New Orleans since 1975. He was named a Fellow in the American Academy of Oral and Maxillofacial Radiology in 1978 and was board-certified by the American Board of Oral and Maxillofacial Radiology in 1981.
Oral and Maxillofacial Surgery
Karl Koerner, DDS, FAGD, is a
is assistant professor of Oral Medicine, Infection and Immunity at Harvard School of Dental Medicine. She is board-certified in Oral and Maxillofacial Pathology and Oral Medicine and practices both specialities in the Boston/ Cambridge area in Massachusetts.
Dental Service, at VA Salt Lake City Health Care System and Clinical Assistant Professor, University of Utah in Salt Lake City.
P. Emile Rossouw, BSc, BChD, BChD(Child-Dent), MChD (Ortho), PhD, is professor and chairman
is a general dentist who practices in New Jersey. He is a Diplomate of both the American Board of Oral Implantology/Implant Dentistry and the International Congress of Oral Implantologists, and a Fellow of the American Academy of Implant Dentistry.
Sebastian Ciancio, DDS, is Distinguished Service Professor and Chair, Department of Periodontics and Endodontics, Adjunct Professor of Pharmacology, and Director of the Center for Dental Studies at the University at Buffalo, State University of New York.
Sook-Bin Woo, DMD, MMSc,
Wesley Blakeslee, DMD, FAGD,
of the American Board of Pediatric Dentistry, has authored numerous articles in the dental literature, and has been recognized as a leader in continuing education. She maintains a private practice in Allison Park, Pennsylvania.
is Past President, International Association for Orthodontics; a Fellow of the American Academy of Craniofacial Pain; and a member of the American Academy of Dental Sleep Medicine. He maintains a general practice in Mt. Holly, New Jersey.
Jane Soxman, DDS, is a Diplomate
Lea Erickson, DDS, MSPH, is Chief,
general dentist in Utah who performs oral surgery exclusively. He lectures extensively on oral surgery in general practice and has made articles, books, and video presentations available to general practitioners.
Stephen Cohen, DDS, is one of the
foremost endodontic clinicians in the country and lectures worldwide on endodontics. A board-certified endodontist, Dr. Cohen specializes exclusively in the diagnosis and treatment of endodontic infections.
Henry A. Gremillion, DDS, MAGD, is dean of the Louisiana State
Yosh Jefferson, DMD, FAGD,
Daniel E. Myers, DDS, MS, is a
member of the Oral Diagnosis Department, Dental Associates of Wisconsin, Ltd. in Wauwatosa.
Joseph Massad, DDS, is currently the Director of Removable Prosthodontics at the Scottsdale Center for Dentistry in Arizona. He is adjunct faculty at Tufts University School of Dental Medicine in Boston and the University of Texas Dental School at San Antonio. Jack Piermatti, DMD, is a Diplomate of the American Board of Prosthodontics, the American Board of Oral Implantology, and the International Congress of Oral Implantologists. He is a board-certified prosthodontist in private practice in Voorhees, New Jersey.
of the Department of Orthodontics, University of North Carolina at Chapel Hill School of Dentistry. He has published and lectured on clinical orthodontic research nationally and internationally. He maintains a part-time clinical practice in addition to his academic responsibilities.
De-stress and enjoy life
od has subtle and not so subtle ways of telling us when we need to slow down. Last June, I thought I was having another kidney stone attack when I began to experience familiar symptoms (pain, emesis, and nausea). After a day of waiting for the stone to pass, my wife, to my eternal blessing, insisted that I go to the emergency room when I began to have trouble putting sentences together. Because my physician, who is also my brother, lives 100 miles away, I didn’t wait any longer. Once at the ER, a CT scan revealed a small bleed in the left occipital lobe of my brain, and I was immediately rushed by helicopter to a larger hospital with an excellent neurosurgery intensive care unit. Fortunately, the bleed was small—the result of a 225/125 spike in my blood pressure—and not an aneurysm. Within two days, my symptoms had subsided, as medication brought my blood pressure back under control. I was released from the hospital, and follow-up CT, MRI, and MRA scans revealed complete healing with no side effects. I felt tremendously blessed, but fully forewarned about the dangers of stress. For too many of us, the stresses of life have zapped us of our ability to do our best, be our best, and enjoy our daily activities. Somehow, we need to find the balance and focus in our lives to capitalize on the productive elements of stress, even as we avoid becoming overwhelmed by its negative elements. Obviously, physical stress management is not my forte (hence the kidney stones and high blood pressure), but I would like to impart some mental stress management strategies that I have learned during my 40 years of dental practice. For starters, you need to take charge of your life. Emotionally healthy dentists tend to maintain a higher degree of control over what happens in their lives, and this feeling of being in control can help to reduce feelings of stress. You might not be able to control all of
life’s events, patient demands, or practice pressures, but you can definitely decide how to respond to them. Dentists who pursue their dreams passionately and view change as a challenge instead of a threat aren’t negatively affected by stress. And dentists who aren’t negatively affected by stress have a personal mission that adds direction, meaning, and a feeling of empowerment during stressful times. Without that sense of purpose, stress can throw us off balance. As dentists, sometimes we allow the problems of our patients to become our own. This causes us to worry too much, which restricts our ability to think clearly and act effectively. We need to find a way to put these problems into perspective, because most stress at the office is caused by patients who overestimate their own problems. We should use our professional strengths and abilities to make the best of difficult situations, break problems down into manageable pieces, and work on creating resolutions. The best cure I know for worry is action. Taking action against our worries allows us to break free of the unnecessary, strangling effects of stress. The dichotomy of experiencing too little stress can cause irritability, boredom, dullness, and apathy, while too much stress can produce comparable results along with feelings of being overwhelmed. Hungarian endocrinologist Hans Selye said, “The most frequent causes of stress are an inability to adapt and not having an established code of behavior to guide our actions.” Stress is an inside job caused by what happens between our ears and how we look at, think about, and respond to events. I am using medicines and dietary restrictions to manage my physical stress. To manage my mental stress, I am trying to keep life in perspective by concentrating on the positive, approaching failures and mistakes as opportunities to learn and grow, and nurturing my enthusiasm for life. I am persevering in difficult times because better days are ahead, and every day is a new opportunity to thrive.
Roger D. Winland, DDS, MS, MAGD Editor Comment
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New antiplatelet and anticoagulant drugs Richard L. Wynn, PhD
he antiplatelet drugs prasugrel (Effient) and ticagrelor (Brilinta, AstraZeneca LP) and the anticoagulant drugs dabigatran (Pradaxa, Boehringer Ingelheim Pharmaceuticals, Inc.) and rivaroxaban (Xarelto, Janssen Pharmaceuticals, Inc.) have gained FDA approval within the past two years. Prasugrel is a platelet aggregation inhibitor approved for the reduction of thrombotic cardiovascular events (including stent thrombosis) in patients with acute coronary syndromes who are managed with percutaneous coronary intervention.1,2 Prasugrel is an antiplatelet agent within the same class of platelet inhibitors as clopidogrel (Plavix). The official labeled indications are to reduce the rate of thrombotic cardiovascular events (for example, stent thrombosis) in patients with unstable angina, non-ST-segment elevation MI, or ST-elevation MI (STEMI) managed with percutaneous coronary intervention (PCI).1 A description of the medical use, effects on bleeding, and other dental considerations for prasugrel was published in this column in 2010.2 The remainder of this column will describe the other three new drugs.
Dabigatran—A new anticoagulant drug Dabigatran has received FDA approval for the prevention of stroke and systemic embolism (blood clots) in patients with atrial fibrillation. It is the first replacement for warfarin (Coumadin) to win FDA approval since warfarin was approved in 1954.3,4 Replacement drugs for warfarin are critically important as the aging population becomes more vulnerable to atrial fibrillation (which affects more than 2 million Americans) and other cardiovascular conditions that can cause blood clots.5 Dabigatran is an anticoagulant that acts by inhibiting thrombin, an enzyme in the blood involved in blood clotting.6 Because thrombin (serine protease) enables the conversion of fibrinogen to fibrin during the coagulation cascade, it prevents the development of a thrombus. The recommended dose is a 150 mg capsule taken orally twice a day in patients with creatinine clearance exceeding 30 mL/min.7 For patients with creatinine clearance from 15–30 mL/min, the recommended dose 8
is 75 mg twice daily.7 Warfarin therapy requires patients to undergo periodic monitoring with blood tests; such monitoring is not necessary for dabigatran.7,8 Measure of effect of dabigatran
At recommended therapeutic doses, dabigatran prolongs the activated partial thromboplastin time (aPTT).9 With an oral dose of 150 mg twice daily, the median peak aPTT is approximately twice that of control values. Twelve hours after the last dose, the median aPTT is 1.5x control. The INR test is relatively insensitive to the activity of dabigatran and might not be elevated in patients on dabigatran.9 Absorption and metabolism
Peak blood level occurs one hour after administration of dabigatran. The half-life of dabigatran is 12–17 hours.10,11 Dabigatran is not metabolized by liver enzymes.12 After oral administration, dabigatran etexilate is converted to dabigatran through esterase-catalyzed hydrolysis of the molecule in plasma. Dabigatran is subject to conjugation with glucuronic acid-forming, pharmacologically active acyl glucuronides.12 Clinical efficacy study
The clinical study that defined the efficacy of dabigatran is known as the Random Evaluation of Long-Term Anticoagulation Therapy (RE-LY) trial.7 This trial randomly assigned 18,113 patients who had atrial fibrillation and a risk of stroke fixed, blinded doses of either 110 or 150 mg of dabigatran twice daily, or adjusted, unblinded doses of warfarin. The primary assessed outcome was the incidence of stroke or systemic embolism over the study period of two years. The adjusted dose of warfarin was defined as dosing to achieve an INR value of 2–3. Results of the RE-LY study
The rate of stroke or systemic embolism was 1.69% per year in the warfarin group, 1.53% in the dabigatran 110 mg twice daily group, and 1.11% in the dabigatran 150 mg twice daily group, which marks a significant reduction compared to the warfarin group. The rate of major bleeding in the warfarin group was 3.36% per year,
compared with 2.71% per year in the group receiving 110 mg of dabigatran twice daily and 3.11% per year in the group receiving 150 mg of dabigatran twice daily. The rate of hemorrhagic stroke was 0.38% per year in the warfarin group, compared with 0.12% per year in the dabigatran 110 mg twice daily group and 0.10% per year in the dabigatran 150 mg twice daily group. The mortality rate was 4.13% per year in the warfarin group, compared with 3.75% per year in the dabigatran 110 mg twice daily group and 3.64% per year in the dabigatran 150 mg twice daily group. A summary of the results showed that in patients with atrial fibrillation, dabigatran administration at a dose of 150 mg twice daily was associated with lower rates of stroke and systemic embolism but with similar rates of major bleeding when compared to warfarin.7 At a dose of 110 mg twice daily, dabigatran was associated with rates of stroke and systemic embolism similar to those of warfarin but with significantly lower rates of major bleeding. The rate of hemorrhagic stroke with both doses of dabigatran was less than one-third that of warfarin, without any reduction in the efficacy against ischemic stroke. This was suggested as an important advantage over warfarin. Risk of bleeding
According to the manufacturer’s labeling, dabigatran increases the risk of bleeding and can cause significant and sometimes fatal bleeding.3 Drugs that can increase the risk of bleeding in patients taking dabigatran include anti-platelet agents and NSAIDs used chronically.13 In the RE-LY trial, life-threatening bleeding occurred at an annualized rate of 1.5% for dabigatran (150 mg) and 1.8% for warfarin.7 Discontinuing anticoagulants, including dabigatran, for elective surgery or invasive procedures places patients at an increased risk of stroke.3 If anticoagulation with dabigatran must be discontinued for any reason, therapy should be restarted as soon as possible.14 Dental patients who might have a high risk of bleeding when taking dabigatran include those over the age of 75 or those who are taking aspirin, long-term NSAIDs, or clopidogrel or prasugrel.15 The drawbacks to warfarin
Warfarin is a vitamin K antagonist. It decreases the coagulation of blood by competitively inhibiting the enzyme vitamin K epoxide reductase. Normally, this enzyme recycles oxidized vitamin K, converting it back to its reduced form. The reduced vitamin K is required for the carboxylation and activation of vitamin K-dependent coagulation factors II, VII, IX, and X. When this enzyme is suppressed
by warfarin, no activation of these factors occurs and the coagulation pathway is essentially broken.16 Foods high in vitamin K inhibit warfarin’s anticoagulant effect. These include beef liver, pork liver, green tea, and leafy green vegatables.16 A balanced diet with consistent intake of vitamin K is essential to maintain optimal anticoagulant efficacy.16
Rivaroxaban—A new anticoagulant drug Rivaroxaban was approved for the prophylaxis of deep vein thrombosis (DVT), which can lead to pulmonary embolism in patients undergoing knee or hip replacement surgery.17,18 The dose is 10 mg taken orally once daily with or without food. The initial dose should be taken at least 6–10 hours after surgery once hemostasis has been established.17 Adverse reactions
The most common adverse reactions with rivaroxaban were bleeding complications.17 From hip surgery studies, 201 of 3,281 patients exhibited bleeding labeled as “any bleeding event,” amounting to an incidence of 6.1%.17 From the knee surgery study, 60 of 1,206 patients exhibited bleeding labeled as “any bleeding event,” amounting to an incidence of 5.0%. These bleeding events occurred at any time between the first dose of medication and two days after the last dose. In addition to bleeding, adverse effects included pain in extremities (1.7%), muscle spasm (1.2%), and syncope (1.2%).17 Mechanism of action
Rivaroxaban is an orally administered factor Xa inhibitor. In the blood coagulation cascade, activation of factor X to factor Xa is central in the cascade to produce fibrin, resulting in blood coagulation.19 Inhibition of factor Xa derails fibrin production, resulting in decreased blood coagulation.19 Measurement of effect
Rivaroxaban prolongs prothrombin time (PT) and activated partial thromboplastin time (aPTT).19,20 According to labeling, there is no data on the use of the INR values to measure the effects of rivaroxaban.17 The predictive value of the coagulation parameters of PT and aPTT for bleeding risk or dosing efficacy has not been established. Dosing
The recommended dose of rivaroxaban is 10 mg taken orally once daily with or without food.17 For patients undergoing hip replacement surgery, treatment duration of 35 days is recommended.19 For patients undergoing
knee replacement surgery, treatment duration of 12 days is recommended.19 Patient information from product labeling
Labeling states that patients should not discontinue rivaroxaban prematurely without talking to their doctor first.17 Patients who are taking rivaroxaban should tell their physicians and dentists if they are taking or planning to take any prescription drugs such as pain relievers, OTC drugs, or herbal supplements so that the health care provider can evaluate potential interactions.17 Dental considerations
With invasive procedures, increased bleeding could occur in patients taking a 10 mg daily dose of rivaroxaban. There are no coagulation parameters for rivaroxaban to predict the extent of bleeding at this time. Medical consult with a physician is suggested prior to invasive dental procedures. According to product labeling, knee replacement patients will be medicated with rivaroxaban for approximately 12 days postsurgery.17 This means that patients with knee replacements having dental work two weeks or more postsurgery probably will not be taking the drug, although this could change with future unlabeled uses of the drug. Also according to product labeling, hip replacement patients will be medicated with rivaroxaban for approximately 35 days postsurgery.17 This means that patients with hip replacements having dental work five weeks or more postsurgery probably will not be taking the drug, although this could change with future unlabeled uses of the drug. There are no reports of interactions between rivaroxaban and amoxicillin, cephalexin, cefazolin, ampicillin, or clindamycin. Therefore, any of these pre-procedural antibiotics can be used safely in total joint replacement patients who are taking rivaroxaban.
Ticagrelor—A new antiplatelet drug Ticagrelor gained FDA approval to reduce the rate of thrombotic cardiovascular events in patients with acute coronary syndrome (ACS) (unstable angina, non-ST elevation myocardial infarction, or ST elevation myocardial infarction).21 The drug has been shown to reduce the rate of a combined endpoint of cardiovascular death, myocardial infarction, or stroke compared to clopidogrel.21 Adverse reactions
The most common adverse reactions to ticagrelor are bleeding (12%) and dyspnea (labored breathing, shortness of breath) (14%).22 Ticagrelor, like other antiplatelet 10
agents, can cause significant and sometimes fatal bleeding.22 Clinical trials have reported major bleeding events in 11.58% of subjects taking ticagrelor and 11.2% subjects taking clopidogrel.21,22 Non-coronary artery bypass graft major and minor bleeding events were more common with ticagrelor (8.7%) than with clopidogrel (7.0%). Minimal bleeding events (including bruising, bleeding gums, and oozing from injection sites) have been reported. The other adverse reaction occurring at a rate of more than 5% was headache (6.5% incidence).22 Mechanism of action
Ticagrelor is an active reversible platelet inhibitor. The liver enzymes convert it to another active reversible platelet inhibitor, its major active metabolite.23,24 The metabolite’s major route of elimination appears to be biliary instead of urinary excretion.23 Ticagrelor and its metabolite reversibly interact with platelets at a site known as the ADP-receptor. This interaction prevents platelet activation and results in diminished platelet aggregation.25 Dosage
Ticagrelor is supplied as 90 mg tablets. A loading dose of two tablets (180 mg) is followed by one tablet (90 mg) twice daily.21 Ticagrelor has been studied in ACS in combination with aspirin. After a loading dose of aspirin (usually 325 mg), ticagrelor is given along with a daily maintenance dose of aspirin of 75–100 mg (usually an 81 mg tablet). Maintenance doses of aspirin greater than 100 mg reduce the effectiveness of Ticagrelor and should be avoided.21 Patient information from product labeling
According to the product information for Brilinta, “Premature discontinuation of Brilinta increases the risk of myocardial infarction, stent thrombosis, and death. Tell all of your doctors and dentists that you are taking Brilinta. They in turn should talk to the doctor who prescribed Brilinta for you before you have any surgery or invasive procedure.”21 Dental considerations
Ticagrelor should not be discontinued without discussing it with the prescribing physician first. Stopping ticagrelor increases the risk of subsequent cardiovascular events.21 Patients taking ticagrelor could bleed and bruise more easily and have shortness of breath.22 If a patient is taking aspirin together with ticagrelor, the aspirin dose should not exceed 100 mg per day.21 Patients should avoid taking any other medications
containing aspirin. Because of this issue with aspirin, the manufacturer will institute a Risk Evaluation and Mitigation Strategy (REMS) that will alert the doctors to the risk of using higher doses along with the drug.21 At this time, no coagulation parameters have been suggested for ticagrelor to predict the extent of bleeding. A medical consultation with the physician is suggested prior to invasive dental procedures.21 A final note
Ticagrelor is now approved in 39 countries, including the U.S., Brazil, Australia, and Canada under the trade name Brilinta and in the European Union under the trade name Brilique.
Author information Dr. Wynn is a professor of pharmacology, Department of Oral Craniofacial Biological Sciences, Dental School, University of Maryland at Baltimore.
1. Wynn RL. Platelet inhibitors: Update on clopidogrel (Plavix) and the recently approved prasugrel (Effient). Gen Dent 2010;58(1):7-9. 2. U.S. Food and Drug Administration. FDA approves Effient to reduce the risk of heart attack in angioplasty patients. Available at: http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm171497.htm. Accessed September 8, 2011. 3. Dabigatran etexilate (Pradaxa)—A new oral anticoagulant. Med Lett Drugs Ther 2010;52(1351):89-90. 4. Tran A, Cheng-Lai A. Dabigatran etexilate: The first oral anticoagulant available in the United States since warfarin. Cardiol Rev 2011;19(3):154-161 5. Wann LS, Curtis AB, Ellenbogen KA, Estes NA 3rd, Ezekowitz MD, Jackman WM, January CT, Lowe JE, Page RL, Slotwiner DJ, Stevenson WG, Tracy CM. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on dabigatran): A report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines.. J Am Coll Cardiol 2011;57(11):1330-1337. 6. Dubois EA, Cohen AF. Dabigatran etexilate. Br J Clin Pharmacol 2010;70(1): 14-5. 7. Connolly SJ, Ezekowitz MD, Yusuf S, Eikelboom J, Oldgren J, Parekh A, Pogue J, Reilly PA, Themeles E, Varrone J, Wang S, Alings M, Xavier D, Zhu J, Diaz R, Lewis BS, Darius H, Diener HC, Joyner CD, Wallentin L; RE-LY Steering Committee and Investigators. Dabigatran versus warfarin in patients with atrial fibrillation. N Engl J Med 2009;361(12):1139-1151. 8. Ingelmo C, Wazni O. Review of the randomized evaluation of long-term anticoagulation therapy (RE-LY) trial. Curr Cardiol Rep 2011;13(5):357-60. 9. Thompson CA. First oral thrombin inhibitor enters market: Drug does not require clinicians to monitor INR. Am J Health Syst Pharm 2010;67(23):1974, 1976 10. Eriksson BI, Quinlan DJ, Weitz JI. Comparative pharmacodynamics and pharmacokinetics of oral direct thrombin and factor xa inhibitors in development. Clin Pharmacokinet 2009;48(1):1-22. doi: 10.2165/0003088-20094801000001.
11. Stangier J. Clinical pharmacokinetics and pharmacodynamics of the oral direct thrombin inhibitor dabigatran etexilate. Clin Pharmacokinet 2008;47(5):285295. 12. Ebner T, Wagner K, Wienen W. Dabigatran acylglucuronide, the major human metabolite of dabigatran: In vitro formation, stability, and pharmacological activity. Drug Metab Dispos 2010;38(9):1567-1575. 13. Stangier J, Stahle H, Rathgen K, Fuhr R. Pharmacokinetics and pharmacodynamics of the direct oral thrombin inhibitor dabigatran in healthy elderly subjects. Clin Pharmacokinet 2008;47(1):47-59. 14. Eikelboom JW, Wallentin L, Connolly SJ, Ezekowitz M, Healey JS, Oldgren J, Yang S, Alings M, Kaatz S, Hohnloser SH, Diener HC, Franzosi MG, Huber K, Reilly P, Varrone J, Yusuf S. Risk of bleeding with 2 doses of dabigatran compared with warfarin in older and younger patients with atrial fibrillation: An analysis of the randomized evaluation of long-term anticoagulant therapy (RELY) trial. Circulation 2011;123(21):2363-2672. 15. Legrand M, Mateo J, Aribaud A, Ginisty S, Eftekhari P, Huy PT, Drouet L, Payen D. The use of dabigatran in elderly patients. Arch Intern Med 2011;171(14): 1285-1286. 16. Nutescu E, Chuatrisorn I, Hellenbart E. Drug and dietary interactions of warfarin and novel oral anticoagulants: An update. J Thromb Thrombolysis 2011; 31(3):326-343. 17. Janssen Pharmaceuticals, Inc. Prescribing information for Xarelto. Available at: http://www.xareltohcp.com/sites/default/files/pdf/xarelto_0.pdf#zoom=100. Accessed September 7, 2011. 18. Rivaroxaban (Xarelto)—A new oral anticoagulant. Med Lett Drugs Ther 2011; 53(1371):65-67 19. EINSTEIN Investigators, Bauersachs R, Berkowitz SD, Brenner B, Buller HR, Decousus H, Gallus AS, Lensing AW, Misselwitz F, Prins MH, Raskob GE, Segers A, Verhamme P, Wells P, Agnelli G, Bounameaux H, Cohen A, Davidson BL, Piovella F, Schellong S. Oral rivaroxaban for symptomatic venous thromboembolism. N Engl J Med 2010;363(26):2499-2510. 20. Misselwitz F, Berkowitz SD, Perzborn E. The discovery and development of rivaroxaban. Ann NY Acad Sci 2011;1222:64-75. doi: 10.1111/j.17496632.2011.05971.x. 21. AstraZeneca LP. Prescribing information for Brilinta. Available at: http://www1. astrazeneca-us.com/pi/brilinta.pdf. Accessed September 7, 2011. 22. Storey RF, Becker RC, Harrington RA, Husted S, James SK, Cools F, Steg PG, Khurmi NS, Emanuelsson H, Lim ST, Cannon CP, Katus HA, Wallentin L. Pulmonary function in patients with acute coronary syndrome treated with ticagrelor or clopidogrel (from the Platelet Inhibition and Patient Outcomes [PLATO] pulmonary function substudy). Am J Cardiol 2011;108(11):1542-1546. 23. Traynor K. Ticagrelor approved for acute coronary syndrome. Am J Health Syst Pharm 2011;68(17):1568. 24. Deeks ED. Ticagrelor: A review of its use in the management of acute coronary syndromes. Drugs 2011;71(7):909-933. doi: 10.2165/11206850-00000000000000. 25. James SK, Roe MT, Cannon CP, Cornel JH, Horrow J, Husted S, Katus H, Morais J, Steg PG, Storey RF, Stevens S, Wallentin L, Harrington RA; PLATO Study Group. Ticagrelor versus clopidogrel in patients with acute coronary syndromes intended for non-invasive management: substudy from prospective randomized PLATelet inhibition and patients Outcomes (PLATO) trial. BMJ 2011;342: d3527. doi: 10.1136/bmj.d3527.
AstraZeneca LP, Wilmington, DE 800.236.9933, www.astrazeneca-us.com Boehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, CT 800.243.0127, us.boehringer-ingelheim.com Janssen Pharmaceuticals, Inc., Titusville, NJ 800.526.7736, www.janssenpharmaceuticalsinc.com
Creating an improved environment for restorative dentistry using periodontal surgery and the Broadrick flag occlusal plane analyzer Bruce W. Small, DMD, MAGD
ong-lasting restorative dentistry requires an environment with enough room to prepare and place restorations and a minimum occlusogingival height of the preparations. In addition, the occlusal planes of Spee and Wilson should be obtained in order to prevent posterior interferences, which could lead to breakage of restorations, muscular pain, or loosening of teeth.
The following case report will show an inadequate restorative environment that was changed using periodontal surgery and pre-prosthetic laboratory work in order to obtain a more ideal occlusion leading to a longer restorative prognosis. (Note: This case is still in treatment and does not include the final restorations.)
Fig. 1. Preoperative lateral view.
Fig. 2. Preoperative occlusal view of the maxillary abutments.
Fig. 3. Radiograph of the mandibular teeth.
Fig. 4. Radiograph of the maxillary teeth.
Fig. 6. The Broadrick flag in use. Fig. 5. Lateral view after periodontal surgery.
Case report Diagnosis
A 65-year-old woman came to the office with the chief complaint that a four-unit bridge had been remade and re-cemented many times in the previous few years and her dentist had retired. The left side of the patient’s dentition did not have adequate interarch space to maintain the bridge (Fig. 1). In addition, both teeth had missing restorations and lacked the minimum 3–4 mm occlusogingival height recommended by Goodacre et al (Fig. 2).1 Extraction of the maxillary molar was discussed as was the possibility of implants, which were declined by the patient due to autoimmune disease. The mandibular posterior teeth on the same side were well-supported in bone (Fig. 3), but the occlusal plane exhibited a reverse curve of Spee and very flat occlusal surfaces. The maxillary premolar had adequate osseous support and was adequate as an abutment, but the molar was questionable due to reduced bone support and previous endodontic therapy that could make it more brittle (Fig. 4). After studying the diagnostic models and evaluating the occlusion with the patient, the following treatment plan was decided upon: Refer the patient to a periodontist to perform crown lengthening on both arches; once healing is complete, do a pretreatment wax-up using new mounted study models; construct provisional restorations to test the case, particularly the maxillary bridge; finish four mandibular crowns; and finish a maxillary four-unit bridge.
Fig. 7. Preparations of the mandibular stone model prior to wax-up.
The patient was referred to a board-certified periodontist, who performed crown lengthening and pocket elimination periodontal surgery. Healthier tooth structure was exposed on the two maxillary abutments as well as on the two molars and premolars on the mandibular arch (Fig. 5). After six weeks of uneventful healing, impressions were taken for study models, mounted on a semiadjustable articulator, and evaluated by the author. A Broadrick flag occlusal plane analyzer (Water-Pik, Inc.), which can help to determine the ideal curve of Spee and Wilson while using anatomical landmarks, was used to help determine the ideal occlusal plane (Fig. 6).2 The analyzer was also used to help complete the wax-up. The mandibular posterior teeth and the two maxillary abutments were prepared on the model (Fig. 7).
Fig. 8. Biofit mold being fitted on the model.
Fig. 9. Wax being applied to the internal surface of the mold.
Fig. 10. Wax being added prior to removal of the mold.
Fig. 11. Mold being carefully removed from the die.
Fig. 12. Mold being placed on the mandibular preparation of the model.
Fig. 13. Occlusal view of the completed maxillary wax-up.
A wax-up was completed using the Biofit system (Jensen Dental) to help begin the carving of the occlusal surfaces. The proper size rubber-like molds were selected, filled with wax, and placed carefully on the prepared teeth (Fig. 8–16). Denture teeth were used as pontics in the wax-up. Alginate impressions were taken of the completed wax-ups, and stents for the provisional restorations were made using the Biostar vacuum-forming device (Great Lakes Orthodontics) (Fig. 17 and 18). A bis-acryl product was used to create the provisional restorations, which were seated with temporary cement.
The patient will be evaluated and impressions will be taken for the final restorations when indicated by her function, occlusion, periodontal response, and esthetics.
Discussion In the current case, it might have seemed easier to simply extract both maxillary abutments of the failed bridge, place implants, and make a new bridge. However, since this patient has an autoimmune disease, it was not known whether implants would be rejected by her immune system. In addition, there was little room, if any, to place any type of predictable restoration.
Fig. 15. Lateral view of the completed wax-up, showing normal-sized teeth.
Fig. 14. Occlusal view of the completed mandibular wax-up.
Fig. 16. Alginate impression and model of wax-up poured in hard stone. Fig. 17. Models and stents for provisionals.
Other options, which were not accepted by the patient, were to extract and leave a large space or insert some type of removable appliance. The mandibular crowns on teeth No. 18–20 needed to be replaced, and tooth No. 20 had a large, failing amalgam restoration, so it was easy to acquire more room by removing the old restorations and preparing these teeth. The author believes that it is advantageous to do as much laboratory work as possible yourself. By doing the lab work himself, the author became more familiar with the case, learned precisely how much room was needed, and was able to prepare the teeth more easily than if the work had been done by a commercial laboratory. Knowledge of occlusion and waxing helps, as does having all of the necessary equipment and materials.
Acknowledgements The periodontal surgery was performed by Dr. Raul Figeroa of Lawrenceville, New Jersey.
1. Goodacre CJ, Campagni WV, Aquilino SA. Tooth preparations for complete crowns: An art form based on scientific principles. J Prosthet Dent 2001;85(4): 363-376. 2. Small BW. Occlusal plane analysis using the Broadrick flag. Gen Dent 2005; 53(4):250-252.
Dr. Small is in private practice in Lawrenceville, New Jersey, and is an adjunct professor at the University of Medicine and Dentistry of New Jersey. He is also on the Board of Advisors and a visiting faculty member of the L.D. Pankey Institute in Key Biscayne, Florida. Comment
Fig. 18. Completed maxillary and mandibular provisional restorations.
Great Lakes Orthodontics, Tonawanda, NY 800.828.7626, www.greatlakesortho.com Jensen Dental, North Haven, CT 800.243.2000, www.jensendental.com Water-Pik, Inc., Fort Collins, CO 800.525.2020, professional.waterpik.com
Injection of sodium hypochlorite beyond the apical foramen—A case report Marcelo de Almeida Paschoalino, DDS Ainda Assayag Hanan, DDS Andre Augusto Franco Marques, DDS, MSc, PhD Lucas da Fonseca Roberti Garcia, DDS, MSc, PhD Angela Bittencourt Garrido, DDS, MSc, PhD Emilio Carlos Sponchiado Jr., DDS, MSc, PhD n
The aim of this study was to report a clinical case of extravasation of 1% sodium hypochlorite into the periapical tissues during endodontic treatment. During apical debridement, absence of reflux of the irrigating solution was observed, followed by root canal hemorrhage. The patient immediately complained of intense pain, and a profuse edema and hyperemia was observed on the left side of her face compatible with extravasation of hypochlorite to the periapex. The patient was treated with ibuprofen 600 mg
uxiliary chemical substances complement the physical action of endodontic files during mechanical-chemical preparation, removing tissue remains and accessing difficultto-reach structures, such as the dentinal tubules and ramifications of the main root canals.1,2 Therefore, they should have a powerful antimicrobial action, good capacity to dissolve organic material, lubricant action, low surface stress, and low cytotoxic effect on the periradicular tissues. Sodium hypochlorite solution is the first irrigant of choice due to its excellent chemical-physical properties, low cost, and accessibility. At high concentrations, its efficacy becomes greater because it produces a higher toxic effect on the periapical tissues.2,3 Irrigation with sodium hypochlorite requires a careful technique due to its toxic effect; the primary objective is to restrict the action site of this substance to the root canal. Maintenance of a reflux area, use of a needle of a compatible length
three times per day for three days, a single dose of dexamethasone 4 mg, amoxicillin 500 mg three times per day for seven days, and a cold compress for two days. Regression of the condition began on the fourth day, and normal tissue aspect and absence of sequelae were observed on the 14th day. Received: December 7, 2010 Accepted: March 9, 2011
with the canal, and prevention of excessive pressure all are required to fulfill the objective.4 Accidents are common during endodontic treatments; most of them occur due to a lack of attention to the necessary care to prevent them.5 One accident that can occur during biomechanical preparation is accidental extravasation of sodium hypochlorite into the periapical region, which causes severe discomfort and can lead to lawsuits against the dentist. It is imperative for the clinician to know how to prevent and treat such complications during endodontic treatment.5 This clinical case report of extravasation of sodium hypochlorite to the periapical region shows the effects in detail and discusses the therapy by comparing several other cases found in the literature.
Case report A 24-year-old woman came to the endodontic clinic of the Federal University of Amazonas complaining of pain in tooth No. 16. The patient reported that pain
appeared with cold stimulation, with a pulsating characteristic. The clinical signs were the presence of deep caries as well as positive and prolonged response to a sensitivity test. The radiographic examination did not show the presence of radiolucency in the periapical region. In view of this finding, irreversible pulpitis was diagnosed. The proposed treatment was biopulpectomy by the crowndown technique, using 1% sodium hypochlorite as an auxiliary chemical substance. During biomechanical preparation, absence of reflux of the irrigating solution was observed during the apical debridement stage, followed by hemorrhage of the root canal; the patient complained of a burning feeling over her entire face. Absolute isolation was removed immediately. Tumefaction and hyperemia were observed on the left side of the patient’s face, consistent with signs and symptoms of extravasation of sodium hypochlorite to the periapical tissues (Fig. 1).
Fig. 1. Presence of tumefaction and hyperemia on the left side of the face.
After receiving irrigation with a physiologic solution, the patient was prescribed the following medications: ibuprofren 600 mg every eight hours for three days; a single dose of dexamethasone 4 mg; and amoxicillin 500 mg three times per day for seven days. The patient was also instructed to use a cold-water compress for two days to alleviate pain and reduce edema. She was evaluated every 24 hours during the first three days after the incident. On the second day, the patient had an increased sensation of pain that was expressly felt when the affected region was touched, in addition to increased edema, which extended up to the infraorbital region. Ecchymosis also appeared on the jugal mucosa, the cheek, and near the labial commissure (Fig. 2 and 3). On the third day, the edema and pain stabilized but ecchymosis became more evident, and new ecchymosis appeared in the infraorbital region (Fig. 4). The patient reported that signs and symptoms began regressing after the fourth day. During a clinical examination on the seventh day, complete remission of edema and pain sensation were observed, as was a considerable reduction of
Fig. 2. Ecchymosis of the cheek near the labial commissure.
Fig. 3. Jugal mucosa.
Fig. 4. Ecchymosis of the infraorbital region.
Fig. 5. Regression of signs and symptoms after 14 days, with no signs of sequelae.
intra- and extraoral ecchymosis. After 14 days, all signs and symptoms had regressed completely without any signs of sequelae (Fig. 5).
Discussion There is consensus in some studies that the use of sodium hypochlorite as an irrigating solution is indispensable for the success of endodontic treatment due to its chemical-physical properties, such as the solvent property of the organic material and antimicrobial activity.2,3 However, the same properties that make sodium hypochlorite a good irrigant solution also make www.agd.org
it cytotoxic.6 When it comes into contact with tissues, it causes acute inflammation, the intensity of which depends on pH, concentration, and time of exposure.6 Therefore, it is preferable to use sodium hypochlorite solutions at low concentrations.6-8 Accidents involving sodium hypochlorite are related to lack of care in preventing its contact with vital tissues such as the skin, eyes, mucosa, and periapical tissue.4 Some simple procedures, such as wearing protective glasses, absolute isolation, correct odontometry, and adequate irrigation techniques,
Endodontics Injection of sodium hypochlorite beyond the apical foramen—A case report
could prevent these incidents.6-8 In the present case report, the probable cause of the incident was that the irrigation needle was introduced beyond the apical foramen, injecting sodium hypochlorite directly into the tissues. This might have been avoided if cursors had been used and the needle had been kept short of the apical foramen. Furthermore, during irrigation, care must be taken to prevent the needle from locking in the canal, thus maintaining a reflux area of the injected solution and not using excessive pressure to prevent extravasation to the periapex.5-8 Immediate signs and symptoms observed in the present case report were pain, hemorrhage, and edema, followed by the appearance of ecchymosis and necrosis one day after the incident. This semiologic condition has been found frequently in a similar chronology in several cases in the literature, with pain and edema appearing immediately after contact of sodium hypochlorite with the vital tissues, while ecchymosis, necrosis, and paresthesia usually appear three days later, although there was no paresthesia in the current case report.9-13 Immediate edema is likely the result of the action of sodium hypochlorite in the organic tissues, causing oxidation of protein and tissue lipids, increasing vascular permeability by direct action or activating certain mediators such as histamine and prostaglandins, causing cellular lysis.10,12 Treatment is palliative and prophylactic against secondary infections and tissue necrosis; cold compresses, anti-inflammatories, and antibiotics were used in the current case. However, the clinical condition of the patient and his or her signs and symptoms must be considered as well.14 For this reason, there is no consensus for the choice of pharmacological agents and 18
posture, and therapeutic variations have been described in different cases in the literature.6 There is consensus in the literature as to the use of antibiotics in cases of necrosis and potential risk of secondary infection. In the present report, amoxicillin 500 mg was orally administered every eight hours for seven days because it is a broad spectrum antibiotic active against the most frequently found types of bacteria in the oral cavity.7 This therapeutic procedure is more common and accepted in the literature and was also used by Motta et al, but for 14 days.13 On the other hand, Witton et al administered amoxicillin 1 g intravenously once for one day in a hospitalized patient.11 Another option is to use phenoxymethylpenicillin 500 mg orally every eight hours for seven days or benzylpenicillin 2 megaunits every four hours.10,15 Antibiotic therapy can also be used in cases of sinusitis secondary to the extravasation of sodium hypochlorite to the maxillary sinus. The antibiotic of choice is rifampicin 300 mg and trimethoprim 80 mg every eight hours for 10 days, associated with a decongestant to drain the maxillary sinus; the evaluation of an otolaryngologist is needed.16 To control pain and edema in the present case, ibuprofen 600 mg was administered every eight hours for three days and a single dose of dexamethasone 4 mg was prescribed postincident. Ibuprofen has an action against both pain and edema; its therapeutic effect begins approximately 30 minutes after ingestion. Dexamethasone belongs to the group of long-action duration corticoids, lasting more than 36 hours, and has a higher anti-inflammatory activity, enabling it to be administered in a single dose. However, because its therapeutic effect takes
longer to begin, the option was to combine it with ibuprofen. Motta et al suggested a different administration of dexamethasone: 2 mg daily for four days.13 On the other hand, Ehrich et al affirmed that the duration of therapy should be two to three days postincident.16 Another option is the alternate use of ibuprofen 400 mg and paracetamol 1 g every four hours.4 The development of the condition in the current case occurred in a manner similar to several cases in the literature, with complete remission of signs and symptoms after the patient received the appropriate treatment.
Summary The therapy used was effective in the treatment of the current case, which shows the importance of the dentist being aware of the use of sodium hypochlorite as an irrigating solution and knowing how to prevent, diagnose, and treat any possible accidents.
Author information Drs. Paschoalino, Hanan, Marques, Garrido, and Sponchiado are in the Department of Endodontics, School of Dentistry, Federal University of Amazonas, Manaus, Amazonas, Brazil. Dr. Garcia is in the Department of Dental Materials and Prosthodontics, Ribeirao Preto School of Dentistry, University of Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil.
1. Rai B, Jain R, Kharb S, Miglani S, Anand SC. Comparative anti-microbial activity of 15% EDTA and 15% dimercaptosuccinic acid (DMSA). J Conserv Dent 2006;9(1):32-35. 2. Estrela C, Estrela CR, Barbin EL, Spano JC, Marchesan MA, Pecora JD. Mechanism of action of sodium hypochlorite. Braz Dent J 2002;13(2): 113-117. 3. Guida A. Mechanism of action of sodium hypochlorite and its effects on dentin. Minerva Stomatol 2006;55(9):471-482.
4. Spencer HR, Ike V, Brennan PA. Review: The use of sodium hypochlorite in endodontics—Potential complications and their management. Br Dent J 2007 12;202(9):555-559. 5. Hulsmann M, Hahn W. Complications during root canal irrigation—Literature review and case reports. Int Endod J 2000;33(3):186-193. 6. Mehdipour O, Kleier DJ, Averbach RE. Anatomy of sodium hypochlorite accidents. Compend Contin Educ Dent 2007;28(10):544-546. 7. Kleier DJ, Averbach RE, Mehdipour O. The sodium hypochlorite accident: Experience of diplomates of the American Board of Endodontics. J Endod 2008;34(11):1346-1350. 8. Doherty MA, Thomas MB, Dummer PM. Sodium hypochlorite accident—A complication of poor access cavity design. Dent Update 2009;36(1): 7-8. 9. Caliskan MK, Turkun M, Alper S. Allergy to sodium hypochlorite during root canal therapy: A case report. Int Endod J 1994;27(3):163-167. 10. Mehra P, Clancy C, Wu J. Formation of a facial hematoma during endodontic therapy. J Am Dent Assoc 2000;131(4):67-71. 11. Witton R, Henthorn K, Ethunandan M, Harmer S, Brennan PA. Neurological complications
following extrusion of sodium hypochlorite solution during root canal treatment. Int Endod J 2005;38(11):843-848. 12. Crincoli V, Scivetti M, Di Bisceglie MB, Pilolli GP, Favia G. Unusual case of adverse reaction in the use of sodium hypochlorite during endodontic treatment: A case report. Quintessence Int 2008;39(2):e70-e73. 13. Motta MV, Chaves-Mendonca MA, Stirton CG, Cardozo HF. Accidental injection with sodium hypochlorite: Report of a case. Int Endod J 2009;42(2):175-182. 14. Gatot A, Arbelle J, Leiberman A, Yanai-Inbar I. Effects of sodium hypochlorite on soft tissues after its inadvertent injection beyond the root apex. J Endod 1991;17(11):573-574. 15. Camoes IC, Salles MR, Fernando MV, Freitas LF, Gomes CC. Relationship between the size of patency file and apical extrusion of sodium hypochlorite. Indian J Dent Res 2009;20(4):426430. 16. Ehrich DG, Brian JD Jr, Walker WA. Sodium hypochlorite accident: Inadvertent injection into the maxillary sinus. J Endod 1993;19(4):180182.
2 HOURS CREDIT
Potential correlation between periodontitis and coronary heart disease—An overview T.G. Shrihari, BDS, MDS The role of periodontal disease remains a headline-generating topic. Periodontal disease, caused chiefly by bacteria, is characterized by inflammation, bacteremia, a strong immune response, and loss of connective tissue attachment and bone. It is speculated that a continuous long-term exposure to oral bacteremia and bacterial toxins induces immune responses that could contribute to coronary atherosclerosis and, in conjunction with other risk factors, lead to coronary heart disease and myocardial infarction.
eriodontal disease is an infection of the supporting structures of the teeth. The host response to infection is an important factor in determining the extent and severity of periodontal disease. Systemic factors modify periodontal diseases through their effects on the normal immune and inflammatory mechanisms. The effects of a relevant number of systemic diseases on periodontitis are unclear, and it is often difficult to causally link such diseases to periodontal disease. Severe oral infections, especially periodontal disease, in otherwise healthy individuals appear to place these individuals at increased risk for developing certain health problems, including stroke and myocardial infarction. These effects cannot be explained by other traditional risk factors for heart disease such as smoking, age, cholesterol levels, blood status, exercise, and so on. New research findings raise the possibility that periodontal disease might increase mortality from a myocardial infarction nearly twofold and the risk of stroke nearly threefold.1 The deleterious effects of periodontal disease on cardiovascular
Periodontal disease might initiate pathological changes in blood vessel walls and act as a precursor of atherosclerosis in susceptible hosts. Many causal factors can play a role in heart diseases. Periodontal disease caused by pathogen bacteria as a low-grade inflammation could represent one of several possible causal factors of heart disease. Received: September 29, 2010 Final revisions: February 1, 2011 Accepted: May 10, 2011
health might be as harmful as those of smoking or high cholesterol.
Pathogenesis of periodontitis and how it affects overall health The threat of periodontitis to overall health extends across the lifetime of an individual. Bacteria causes periodontitis, yet the biochemical destruction that leads to clinical signs of disease is the result of the chronic inflammatory process in the periodontal tissues. The inflammation, if uncontrolled, leads to a loss of connective tissue attachment and bone. Three key bacteria are elevated in the subgingival plaque of patients with chronic periodontitis and have been identified as causing periodontal disease: Porphyromonas gingivalis, Treponema denticola, and Bacteroides forsythus. They require a lush biofilm ecosystem to support adherence, growth, and emergence and rely on host serum proteins and blood components for sustenance. These three bacteria have special enzymes and proteins that enable them to trigger mild host inflammation.2
P. gingivalis is capable of evading neutrophil phagocytosis, invading through the epithelium to the tissues into the bloodstream, secreting enzymes that digest host tissues to enable penetration and spreading, and triggering vasopermeability to facilitate hematogenous dissemination. The bacteria have been identified at many distant sites, such as within atheromatous plaques, fetal cord blood, pneumonia areas, brain abscess, and eye and skin inflammatory reactions.3,4 Oral bacteria have been linked to infections of the endocardium, meninges, mediastinum, vertebrae, hepatobiliary system, and prosthetic joints. Antibodies against P. gingivalis have been found in fetal cord blood, indicating that fetal exposure can occur in utero in mothers with periodontal disease.5 During pregnancy, maternal periodontal disease appears to be associated with an increased risk (up to sevenfold) for premature delivery and low birth weight for gestational age. Fetal cord blood obtained at delivery contained maternal oral bacteria that become bloodborne and target the
placenta and fetus.5 In a pregnant woman with periodontal disease, the transient bacteremia associated with periodontitis and periodontal progression appears to represent a special risk.6 Based on extrapolation, periodontal disease appears to be the reason for 18% of pre-term, low birth weight deliveries.6 P. gingivalis avoids activating the acquired immune response and evades immune surveillance and clearance. Other periodontal pathogens also appear to gain systemic egress and become bloodborne. It has been suggested that the periodontal pocket epithelium surface area can approximate a wound site for microbial penetration.7 Periodontal pathogens also create toxic lipopolysaccharide (LPS) that is highly inflammatory. LPS is released within the pockets and penetrates into the tissues, where it interacts with macrophages to stimulate the release of inflammatory mediators (PGE2, IL-1ß, TNF-α). These inflammatory markers cause vasodilation and destruction of the periodontal ligament and activate fibroblasts and osteoclasts, causing tissue destruction and bone resorption.8 Patients who secrete more PGE2, IL-1ß, and TNF-α have more systemic inflammation and more severe periodontal disease. Periodontal diseases do not affect everyone, but all people are exposed to similar oral pathogens. Some individuals never seem to get periodontal disease, no matter how poor their oral hygiene habits are. The key differentials appear to be genetic behavioral differences. Certain genes associated with an excess production of IL-1ß have been associated with severe periodontal disease.9,10 Periodontitis has a genetic component, and much of the susceptibility to disease is inherited. Smoking and diabetes, not plaque accumulation,
enhance the inflammatory response to bacterial LPS while also impairing the ability to fight infection by compromising neutrophil function. This exaggerated inflammatory response results in more severe periodontitis in patients with diabetes and those who smoke.
Periodontal inflammation and cardiac risk In patients with periodontal pathogens, bacteremia initiates a systemic antibody response and activates the hepatic acute-phase response. The liver can be activated by bacteria, bacterial products such as LPS, and cytokines like IL-1ß, TNF-α, and IL-6. This activation results in the synthesis of acute phase proteins such as C-reactive protein (CRP). The increases in CRP seen in patients with periodontitis are modest (two to three times higher) compared to the increases seen in acute infection (100–1,000 times higher). Inflammation and bacteria at a systemic, low-grade level, when aggravated chronically over many years, theoretically can cause severe cumulative damage to systemic health. Ridker reported that serum CRP levels, in addition to cholesterol levels, provide the best diagnostic indicators of risk for future myocardial infarction.11-13 It has been suggested that even mild increases in CRP enhance cardiac risk; the small elevations in CRP elicited by periodontal disease might be considered a potential cardiac risk factor. Slade et al studied the relationship among periodontal status, blood CRP levels, and the severity of subclinical atherosclerosis using B-mode ultrasonography to measure the wall thickness of the carotid vessels.14 Approximately half the linkage between high CRP levels and increased carotid wall thickness appears to be attributable to periodontal disease. www.agd.org
Arbes et al, who analyzed NHANES 111 data, revealed an association between a history of myocardial infarction and increasing periodontal disease severity in a dose-response relationship, with odds ratios >5 for the most severe periodontal disease groups.15 The authors adjusted for age, race, gender, levels of serum cholesterol, low- and high-density lipoproteins, smoking, body mass index, physical activity, hypertension, diabetes mellitus, socioeconomic status, and education. Beck et al indicated an incremental increase in risk for death due to myocardial infarction and stroke with increasing periodontal disease.16 Spahr et al found an association between periodontal disease and coronary heart disease (CHD).17 Joshipura et al and Holmlund et al illlustrated a strong relation between the number of teeth lost due to periodontitis and CHD.18,19 Holmlund et al showed an association between the severity of periodontal disease and hypertension.19 Volzke et al found a correlation between aortic atherosclerosis and myocardial infarction, body mass index, tooth quantity, plasma fibrinogen, and lipoprotein.20 Periodontal disease has an impact on a chronic atherosclerotic process that leads to atheroma formation, impaired perfusion, and vasospasm. Periodontal disease is also associated with elevated serum total cholesterol, CRP, and plasma fibrinogen, which could be the link to increased cardiovascular disease risk.21
Epidemiological studies showing an association between cardiovascular disease and periodontitis One of the earliest epidemiological studies by Matilla et al reported that dental health, including
Periodontics Potential correlation between periodontitis and coronary heart disease
periodontal health, was significantly worse in patients with acute myocardial infarction than in controls.22 In a study by DeStefano et al, participants who had periodontitis had a 25% increased risk of CHD relative to those with minimal periodontal disease.23 Beck et al used combined data from the normative aging study and the dental longitudinal study; they concluded that the levels of bone loss and cumulative incidence of total CHD and fatal CHD indicated a biologic gradient between severity of exposure and occurrence of disease.16 Persson et al studied clinical periodontal conditions, alveolar bone loss, self-reported medical histories, and carotid calcifications from panoramic radiographs in older adults.24 They found an odds ratio of 2:1 for carotid calcifications and periodontitis. In another study based on a subset of participants in the atherosclerosis risk in communities study, Beck et al concluded that clinical signs of periodontal disease were not associated with CHD but that systemic antibody response was associated with CHD in smokers and nonsmokers alike.25 Geismar et al studied the association of periodontal disease and CHD and attempted to explore common risk factors.26 They found a strong association between periodontal disease and CHD in subjects under the age of 60. They also reported that this association could be attributed, to some extent, to diabetes and smoking. A similar finding was reported in a recent study by Dietrich et al.27 In subjects followed for up to 35 years, chronic periodontitis was associated with CHD among men under the age of 60, independent of established cardiovascular risk factors. 22
Longitudinal studies evaluating the effect of periodontal therapy on inflammatory markers Several reports have shown increased serum CRP levels associated with periodontal disease severity. Ebersole et al conducted the initial study measuring serum CRP and heptoglobin levels in patients with periodontal disease.28 Patients with the most severe disease demonstrated nearly a 17-fold increase in CRP levels compared to controls. Their results showed that mechanical debridement did not lower serum CRP levels; however, there was a decrease in heptoglobin levels measured at 12 months. Patients taking 50 mg of the antiinflammatory drug flubiprofen displayed decreased levels of CRP over a two-year period. A number of studies have demonstrated that nonsurgical periodontal therapy led to a decrease in serum CRP at selective times, in conjunction with improved clinical periodontal parameters and endothelial function. The first study to report a decrease in serum CRP levels following nonsurgical periodontal treatment was conducted by Mattilla et al.22 They noted a generalized decrease in CRP in the entire population; however, post-treatment CRP levels did not decrease significantly in all participating subjects, suggesting that patient susceptibility could play a crucial role. D’Aiuto et al treated patients with nonsurgical mechanical therapy, recording serum CRP levels at baseline and at two and six months post-treatment.29,30 They noted that subjects with better clinical responses to periodontal treatment resulted in a greater decrease in CRP levels. They also recorded a statistically significant decrease in
serum CRP at six months but not at two months. They determined that patients who responded better to periodontal therapy were four times more likely to reduce their risk category for cardiovascular disease. Yamazaki et al conducted a study with Japanese subjects who displayed baseline levels of serum CRP much lower than those in Western populations with the same severity of periodontal disease.31 These subjects received nonsurgical mechanical debridement, surgical intervention when indicated, and four days of nonspecified antibiotics. Results showed a trend for decreased CRP levels after treatment. Pitiphat et al conducted a study in a Thai population that displayed lower basal levels of serum CRP compared to Western populations.32 Serum CRP levels correlated with severity of periodontal disease. This study demonstrated that periodontal infection with P. gingivalis could contribute to a systemic inflammatory burden and elevated serum CRP in otherwise healthy individuals. Tonetti et al compared periodontal treatment outcomes and endothelial function.33 Improvement of endothelial function was related to reduction in the number of periodontal lesions. Patients underwent intensive, nonsurgical therapy, resulting at 24 hours in endothelial dysfunction, a decrease in endothelial flow, and an increase in inflammatory markers, including CRP. However, six-month post-treatment CRP levels decreased and patients showed improved endothelial function and an increase in endothelial flow rate. Desvarieux et al reported smoking to be among potential effect modifiers of the periodontal infection/ atherosclerotic vascular disease association.34 Two publications from the normative aging study (NAS) cohort reported positive associations
between periodontal disease and coronary artery disease.34 Recently reported data from Korea and India appear to be among the first publications reporting on associations between periodontal disease and clinical atherosclerotic vascular disease events in Asian populations. These data reinforce previous findings that stem predominantly from European and North American cohorts. The growing diversity of study populations from which results have been reported helps to assuage concerns about spurious findings related to health behaviors (smoking, dietary patterns, and physical activity), health care systems (access to care, clinical guidelines, availability of pharmaceuticals), and environment (tobacco, smoke, pollution, diet).35,36 A recent gene association study identified a common genetic susceptibility locus, shared by both CHD and aggressive periodontitis, that could partially account for observed associations. Unfortunately, very little, if anything, can be done in observational studies to account for this possibility. The remedy for this problem lies in randomization, a key feature of intervention studies testing the oral infection/atherosclerotic vascular disease hypothesis.37 Results from studies using exposure definitions based on antibody titers also need to consider the influence of partial or complete edentulism, because edentulous participants, despite a likely history of periodontal infection, tend to display lower antibody titers compared to their dentate counterparts.38 To date, only one multicenter pilot study has examined the effects of periodontal therapy on the secondary prevention of cardiac events. The periodontitis and vascular events study randomized
patients with periodontitis and a history of severe coronary vascular disease to either community care or a study protocol that consisted of oral hygiene instruction and mechanical periodontal therapy. Over a 25-month follow-up period, adverse cardiovascular events occurred with similar frequency in the community control and the periodontal treatment groups, but periodontal therapy resulted in a rather limited improvement of periodontal status at six months postintervention. Further, these positive effects were not sustainable at the one-year follow-up. What further complicates the interpretation of the findings of this study is the fact that a substantial proportion of the individuals randomized in the community care group received some form of preventive or periodontal care outside the study. Finally, obesity appeared to nullify the effects of periodontal treatment on reduction in serum CRP levels. Important lessons were learned in this pilot trial that will inform the design of future randomized controlled trials, including: the required intensity of the protocol to provide periodontal intervention to result in clinically and biologically meaningful and sustainable positive effects on the periodontal status; the role of coexisting risk factors for atherosclerotic vascular disease that could negate the treatment-induced positive modulation of systemic inflammation; and the overall feasibility of the study design.39
Controversies The corelationship between periodontitis and CHD is not fully established. Whether patients with periodontitis have CHD or patients with CHD have periodontitis remains controversial. www.agd.org
Whether patients with exclusive periodontitis (without other predisposing factors) will have heart disease is still a controversy, because periodontitis without predisposing factors (diabetes, smoking, obesity, and stress) that could lead to CHD must be ruled out and included in the study.
Future research perspective The identification of periodontal microorganisms that could lead to CHD and their mechanism of action requires investigation. Other sensitive and specific microbiologic investigations or biochemical markers to assess the stage of CHD could be developed based on these periodontal biomarkers.
Summary Periodontal bacteria are known to invade the systemic circulation. Oral pathogens and inflammatory mediators (IL-1, TNF-α) from periodontal lesions intermittently reach the bloodstream, inducing chronic, low-level bacteremia and systemic inflammatory reactants (CRP, systemic antibodies), all of which could represent a pathogenetic link between periodontal disease and heart disease. Atherosclerosis is thought to be the underlying cause of approximately 50% of deaths in developed countries and is essentially responsible for a large portion of the clinical problems seen by physicians caring for adult patients. Although the strength of the association between periodontal and cardiovascular diseases remains to be fully established, it is in the interest of public health to address this issue for informed patient care and the development of therapeutic applications.
Author information Dr. Shrihari is an assistant professor, Department of Oral Medicine &
Periodontics Potential correlation between periodontitis and coronary heart disease
Radiology, AB Shetty Memorial Institute of Dental Sciences, Constituent College of Nitte University, Deralakatte, Karnataka, India.
1. Williams RC, Offenbacher S. Periodontal medicine: The emergence of a new branch of periodontology. Periodontol 2000 2000;23:9-12. 2. Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL Jr. Microbial complexes in subgingival plaque. J Clin Periodontal 1998;25(2):134-144. 3. Chiu B. Multiple infections in carotid atherosclerotic plaques. Am Heart J 1999;138(5 pt 2):534536. 4. Haraszthy VI, Zambon JJ, Trevisan M, Zeid M, Genco RJ. Identification of periodontal pathogens in atheromatous plaques. J Periodontol 2000;71(10):1554-1560. 5. Madianos PN, Lieff S, Murtha AP, Boggess KA, Auten RL Jr, Beck JD, Offenbacher S. Maternal periodontitis and prematurity. Part II: Maternal infection and fetal exposure. Ann Periodontol 2001;6(1):175-182. 6. Offenbacher S, Lieff S, Boggess KA, Murtha AP, Madianos PN, Champagne CM, McKaig RG, Jared HL, Mauriello SM, Auten RL Jr, Herbert WN, Beck JD. Maternal periodontitis and prematurity. Part I: Obstetric outcome of prematurity and growth restriction. Ann Periodontol 2001; 6(1):164-174. 7. Page RC, Offenbacher S, Schroeder HE, Seymour GJ, Kornman KS. Advances in the pathogenesis of periodontitis: Summary of developments, clinical implications and future directions. Periodontol 2000 1997;14:216-248. 8. Offenbacher S. Periodontal diseases: Pathogenesis. Ann Periodontol 1996;1(1):821-878. 9. Engebretson SP, Lamster IB, Herrera-Abreu M, Celenti RS, Timms JM, Chaudhary AG, di Giovine FS, Kornman KS. The influence of interleukin gene polymorphism on expression of interleukin-1beta and tumor necrosis factor-alpha in periodontal tissue and gingival crevicular fluid. J Periodontol 1999;70(6):567-573. 10. Shirodaria S, Smith J, McKay IJ, Kennett CN, Hughes FJ. Polymorphisms in the IL-1A gene are correlated with levels of interleukin-1alpha protein in gingival crevicular fluid of teeth with severe periodontal disease. J Dent Res 2000; 79(11):1864-1869. 11. Ridker PM, Glynn RJ, Hennekens CH. C-reactive protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction. Circulation 1998;97(20): 2007-2011. 12. Ridker PM, Buring JE, Shih J, Matias M, Hennekens CH. Prospective study of C-reactive protein and the risk of future cardiovascular events among apparently healthy women. Circulation 1998;98(8):731-733. 13. Ridker PM, Stampfer MJ, Rifai N. Novel risk factors for systemic atherosclerosis. A comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol
screening as predictors of peripheral arterial disease. JAMA 2001;285(19):2481-2485. 14. Slade GS, Ghezzi EM, Heiss G, Beck JD, Riche E, Offenbacher S. Relationship between periodontal disease and C-reactive protein among adults in the Atherosclerosis Risk in Communities Study. Arch Intern Med 2003;163(10):11721179. 15. Arbes SJ Jr, Slade GD, Beck JD. Association between extent of periodontal attachment loss and self-reported history of heart attack: An analysis of NHANES III data. Dent Res 1999; 78(12):1777-1782. 16. Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal disease and cardiovascular disease. J Periodontol 1996;67(10 suppl): 1123-1137. 17. Spahr A, Klein E, Khuseyinova N, Boeckh C, Muche R, Kunze M, Rothenbacher D, Pezeshki G, Hoffmeister A, Koenig W. Periodontal infections and coronary heart disease: Role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal Disease (CORODONT) study. Arch Intern Med 2006;166(5):554-559. 18. Joshipura KJ, Rimm EB, Douglass CW, Trichopoulos D, Ascherio A, Willet WC. Poor oral health and coronary heart disease. J Dent Res 1996; 75(9):1631-1636. 19. Holmlund A, Holm G, Lind L. Severity of periodontal disease and number of remaining teeth are related to the prevalence of myocardial infarction and hypertension in a study based on 4,254 subjects. J Periodontol 2006;77(7):11731178. 20. Volzke H, Schwahn C, Hummel A, Wolff B, Kleine V, Robinson DM, Dahm JB, Felix SB, John U, Kocher T. Tooth loss is independently associated with the risk of acquired aortic valve sclerosis. Am Heart J 2005;150:1198-1203. 21. Schulze A, Busse M. Periodontal disease and heart disease. Clin Sport Med Int J 2008;1(8):912. 22. Mattila K, Vesanen M, Valtonen V, Nieminen M, Palosuo T, Rasi V, Asikainen S. Effect of treating periodontitis on C-reactive protein levels: A pilot study. BMC Infect Dis 2002;2:30. 23. DeStefano F, Anda RF, Kahn HS, Williamson DF, Russell CM. Dental disease and risk of coronary heart disease and mortality. BMJ 1993; 306(6879):688-691. 24. Persson RE, Hollender LG, Powell VL, MacEntee M, Wyatt CC, Kiyak HA, Persson GR. Assessment of periodontal conditions and systemic disease in older subjects. II. Focus on cardiovascular diseases. J Clin Periodontol 2002;29(9):803-810. 25. Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal disease and cardiovascular disease. J Periodontol 1996;67(10 Suppl): 1123-1127. 26. Geismar K, Stoltze K, Sigurd B, Gyntelberg F, Holmstrump P. Periodontal disease and coronary heart disease. J Periodontol 2006;77(9):15471554. 27. Dietrich T, Jimenez M, Krall Kaye EA,Vokonas PS, Gracia RI. Age-dependent associations between chronic periodontitis/edentulism and
risk of coronary heart disease. Circulation 2008; 117(13):1668-1674. 28. Ebersole JL, Machen RL, Steffen MJ, Willman DE. Systemic acute-phase reactants, C-reactive protein and haptoglobin, in adult periodontitis. Clin Exp Immunol 1997;107(2):347-352. 29. D’Aiuto F, Parkar M, Andreou G, Suvan J, Brett PM, Ready D, Tonetti MS. Periodontitis and systemic inflammation: Control of the local infection is associated with a reduction in serum inflammatory markers. J Dent Res 2004;83(2): 156-160. 30. D’Aiuto F, Ready D, Tonetti MS. Periodontal disease and C-reactive protein associated cardiovascular risk. J Periodontal Res 2004;39(4): 236-241. 31. Yamazaki K, Honda T, Oda T, Ueki-Maruyama K, Nakajima T, Yoshie H, Seymour GJ. Effect of periodontal treatment on the C-reactive protein and proinflammatory cytokine levels in Japanese periodontitis patients. J Periodontal Res 2005;40(1):53-58. 32. Pitiphat W, Savetsilp W, Wara-Aswapati N. C-reactive protein associated with periodontitis in a Thai population. J Clin Periodontol 2008;35(2): 120-125. 33. Tonetti MS, D’Aiuto F, Nibali L, Donald A, Storry C, Parkar M, Suvan J, Hingorani AD, Vallance P. Treatment of periodontitis and endothelial function. N Engl J Med 2007;356(9):911-920. 34. Desvarieux M, Demmer RT, Jacobs DR Jr, Rundek T, Boden-Albala B, Sacco RL, Papapanous RN. Periodontal bacteria and hypertension: The oral infections and vascular disease epidemiology study (INVEST). J Hypertens 2010;28(7):14131421. 35. Choe H, Kim YH, Park JW, Kim SY, Lee SY, Jee SH. Tooth loss, hypertension and risk for stroke in a Korean population. Atherosclerosis 2009; 203(2):550-556. 36. Pradeep AR, Hadge P, Arjun Raju P, Shetty SR, Shareef K, Guruprasad CN. Periodontitis as a risk factor for cerebrovascular accident: A casecontrol study in the Indian population. J Periodontal Res 2010;45(2):223-228. 37. Schaefer AS, Richter GM, Groessner-Schreiber B, Noack B, Nothnagel M, El Mokhtari NE, Loos BG, Jepsen S, Schreiber S. Identification of a shared genetic susceptibility locus for coronary heart disease and periodontitis. PLoS Genet. 2009;5(2):e1000378. 38. Vlachojannis C, Dye BA, Herrera-Abreu M, Pikdoken L, Lerche-Sehm J, Pretzl B, Celenti R, Papapanous RN. Determinants of serum IgG responses to periodontal bacteria in a nationally representative sample of US adults. J Clin Periodontol 2010:37(8):685-696. 39. Offenbacher S, Beck JD, Moss K, Mendoza L, Paquette DW, Barrow DA, Couper DJ, Stewart DD, Falkner KL, Graham SP, Grossi S, Gunsolley JC, Madden T, Maupome G, Trevisan M, Van Dyke TE, Genco RJ. Results from Periodontitis and Vascular Events (PAVE) study: A pilot multicentered, randomized, controlled trial to study effects of periodontal therapy in a secondary prevention model of cardiovascular disease. J Periodontol 2009;80(2):190-201.
self CDE 2 HOURS instruction CREDIT
Exercise No. 297
Periodontics Subject Code 490 The 15 questions for this exercise are based on the article “Potential correlation between periodontitis and coronary heart disease—An overview” on pages 20-24. This exercise was developed by Daniel S. Geare, DMD, in association with the General Dentistry Self-Instruction committee. Reading the article and successfully completing the exercise will enable you to understand: • the contributing causalities of periodontal disease; • the relationship between periodontal disease and coronary heart disease (CHD); and • the physiological risk factors of periodontal disease and CHD.
5. The bacteremia from periodontal disease in a mother accounts for what percentage of low birth weight babies? A. 5 B. 15 C. 18 D. 24
6. Porphyromonas gingivalis activates the host immune response after it penetrates the periodontal pockets. These bacteria release a lipopolysaccharide that triggers the T cell response in inflammation. A. Both statements are true. B. The first statement is true; the second is false. C. The first statement is false; the second is true. D. Both statements are false.
1. What is the estimated range of prevalence for severe periodontal disease in the U.S.? A. 0–9% B. 10–30% C. 40–60% D. 70–90% 2. The increased health risks from periodontal disease include all of the following except one. Which is the exception? A. Myocardial infarction B. Diabetic peripheral neuropathies C. Exotoxin-induced peripheral neuropathies D. Stroke
3. Which bacterium is known to cause periodontal disease? A. Porphyromonas gingivalis B. Lactobacillus salivarius C. Bifidiobacterium adolescentis D. Bacteriodes pyogenes
4. How can fetal tissue be exposed to oral bacteria? A. Through the birth canal B. Through the mother’s milk C. Through oral contact between the mother and baby D. Through fetal cord blood
7. What is the dominant feature of resistance to periodontal disease? A. Genetic behavioral differences B. Environmental and locational differences from age 1–5 C. Whether the parents/siblings smoked D. Acquired brushing/hygiene habits
8. Studies associating periodontal disease and CHD show all of the following except one. Which is the exception? A. Patients with heart attacks showed significant periodontitis present. B. Although periodontal disease was correlated with CHD, antibody response between CHD and periodontal disease was not. C. There is a strong age correlation between CHD and periodontal disease in patients under the age of 60. D. There is a ratio of 2:1 between periodontal disease and carotid artery calcifications.
9. Why is measuring C-reactive protein (CRP) important in periodontal disease? A. CRP is produced in the periodontal ligament space. B. CRP varies with the severity of periodontal disease. C. CRP causes heart disease. D. CRP is produced in inflamed heart tissue.
10. Which of the following is not a characteristic of periodontitis? A. Inflammation B. Bacteremia C. Poor host response D. Strong immune response 11. Pathological bacteria causing periodontal disease could be a factor in heart disease development. This is because periodontal disease causes changes in blood vessel walls. A. Both statements are true. B. The first statement is true; the second is false. C. The first statement is false; the second is true. D. Both statements are false.
12. By what factor might periodontal disease increase the risk of having a stroke? A. Two B. Three C. Four D. Six 13. The threat of periodontitis to overall health occurs primarily A. during the entire lifetime. B. during periods of chronic illness. C. after age 70. D. during an acute illness. 14. Oral bacterial infections have been linked to all of the following except one. Which is the exception? A. Pneumonia B. Gout C. Brain abscess D. Endocarditis 15. All of the following are possible indicators of periodontal disease and CHD except one. Which is the exception? A. Bacteremia B. CRP C. Systemic antibodies D. Bacterial exotoxins
Answer form and Instructions are on pages 79-80. Answers for this exercise must be received by December 31, 2012.
Influence of increment thickness on the similarity of composite shade: A pilot study Lourenco de Moraes Rego Roselino, DDS Lucas da Fonseca Roberti Garcia, DDS, MSc, PhD Ana Beatriz Silva Sousa, DDS Fernanda de Carvalho Panzeri Pires-de-Souza, DDS, MSc, PhD n
The aim of this study was to evaluate the similarity in shade between increments of different composite thicknesses. Fifty test specimens 12 mm in diameter were fabricated and separated into five groups ( n = 10) according to sample thickness: 0.5 mm, 1.0 mm, 1.5 mm, 2.0 mm, and 2.5 mm. Specimens were polished with water abrasive papers and silicone points. Next, based on the CIE L*a*b* system, test specimens were submitted to color readouts, and the values obtained for the coordinates L*, a*, and b* for each thickness were compared using one-way ANOVA and a Tukey test ( P < 0.05). The results demonstrated that there was a reduction in coordinate L* as the test specimen thickness increased, with statistically significant differences (P < 0.05), except for 2.0 mm and 2.5 mm
s an optical property, color is not simply a property of light, but the result of the effect of light waves reflected from restorative materials, which can be opaque or translucent.1 Various factors are involved in color determination, such as the characteristics of the light under which the object is observed; the way in which the waves of light incident on the object are absorbed, transmitted, or reflected; and the effects of the environment on the observer.2,3 The color and opacity of an illuminated object are directly related to the scattering and absorption of the light emitted by the source; in turn, light scattering is caused by its refraction upon falling on the object.4 The light can be absorbed, reflected, or transmitted by the interior of the object; the light is scattered with greater intensity in opaque objects and more transmission and less scattering occurs in transclucent objects.5
thicknesses (P > 0.05). Samples 1.5 mm thick presented less variation of a*, while a greater variation occurred for samples 2.5 mm thick, with a significant difference in comparison with the other thicknesses (P < 0.05), except for 2.0 mm (P > 0.05). Samples 0.5 mm thick presented a greater variation of b*, while the lowest variation in this coordinate occurred for samples 2.5 mm thick, which was significantly different from the other samples (P < 0.05). It was concluded that different composite thicknesses do not present similarity of color and have an influence on the final result of esthetic restorations. Received: September 3, 2010 Final revisions: January 25, 2011 Accepted: April 19, 2011
The development of composites, particularly with respect to adhesive systems and physicomechanical properties, allied with the characteristic of re-establishing the natural appearance of teeth with respect to color and translucence, has made this material one of the main choices among esthetic restorative materials used in dentistry.6,7 Nevertheless, to obtain a restoration with the most natural appearance, various hues with different nuances of color and opacity are necessary for creating a single restoration.4 In the past, esthetic restorative material manufacturers were more concerned about offering composites with a large variety of shades. Recently, however, composites with different degrees of opacity have been introduced, making it possible to imitate more natural aspects of the tooth, such as high marginal and incisal translucence and the reflection www.agd.org
from the tooth surface of the cavity walls.4,5 Even so, creating a restoration with an appearance as close to that of the natural tooth as possible continues to be problematic and depends on a sophisticated mixture of shades and increments of different opacities and thicknesses, the latter two factors being preponderant in simply selecting the adequate shade for the restoration.4,5,8,9 The aim of this study was to evaluate the similarity in shade between increments of different thicknesses of a composite. The null hypothesis tested was that the different thicknesses evaluated would present no difference in the similarity of shade between them.
Materials and methods For this study, the composite Filtek Z250 (3M ESPE) in shade A 3.5 was used; its properties are described in Table 1.
Cosmetic Dentistry Influence of increment thickness on the similarity of composite shade: A pilot study
Table 1. Composite used in the current study.
Table 2. Mean values and standard deviations for the coordinates L*, a*, and b*.
-0.82 ± 0.23a
13.54 ± 0.56a
56.28 ± 3.06b
-0.72 ± 0.15a
12.81 ± 0.72a
50.28 ± 1.61
-0.59 ± 0.16
9.99 ± 0.53b
47.77 ± 1.14d
-0.99 ± 0.14ab
7.24 ± 0.64b
UDMA = Urethane dimethacrylate
46.82 ± 1.17
-1.22 ± 0.25
6.37 ± 0.42b
Bis-EMA = bisphenol-A glycidyl dimethacrylate ethoxylate.
Note: Different superscript letters indicate statistically significant differences ( P < 0.05).
Monomers Filtek Z250 (microhybrid)
Bis-GMA, UDMA, Bis-EMA
Bis-GMA = bisphenol-A glycidyl dimethacrylate
Fig. 1. Composite test specimens in ascending order of thickness (top to bottom: 0.5, 1.0, 1.5, 2.0, and 2.5 mm).
L* 61.40 ± 2.26a
Fifty test specimens were fabricated with the use of a Teflon matrix 12 mm in diameter and randomly separated into five groups (n = 10) according to sample thickness: Group 1, 0.5 mm; Group 2, 1.0 mm; Group 3, 1.5 mm; Group 4, 2.0 mm; and Group 5, 2.5 mm. The composite was inserted into the matrix according to the incremental technique and photoactivated for 20 seconds using an LED appliance (FlashLite 1401, Discus Dental) at 1,100 mW/cm2 with a wavelength of 460–480 nm, in accordance with the manufacturer’s recommendations. The last layer of composite was protected with a 1.0 mm thick glass slide before photoactivation to allow for compaction and flow of the material and to prevent bubble formation in the test specimens. After 24 hours, specimens were polished with water abrasive paper (Norton Abrasives) in decreasing order of granulation (320, 600, and 1200) and with silicone points (Astropol, Ivoclar Vivadent Inc.) mounted at low speed (MRS 400, Dabi Atlante). After polishing, the thickness of every test specimen was checked with a digital pachymeter (Digimess Instrumentos de Precisao). The test specimens were submitted to color readouts with a PCB 687 spectrophotometer
(BYK-Gardner USA), based on the CIE L*a*b* system, against a white standard background (standard white 45 degrees, 0 degrees reflectance, BYK-Gardner USA), as described by Pires-de-Souza et al.10 The similarity in shade between the test specimens was determined by using a one-way ANOVA and a Tukey test (P < 0.05) to compare the mean values of coordinates L*, a*, and b* obtained for each sample.
Results The mean values corresponding to the coordinates L*, a*, and b* for each thickness of the test specimens are shown in Table 2. Statistical analysis showed that for coordinate L*—which represents the luminosity of the object—the greater the thickness, the lower the luminosity values, with a statistically significant difference among the different thicknesses (P < 0.05), except for Groups 4 and 5 (P > 0.05). The smaller the thickness (0.5 mm), the lighter the sample appears when compared with thicker samples (Fig. 1). Mean values for coordinates a* (variation between green/red) and b* (variation between blue/ yellow) for the different thicknesses indicate less alteration than for coordinate L*. For coordinate a*, there was no statistically significant
difference among the thicknesses evaluated (P > 0.05), except for Group 5 (P < 0.05), indicating a tendency to green. For coordinate b*, the mean values decreased as the thickness of the test specimens increased, which means lower color saturation for thicker samples. The smaller thicknesses, 0.5 mm and 1.0 mm, presented mean values statistically different from Groups 3–5 (P < 0.05), which demonstrated statistically similar mean values to each other (P > 0.05).
Discussion The characteristic of light transmission is an important esthetic property of a composite.11 Translucence and opacity are opposite terms and are used to describe the quantity of light that is allowed or prevented from passing through a certain material.11 The translucence and opacity of a composite can be determined by taking a color reading of the sample, in which only the values of the coordinate L* (luminosity) are considered.4 To allow for the reproduction of the esthetic aspects of natural teeth, color, texture, opacity, and translucence are important characteristics.4 The results obtained in the current study demonstrated that the thicker the specimen, the lower its translucence and, therefore, the greater its opacity, leading to rejection of the null hypothesis.12,13 Light transmission through composite restorations occurs by diffuse and straight line transmissions, due to the light scattering caused by the load particles. In other words, the thicker the increment, the greater the light scattering.12 Therefore, the thickness of the increment of composite used while making a restoration is of fundamental importance in the esthetic result. For cases in which there is insufficient dental structure remaining on the
lingual wall of a tooth that must be restored, such as in extensive Class III or Class IV cavities, the index of translucence of the composite could result in an esthetic failure caused by the grayish appearance of the restorative material in contrast with the darkness of the oral cavity when compared to the adjacent dental structure.14 Therefore, a composite with an opaque hue or thicker increment must be used to promote better esthetic results.12,15 The results of the present study demonstrated that the thicker the sample, the greater the trend toward blue, which, in a restoration, can be confused with its grayish appearance.16 Therefore, the clinician must have accurate knowledge of the optical behavior of each composite and the interaction between the different hues in order to obtain restorations of a high esthetic quality.4 Another important situation that must be considered with regard to the thickness of increments when making esthetic restorations is the stress generated during polymerization shrinkage and bubble formation.17-19 Clinically, the effects of polymerization shrinkage of a composite can be minimized by using techniques for making restorations in layers or in small increments that are photoactivated later.20 For this reason, the maximum thickness evaluated in the current study was 2.5 mm, a thickness compatible with making a restoration, avoiding bubble formation, and diminishing the C-factor.17-19 Even so, none of the techniques described are capable of completely eliminating the stress generated by the polymerization shrinkage of a composite.20 With the intention of combining mechanical resistance and a smoother surface in addition to facilitating polishing and enhancing the esthetic appearance of www.agd.org
restorations, the application of hybrid and microparticle systems in conjunction has been suggested. However, due to the difficulty of performing this technique, microhybrid composites were developed. Microhybrid composites combine the facility of polishing, the natural aspect, and the depth of shade present in microparticle composites with the mechanical resistance to wear that is characteristic of the hybrid systems.21,22 Nevertheless, in spite of favorable mechanical and optical behavior, microhybrid composites have a concentration of load particles of approximately 60%, promoting less light scattering; this phenomenon alters the observer’s perception of light.23-25 The combination of increments of different shades, opacities, and especially thicknesses is still necessary to obtain a satisfactory esthetic result, as proven by the results of the current study, which demonstrated that different thicknesses presented a different optical behavior in relation to the coordinates evaluated with regard to similarity in color.4 Profound knowledge of the dental structure and its morphology is also key for satisfactory esthetic results. The color of a tooth can be identified on the basis of its appearance, hue, saturation, and brightness.26 In general, dentin (covered by enamel, which, in turn, is translucent) presents different nuances of hue and fluorescence and has a certain degree of opalescence.26 To minimize these different characteristics of the two tissues, a technique that uses various increments of different thicknesses is recommended. Also, according to Vichi et al, only small restorations can be made with a duly satisfactory esthetic result when using a single increment.4
Cosmetic Dentistry Influence of increment thickness on the similarity of composite shade: A pilot study
Conclusion Based on the results of the current study, it can be concluded that the thickness of the increment used while making a restoration plays a fundamental role in the final esthetic result, particularly regarding luminosity. However, other factors such as opacity, correct shade selection, and the individual professional’s skill and knowledge with respect to the optical properties of composites are extremely relevant for successful treatment.
Disclaimer The authors of this study deny any conflict of interest.
Author information Drs. Roselino, Garcia, Sousa, and Pires-de-Souza are in the Department of Dental Materials and Prosthodontics, Ribeirao Preto School of Dentistry, University of Sao Paulo, Brazil.
1. Jonhston WM, Reisbick MH. Color and translucency changes during and after curing of esthetic restorative materials. Dent Mater 1997; 13(2):89-97. 2. Schanda JD. Colorimetry. In: DeCusatis C. Handbook of applied photometry, ed. 2. New York: Optical Society of America Springer-Verlag:1998; 327-412. 3. Janda R, Roulet JK, Latta M, Steffin G, Ruttermann S. Color stability of resin matrix restorative materials as a function of the method of light activation. Eur J Oral Sci 2004;112(3):280285. 4. Vichi A, Fraioli A, Davidson CL, Ferrari M. Influence of thickness on color in multi-layering technique. Dent Mater 2007;23(12):1584-1589.
5. Lee YK, Powers JM. Color changes of resin composites in the reflectance and transmittance modes. Dent Mater 2007;23(3):259-264. 6. Sarafianou A, Iosifidou S, Papadopoulos T, Eliades G. Color stability and degree of cure of direct composite restoratives after accelerated aging. Oper Dent 2007;32(4):406-411. 7. Samra AP, Pereira SK, Delgado LC, Borges CP. Color stability evaluation of aesthetic restorative materials. Braz Oral Res 2008;22(3):205-210. 8. Lee YK, Lim BS, Rhee SH, Yang HC, Powers JM. Color and translucency of A2 shade resin composites after curing, polishing and thermocycling. Oper Dent 2005;30(4):436-442. 9. Lee YK, Lim BS, Kim CW, Powers JM. Color characteristics of low-chroma and high-translucence dental resin composites by different measuring modes. J Biomed Mater Res (Appl Biomater) 2001;58(1):613-621. 10. Pires-de-Souza Fde C, Casemiro LA, Garcia Lda F, Cruvinel DR. Color stability of dental ceramics submitted to artificial accelerated aging after repeated firings. J Prosthet Dent 2009;101(1): 13-18. 11. Kim JH, Lee YK, Powers JM. Influence of a series of organic and chemical substances on the translucency of resin composites. J Biomed Mater Res B Appl Biomater 2006;77(1):21-27. 12. Arimoto A, Nakajima M, Hosaka K, Nishimura K, Ikeda M, Foxton RM, Tagami J. Translucency, opalescence and light transmission characteristics of light-cured resin composites. Dent Mater 2010;26(11):1090-1097. 13. Lee YK. Influence of filler on the difference between the transmitted and reflected colors of experimental resin composites. Dent Mater 2008;24(9):1243-1247. 14. Ikeda T, Murata Y, Sano H. Translucency of opaque-shade composites. Am J Dent 2004; 17(2):127-130. 15. Kawaguchi M, Fukushima T, Miyazaki T. The relationship between cure depth and transmission coefficient of visible-light-activated resin composites. J Dent Res 1994;73(2):516-521. 16. Kamishima N, Ikeda T, Sano H. Color and translucency of resin composites for layering techniques. Dent Mater J 2005;24(3):428-432. 17. Ferrari M, Goracci C, Sadek F, Eduardo P, Cardoso C. Microtensile bond strength tests: scanning electron microscopy evaluation of sample integrity before testing. Eur J Oral Sci 2002;110(5): 385-391. 18. Choi KK, Ryu GJ, Choi SM, Lee MJ, Park SJ, Ferracane JL. Effects of cavity configuration on
composite restoration. Oper Dent 2004;29(4): 462-469. 19. Versluis A, Tantbirojn D, Pintado MR, DeLong R, Douglas WH. Residual shrinkage stress distributions in molars after composite restoration. Dent Mater 2004;20(6):554-564. 20. Ferracane JL. Developing a more complete understanding of stresses produced in dental composites during polymerization. Dent Mater 2005;21(1):36-42. 21. Fahl N Jr. Predictable aesthetic reconstruction of fractured anterior teeth with composite resins: A case report. Pract Periodontics Aesthet Dent 1996;8(1):17-31. 22. Mitra SB, Wu D, Holmes BN. An application of nanotechnology in advanced dental materials. J Am Dent Assoc 2003;134(10):1382-1390. 23. Inokoshi SMB, Burrow MF, Kataumi M, Yamada T, Takatsu T. Opacity and color changes of toothcolored restorative materials. Oper Dent 1996; 21(2):73-80. 24. Schulze KA, Marshall SJ, Gansky SA, Marshall GW. Color stability and hardness in dental composites after accelerated aging. Dent Mater 2003;19(7):612-619. 25. Campbell PM, Johnston WM, O’Brien WJ. Light scattering and gloss of an experimental quartzfilled composite. J Dent Res 1986;65(6):892894. 26. Duarte S, Perdigao J, Lopes M. Composite resin restorations. Natural aesthetic and dynamic of light. Pract Proced Aesthet Dent 2003(1);15: 657-664.
BYK-Gardner USA, Columbia, MD 301.483.6500, www.byk.com/instruments Dabi Atlante, Ribeirao Preto, SP, Brazil 55.16.3512.1212, www.dabiatlante.com.br Digimess Instrumentos de Precisao, Sao Paulo, SP, Brazil 55.11.2696.5700, www.digimess.com.br Discus Dental, Culver City, CA 800.422.9448, www.philipsoralhealthcare.com Ivoclar Vivadent Inc., Amherst, NY 800.533.6825, www.ivoclarvivadent.us.com Norton Abrasives, Worcester, MA 254.918.2313, www.nortonindustrial.com 3M ESPE, St. Paul, MN 800.634.2249, http://solutions.3m.com
2 HOURS CREDIT
Adult minimal oral sedation in the general practice setting K. David Stillwell, DDS, MAGD
Barbara J. Anderson, DMD
Patients who are phobic, elderly, physically disabled, or mentally impaired pose unique challenges in the dental operating environment. Reducing stress during the dental appointment allows for improved cooperation, safety, and clinical efficiency. There is an increased need for dentists who are able to confidently and
his article provides detailed information on a systematic sedation protocol currently employed in a hospital-based general practice residency program. The protocol outlined here is termed adult minimal oral sedation (AMOS), defined as a minimally depressed level of consciousness produced by a pharmacologic method in which ventilatory and cardiovascular functions are unaffected while yielding a patient who can respond normally to tactile stimulation and verbal commands.1 This protocol has been observed to be a valuable and reliable adjunct to patients that can be reproduced in other practice environments. Replication and implementation of a similar outpatient sedation program into the general practice setting requires supplemental training and resources by the dentist and staff. For those interested, the authors have thoroughly outlined an in-office AMOS methodology, comprising proper patient selection for minimal sedation; use of an appropriate preoperative physical status assessment tool like the American Society of Anesthesiologists (ASA) classification method; effective preoperative physical evaluation procedures; medical risk assessment
competently render care to these patients. Adult oral conscious sedation at the minimal level is a valuable way to more effectively manage the specific dental needs of this growing population. Received: January 24, 2011 Accepted: April 19, 2011
and informed consent; and practice logistics, information flow, and instrumentation. A short list of well-studied sedative and anxiolytic drugs (AMOS Drug Protocol) will be discussed individually to highlight their indications and usage. Appropriate monitoring, documentation, and recovery of the sedated patient will also be covered. When properly structured and administered, minimal sedation of the adult patient is a safe, effective professional service to be integrated into the dental office.
Background and evolution of AMOS Due to the high cost of effective dental care in a hospital setting, there is an escalating need for adult patients with special needs to receive treatment in the traditional office environment. The administration of sedation has been a part of dentistry since the 1840s and continues to have a remarkable record of safety, yet necessary dental care is often neglected due to fear, anxiety, or lack of access to competently trained professionals in an appropriately equipped treatment facility. Thus, many physically and mentally challenged individuals fail to receive comprehensive dental www.agd.org
care that relieves pain and restores form and function. As the adult special needs segment of the population continues to grow, there is an increased need for dentists who are able to safely and routinely render care to these patients. Standards of care continue to evolve as new evidence on sedative agents and technique is reported. This has prompted most state dental boards to recently revise their regulation of the enteral (oral, sublingual, and rectal) administration of sedatives to be consistent with the American Dental Association’s 2007 Guidelines for the use of sedation and general anesthesia by dentists.2 In addition to certification in basic life support for health care providers, many states now mandate the completion of 16 hours of formal training in minimal oral sedation technique for patients over the age of 12. This basic training includes experiences in managing a compromised airway critical to the prevention of life-threatening emergencies. Dentists considering the use of in-office sedative techniques are reminded to carefully review all jurisdictional rules and regulations related to additional training and education, issuance of permits, and requirements for administration of
Conscious Sedation Adult minimal oral sedation in the general practice setting
Table 1. Evaluation of preoperative health status prior to AMOS. ASA category Preoperative health status
Organ system status
Normal healthy patient
All organ systems intact.
Patient with mild systemic disease
No functional limitations. Has well-controlled disease of one body system. Controlled hypertension or diabetes without systemic effects, cigarette smoking without COPD, mild obesity, pregnancy. Update medical history and cross-check for medication interactions.
Patient with severe systemic disease
Some functional limitation. Has controlled disease of more than one body system or major organ. No immediate danger of death. Controlled congestive heart failure (CHF), stable angina, previous heart attack, poorly controlled hypertension, morbid obesity, chronic renal failure, bronchospastic disease with intermittent symptoms. Strongly encourage physician consult.
INDICATED WITH PRECAUTIONS
Patient with severe systemic disease that is a constant threat to life
Has at least one severe disease that is poorly controlled or at end stage. Possible risk of death. Unstable angina, symptomatic COPD, symptomatic CHF, hepatorenal failure. Obtain physician consult and review current laboratory values.
Patient not expected to survive >24 hours without surgical intervention
Multi-organ failure. Hypothermia, poorly controlled coagulopathy.
Patient declared brain dead
Organs are being removed for donor purposes.
Adapted from: http://my.clevelandclinic.org/services/Anesthesia/hic_ASA_Physical_Classification_System.aspx.4,7
oral conscious sedation; significant differences continue to exist from state to state. Expanding the capabilities of a practitioner to safely implement and provide outpatient sedation hinges on the individual’s willingness to seek out appropriate and frequent continuing education courses and to dedicate sufficient time, resources, and training within the office environment. Minimal sedation training should include updates in patient evaluation, informed consent, monitoring, discharge criteria, documentation, facilities, equipment, and personnel. The treatment environment must be properly equipped with redundant suction devices, physiologic 32
monitoring equipment, a positivepressure oxygen delivery system, and emergency drugs including the benzodiazepine reversal agent, flumazenil. In-office protocols for the delivery of dentistry under sedation must be developed to include assessment of recovery for home readiness and activation of emergency management services (EMS). Training programs for staff should be held at frequent intervals and documented to maintain compliance with regulatory agencies.3 AMOS can be safely rendered by more practitioners once these training programs are completed, additional equipment is obtained, and office procedures are modified to incorporate all of the defined regulatory requirements.
Patient evaluation and risk assessment Advances in medical care have resulted in dental outpatients who are both medically and pharmacologically complex. Many adult patients require sedation to complete a thorough oral examination and subsequent care because of behavioral, communicative, and/or complex medical problems. For patients with a compromised medical status, lack of a physiologic reserve capacity coupled with the stress and anxiety of a dental procedure can precipitate a medical emergency or urgency outside the scope of a dentist’s management expertise. AMOS can be considered an important adjunct in the treatment of such patients to
minimize stress and the resultant autonomic response.4,5 Prudent risk management indicates that dentists should limit the use of sedation to those patients who require the modality after careful screening and physical assessment; sedation should be administered only when the practitioner has adequate training, monitoring equipment is in place, and emergency preparedness scenarios are established.3 The physical evaluation consists of a current medical history, including a written review of systems, a review of medication, and a basic physical inspection. The pharmacologic history should include prescription medications, OTC medications, and dietary supplements (herbals, alternative medicines, and so forth) as well as a complete list of all allergies and major side effects.4 It has been demonstrated that 30% of patients receiving treatment will have a history of at least one medical condition. Several studies have determined a 50% chance of a significant drug interaction for a patient taking five medications, while the likelihood for a patient taking eight prescription drugs is 100%.6 It is also helpful to discuss with the patient any history with sedative procedures, including general anesthesia. Baseline vital signs should be noted during the preliminary evaluation. Often, with the elderly and in patients with medically complex situations, a physician consult is needed to confirm specific information pertinent to decision making prior to routine dental care, including sedation procedures. The ASA has formulated the most commonly used system to assess physical status or risk (ASA I–VI).7,8 The ASA status of each potential sedation patient should be classified and recorded. With significant physical findings from the examina-
tion captured, eligibility for receiving sedative therapies in clinic will bear a close dependence on the ASA status of the candidate patient. In the authors’ clinic, minimal sedation is offered routinely to patients classified as ASA I or II. Patients who are classified as ASA III or IV should be considered for minimal sedation only after medical clearance from the primary care physician and/or relevant specialist. Treatment modifications are often necessary for patients who have ASA III or IV classifications (Table 1).
Preoperative and intraoperative responsibilities The policy at the authors’ clinic for the administration of AMOS is to strongly recommend to patients that all sedatives be administered in the dental office for maximum safety. After careful and thorough evaluation, some extremely apprehensive patients will be candidates to receive medication to assist with restful sleep the night prior to their scheduled appointment. A preoperative office visit is scheduled to obtain informed consent for the sedation procedure and to verbally review written pre- and postoperative instructions with each patient. Each patient must identify a responsible adult companion; that companion is informed that his or her cooperation is required to deliver the patient to the clinic, to remain in the clinic and be available for the duration of the appointment, and to transport the patient home and remain with that patient for an extended period of observation. The companion/guardian should be given copies of the specific written patient care instructions and should agree to provide that care. All patients are required to remain NPO (nulla per os, or nothing by mouth) after midnight for morning AMOS procedures. For patients www.agd.org
receiving oral sedation in the afternoon hours, the authors encourage the intake of small amounts of clear fluid with dry toast or crackers to avoid dehydration and to absorb gastric secretions. Patients who regularly take prescribed medications in the morning should do so with a small sip of water. Diabetic patients are encouraged to schedule morning dental appointments for AMOS; these patients should not postpone their antihyperglycemic medications prior to the sedation procedure. To avoid a hypoglycemic event, each patient is administered small amounts of apple juice once seated in the operatory to stabilize blood glucose levels. A glucometer is kept nearby along with a concentrated glucose source (cake icing) to allow rapid assessment and/or management of intraoperative hypoglycemia. From the moment the patient enters the clinic for the scheduled AMOS procedure, the entire office staff understands the special obligation assumed to safeguard patients who are under the influence of medications. From the time the patient is seated in the operatory until he or she is officially discharged, the dentist or a basic life support-trained staff member must remain with the patient at all times. Physiologic and visual monitoring of the patient should commence as soon as he or she is seated and all anticipated procedures have been reviewed. Monitoring must include oxygenation, ventilation, and circulation, and a consistent method of recording must be established. A pulse oximeter and use of an integrated blood pressure cuff are the standard of care to ensure proper oxygenation and circulation. Percentage hemoglobin oxygen saturation (SpO2) as tracked by the pulse oximeter typically ranges from 93–100%; when SpO2 falls to 92%,
Conscious Sedation Adult minimal oral sedation in the general practice setting
Fig. 1. Sample anesthesia record.
the device is programmed to emit an audible warning. The patient is instructed to take one or two deep breaths, and the lowered oxygen saturation level typically responds by moving back into the acceptable range within a few seconds. In addition to monitoring the above instruments, chest excursions, respiration, and the mucosa color should be continuously observed. Vital signs are recorded preoperatively, postoperatively, and 34
intraoperatively at specific intervals. For patients receiving AMOS, blood pressure is recorded at 15-minute intervals and heart rate and oxygen saturation are recorded continuously. Proper patient documentation should include a paper printout of the pulse oximeter readings throughout the procedure. It might be appropriate to include a supplemental anesthesia record (Fig. 1). With vital signs assessed as stable, all consents properly executed, and
the responsible adult companion present in the office, the sedation procedure can begin. A sedative agent is selected and administered that best matches the patient’s medical profile and coordinates the agent’s half-life with the anticipated length of the dental procedure. No additional medication is administered as long as the patient displays signs of sedation and tolerates dental treatment. The operatory configuration during dental procedures under oral sedation is altered only by the presence and use of the pulse oximeter unit (Fig. 2). Certain patient factors might require an increased dosing or a repeated dosing during AMOS; these factors include extreme anxiety or fear, liver enzyme induction, increased body mass or fat, heavy use of stimulants (such as caffeine or tobacco), and admitted drug tolerance related to past use. Based on known distribution curves, it should be acknowledged that any standard oral dosing regimen will be effective for only two-thirds of a patient population. This infers that, for the remaining one-third of the population, smaller or larger doses will be required to increase tolerance of dental treatment.6 Certain patients will be extreme hyporesponders, exhibiting little or no sedative effect after receiving typical doses. These individuals are candidates for a deeper level of sedation and need to be recognized early on in the AMOS procedure and referred appropriately.6 Under no circumstance should a hyporesponder be administered excessive dosages outside of the established in-office sedation protocol. Instead, the dental visit should be terminated, with all routine dismissal procedures followed prior to releasing the patient to the responsible adult companion.
The opposite situation, when individuals are found to be extreme hyperresponders, carries with it the more significant risk for creating an overdosing situation. These patients frequently react to medications in an idiosyncratic or exaggerated fashion. Often, during the physical evaluation, a hyperresponder will provide a long list of medication allergies; when properly researched, these medication lists are often found to include common manifestations of known side effects instead of true anaphylactic reactions. Dose reductions for AMOS should be strongly considered in an identified hyperresponder, particularly if the patient is taking concurrent medications or herbal supplements known to decrease metabolic clearance or inhibit hepatic enzyme systems. Wellpublicized lists include commonly prescribed medications that are known to be moderate to potent inhibitors of the cytochrome P450 CYP3A4 hepatic enzyme.9 Coadministration of sedative agents in an individual suspected of having attenuated function of cytochrome P450 will significantly increase the potential to oversedate, which can inadvertently take the patient into a deeper level of anesthesia. Patients can move swiftly from minimal sedation into moderate or deep sedation; if this happens, it could require intensive management of an unintended sedation complication. Minimal, moderate, and deep sedation and general anesthesia should be viewed as a continuum (Table 2).1 It is important to understand that every level in this continuum can be reached, regardless of the route of administration or tendency for hyperresponse. Reduced dosage (50% less than the maximum recommended dose) has been advocated when sedating patients over the age
Fig. 2. A 24-year-old patient with rampant dental caries and a history of unsuccessful dental treatment under local anesthesia is well-managed under the influence of 0.375 mg oral triazolam and 40% nitrous oxide-oxygen inhalation analgesia. A properly positioned pulse oximeter with integrated blood pressure cuff and SpO2 sensor is a mandatory operatory addition.
Table 2. Continuum of sedation and anesthesia. Minimal sedation
Responsiveness Normal response to verbal stimulation
Purposeful response to verbal and tactile stimulation
Purposeful response after repeated or painful stimulation
Unarousable, even with painful stimulation
No intervention required
Intervention could be required
Intervention often required
Might be inadequate
Could be impaired
of 65, primarily due to polypharmacy, drug interaction potential, and reduced metabolic clearance.4,6,10 Acknowledging the potential for an unplanned progression of sedation to a deeper plane is the rationale for the 2007 ADA guidelines to include training in compromised airway management. Respiration support is an essential www.agd.org
skill for those undertaking sedative procedures. Airway repositioning (chin lift procedures), placement of oral airways, and administration of positive-pressure ventilation is often all that is required to prevent the development of a life-threatening emergency while the effects of a mild oversedation wane. However, intraoperative recognition of an
Conscious Sedation Adult minimal oral sedation in the general practice setting
Table 3. Drugs recommended in the AMOS protocol. Generic name (brand names) Drug class
Dosage range (mg)
Onset (minutes) Half-life (hours) Formulations
Hydroxyzine (Atarax, Vistaril)
Antihistamine (H1 receptor antagonist)
Syrup: 10 mg/5 mL Capsules: 10, 25, 50, 100 mg Oral Suspension: 25 mg/5 mL
Tablets: 0.125 and 0.25 mg
Oral solution: 2.0 mg/mL Tablets: 0.5, 1.0, 2.0 mg
Capsules: 5.0, 10 mg
Ampule: 0.1 mg/mL
Syrup: 2.0 mg/mL Ampule: 5.0 mg/mL
Tablets: 5.0, 10 mg
Z drug precautions
• Cannot be reversed • Potentiates opioids, barbiturates, and anti-anxiety drugs • Does not reduce seizure threshold • Blurred vision, dizziness, and xerostomia • Decrease dosage in elderly due to exaggerated effects or extrapyramidal reactions • Avoid during early pregnancy
• Exercise caution with concurrent use of antifungals, macrolide antibiotics (erythromycin), proton pump inhibitors, protease inhibitors, SSRIs, contraceptives, and grapefruit juice, as concurrent use can significantly increase sedative clearance time • Powerful anterograde amnesia properties • Contraindicated with narrow angle glaucoma • Past reports of relatively high addictive liability • Rebound anxiety, amnesia, confusion, and psychiatric symptoms reported (especially triazolam) • Flumazenil will reverse • Benzodiazepine abusers, seizure patients, tricyclic antidepressant user/abusers can exhibit withdrawal/seizures with reversal • Decrease dosage in elderly (50% reduction over age 65)
• Poor anticonvulsant and muscle relaxant properties • Some anterograde amnesia reported • Might be habit-forming • Exercise caution with impaired renal or hepatic function • Increased CNS depression when given with benzodiazepine • Flumazenil will reverse (same precautions as with benzodiazepine reversal) • Decrease dosage in elderly (50% reduction over age 65)
Note: These are guidelines only; seek appropriate training and physician input.
inadvertently oversedated patient is a critical skill. Training in the use of an appropriate sedative reversal agent (such as flumazenil) and keeping the agent as part of the in-office emergency drug kit will ensure adequate preparedness for the rare occasion when an anesthesia rescue procedure is necessary. 36
Strategically selected sedative agents (the AMOS drug protocol) Many agents are available to clinicians to aid in sedation and anxiety control of the adult patient. The authors have identified a short list of well-studied sedative and anxiolytic drugs proven to be predictable and
effective in the authors’ practice and educational setting. The most significant factors that will dictate the AMOS medication selected for use are age, weight, concurrent medications, ASA physical status classification, anxiety level, and duration of the dental procedure to be performed.
The following sections will focus on seven medications from four drug classes (Table 3). Information on the formulations, dosage range, onset, half-life, and precautions found in Table 3 was compiled from numerous reference documents, with emphasis on Malamed’s text.3,5,6,9-17
Comments Good for substance abuse patients and heavy smokers Significant anticholinergic effects favor use in asthma and COPD patients Antisialogogue (reduces salivary flow) Anti-emetic (reduces nausea and vomiting) Prepare and administer as oral cocktail in apple juice, Liquid Tylenol, Liquid Advil Rapid onset Short duration No active metabolites
Good for short to moderate cases (two to four hours) Sublingual dosing (bitter) produces faster onset and increased bioavailability No active metabolites Good for longer cases (more than three hours) Excellent anxiolytic (night before dosing for severe phobics) Good for patients with active liver disease and smokers No active metabolites Good for moderate cases (one to three hours) Not contraindicated in pregnancy No active metabolites Good for short appointments Not contraindicated in pregnancy No active metabolites Rapidly reverses sedative effects of benzodiazepines and Z drugs Deliver initial 0.2 mg dose sublingually via 16 gauge needle unless IV port is available Reversal precautions • Initiation of convulsion is potential adverse event after reversal, especially in patients with epilepsy • Severe cardiac arrhythmias possible when used with high-dose tricyclic antidepressants • Withdrawal symptoms possible in patients with long-term exposure to benzodiazepine • Residual benzodiazepine in the circulation after reversal can lead to resedation (extended monitoring prior to discharge)
For maximum safety, the authors dispense all sedative agents directly to each patient; this avoids the potential of preoperative self-sedation outside of a controlled environment. A small inventory of the various AMOS agents is stored in the dental practice in a double-locked drug box together with all state-regulated dispensing
records required to properly document use of these medications. In many institutional settings, automated medication dispensing machines are employed to support the workflow of anesthesia providers during surgery, while ensuring compliance, medication safety, and accurate reporting for the pharmacy. www.agd.org
The antihistamine class includes a number of H1 antagonists that possess sedative, anti-emetic, antispasmodic, and anticholinergic properties. As a clinically useful histamine blocker, hydroxyzine is classified as a diphenylethane and offers an excellent sedative choice for patients who are heavy smokers or who have asthma. It has been reported that benzodiazepines have not been as effective in patients who smoke due to up-regulated liver enzymes that speed up benzodiazepine metabolism. Hydroxyzine’s sedative actions are produced not by cortical depression but instead through suppression of hypothalamic nuclei and by peripheral actions on sympathetic pathways. Hydroxyzine’s anticholinergic effects are useful in dentistry through its antisialogogue and anti-emetic actions. Patients with asthma often benefit from these supplemental actions as well as from the sedative effect. Some precautions should be observed with antihistamine sedatives, which are known to potentiate opioids, barbiturates, sedativehypnotics, and anti-anxiety drugs. Malamed has suggested that dosages of all CNS depressants be reduced by 50% when administered concurrently with hydroxyzine.17 This drug does not reduce seizure threshold. Blurred vision, dizziness, and xerostomia are commonly reported side effects. Yagiela noted the need to decrease dosage in the elderly
Conscious Sedation Adult minimal oral sedation in the general practice setting
due to exaggerated effects or extrapyramidal reactions.11 Hydroxyzine is metabolized in the liver and excreted in the urine. Fatal overdose is extremely rare, and withdrawal reactions after long-term therapy have never been reported. Hydroxyzine dosing
Although it cannot be reversed after administration, hydroxyzine enjoys a wide therapeutic range, a reasonably short onset, and a manageable halflife. Use should be avoided in early pregnancy. Two forms of this drug are available: hydroxyzine hydrochloride (Atarax) and hydroxyzine pamoate (Vistaril). It is available as a syrup, capsules, or oral suspension. Hydroxyzine combined with inhalation analgesia (N2O-O2) is more effective in patients with severe anxiety than as a sole agent. For AMOS, the authors administer 50–100 mg as a single dose (100 mg maximum), with dose determined by age, weight, and ASA classification. Benzodiazepines
The benzodiazepines are the most commonly used medications for adult oral sedation. The benzodiazepine mechanism of action resides in the ability to slow the uptake of the inhibitory neurotransmitter gammaaminobutyric acid (GABA), which causes muscle relaxation, anxiolysis, and an anticonvulsant effect. This drug class has a wide therapeutic dosage range that reduces unwanted side effects and toxicity. Even acute overdose situations do not affect the respiratory system like barbiturates, opiates, or alcohol because the GABA-benzodiazepine receptors are located in the limbic system rather than in the respiratory control centers of the brain stem.9 Benzodiazepine biotransformation occurs in the liver but without induction of hepatic microsomal 38
cytochrome P450 enzymes, so patients with hepatic dysfunction can receive these drugs without increased risk of side effects. Many benzodiazepines are long-acting and have biotransformation products that are pharmacologically as active as the parent compound. Selecting a benzodiazepine without intermediate metabolites for use in AMOS will reduce the potential for oversedation or resedation.9,17 Certain precautions should be observed with this drug class. Exercise caution using benzodiazepines concurrently with antifungals, macrolide antibiotics (erythromycin and others), proton pump inhibitors, protease inhibitors, selective serotonin reuptake inhibitors (SSRIs), oral contraceptives, and grapefruit juice, as sedative clearance time can be increased significantly. Powerful amnesia effects are generally helpful to minimize the memory of dental interventions, but they restrict the capability for patients to recall important postoperative instructions. Benzodiazepines are contraindicated for patients with acute narrow angle glaucoma. There are reports of relatively high addictive liability for patients prone to psychological dependence. Rebound anxiety, amnesia, confusion, and psychiatric symptoms have been reported (especially with triazolam). Overt medical complexity and poor reserve capacity warrant a reduction in the maximum cumulative doses in the elderly (50% reduction for patients over the age of 65 judged to be ASA III).6,9,10,17 Strong inducers of the P450 CYP3A4 hepatic enzyme (phenytoin, rifampin, barbiturates, St. John’s wort) have the potential to cause therapeutic failure by increasing the rate of metabolism of all benzodiazepines while decreasing serum concentrations.9
Even with certain precautions noted, benzodiazepine compounds continue to represent the most nearly ideal drugs for the management of anxiety. Importantly, all benzodiazepines can be reversed with flumazenil (Romazicon). Midazolam (Versed) dosing
This short-acting benzodiazepine has a rapid onset, short duration, and inactive metabolites. It is available as a syrup or by ampule. For AMOS use, the authors prepare and administer midazolam as an oral cocktail in apple juice, liquid acetaminophen, or liquid ibuprofen. Apple juice is an effective taste-masking agent and provides a low pH that has been suggested to increase absorption and bioavailability of orally administered midazolam.18 Suspensions of acetaminophen or ibuprofen provide the benefit of supplemental pain control related to intraoperative trauma. The initial oral dose of midazolam is 10–15 mg, with one incremental dose as needed up to a maximum dose of 20 mg. Triazolam (Halcion) dosing
The rapid onset (15–30 minutes) and moderately long half-life (1.5–5 hours) of triazolam makes it an excellent choice for short to moderate cases of two to four hours in length. No active metabolites are produced. For AMOS use, the authors administer triazolam at an initial dose of 0.125–0.375 mg, with one incremental dose at hour 2 of the dental procedure when needed, up to a maximum dose of 0.5 mg. For redosing, sublingual administration produces faster onset and increased bioavailability by avoiding the first-pass hepatic effect; however, triazolam is bitter and might not be tolerated well sublingually by some patients.13
Lorazepam (Ativan) dosing
Lorazepam is a highly effective, moderately long-acting benzodiazepine with excellent anti-anxiety and hypnotic properties which provides a rapid oral onset (30 minutes) and produces no active metabolites. Hepatic dysfunction (hepatitis and cirrhosis) does not alter biotransformation, making it a good choice for patients with active liver disease and those who smoke. For AMOS use, the authors use lorazepam for longer cases, administering a single 2.0–4.0 mg dose depending on age, weight, and ASA classification. No supplemental intraoperative doses are used. The amnesic properties of lorazepam are impressive and include anterograde and a degree of retrograde amnesia. Some ambulatory patients might not be comfortable feeling as if they have “lost a day.”17 Due to the excellent anxiolytic properties of lorazepam, administration of the same dose (2.0–4.0 mg) the evening before treatment can ensure a restful night’s sleep. Non-benzodiazepine hypnotic drugs
The relatively new non-benzodiazepine hypnotics, often referred to as Z drugs, have hypnosedative actions comparable with those of the benzodiazepines, yet they display specific pharmacokinetic and pharmacodynamic properties. These agents are selective compounds that interact preferentially by binding to neural transmembrane chloride channel subunits known as omega-1 receptors to produce their sedative effects (benzodiazepines bind to both omega-1 and omega-2 receptors, generating adverse effects on cognitive performance and memory).16 The Z drugs are strong sedatives but exhibit only mild anxiolytic, myorelaxant, and anticonvulsant properties. This drug class better
preserves psychomotor tasks and memory capacities compared to benzodiazepine compounds. The Z drugs have fast-acting clinical onsets, relatively short half-lives, and limited duration of action, which make them a good choice for short appointments. Caution should be exercised for patients with impaired renal or hepatic function. Elevated blood levels should be expected if Z drugs are administered concurrently with other drugs that inhibit the CYP3A4 liver enzyme metabolic pathway. Increased CNS depression occurs when Z drugs are given with benzodiazepines. It has been recommended to decrease dosage in elderly patients (50% reduction for patients over the age of 65). These drugs are not contraindicated in pregnant patients or patients with narrow angle glaucoma.11,15 Zolpidem (Ambien) dosing
As an imidazopyridine, zolpidem tartrate has a short half-life (one to three hours) and no active metabolites, making it an excellent choice for short to moderately long dental appointments. Occasional side effects reported include headache, nausea, and muscle pain. Flumazenil will reverse sedative effects, so clinicians should observe the same precautions as with benzodiazepine reversal. For AMOS use, the authors administer 5.0–10 mg of zolpidem, with one incremental dose if needed up to a maximum dose of 10 mg. Zaleplon (Sonata) dosing
Also an imidazopyridine, zaleplon has an ultrashort half-life (0.5–1.0 hours) and no active metabolites. This combination provides clinicians with an oral agent that can be employed effectively for those short dental appointments (crown delivery/soft tissue management, and so forth.) when the patient must be sedated www.agd.org
but when other AMOS agents would oversedate and result in an extended monitoring period prior to discharge. For AMOS use, the authors suggest administration of a single dose of 5.0–20 mg, depending on age, weight, and ASA status. Flumazenil will reverse the sedative effects.
Respiratory support and supplemental inhalation analgesia There are very few patient conditions that contraindicate the use of supplemental oxygen administration during dental care. As part of the AMOS protocol, the authors set up and deliver 100% oxygen by nasal hood or cannula at the beginning of the sedation induction. Later, coadministration of nitrous oxide during local anesthesia delivery and more challenging portions of the dental procedure can effectively utilize the analgesic properties of N2O-O2. This additional analgesia will assist in preserving the sedation result. At appropriate intervals, the treating dentist can revert to 100% oxygen. This process of intermittent nitrous oxide administration will decrease the risk of nausea often associated with the length of time an individual is carried on N2O-O2. The use of nitrous oxide/oxygen analgesia as a supplement to any of the medications in the AMOS drug protocol will convey supplementary levels of anxiety relief with minimal effects on respiration, consciousness, and cardiovascular stability. At the conclusion of the active dental treatment, the authors recommend administration of 100% oxygen for five minutes in preparation for evaluation of discharge readiness.4,13
Recovery and reversal of the AMOS patient Effective selection of a sedative drug directly affects recovery. Choosing
Conscious Sedation Adult minimal oral sedation in the general practice setting
an agent from the AMOS drug protocol for a patient who has been properly assessed for sedation reliability prior to administration and with dental treatment sequenced and executed to effectively coincide with the duration of the sedative will routinely result in an uneventful recovery. AMOS patients will normally be observed emerging from sedation in a timely fashion, free from major anxiety and fully capable of preparing themselves for departure from the operating environment. By limiting the duration of dental treatment to four hours and by specifically limiting the type and amount of sedative agent employed, it is a rare occurrence in the authors’ practice to find a patient in an oversedated state who is unable to meet discharge criteria. For this reason, the administration of a reversal agent has rarely been necessary. Reversal is contemplated when a patient moves out of a minimal sedation state into undesired deeper planes of anesthesia, necessitating discontinuance of the dental procedure or delaying full recovery following completion of treatment. Avoidance of oversedation is the paramount goal, but safety is enhanced due to the availability of a highly effective reversal method. Flumazenil (Romazicon) is a specific benzodiazepine receptor antagonist. Upon administration, it causes a rapid reversal of unconsciousness, sedation, amnesia, and psychomotor dysfunction. Onset is rapid, with peak effect occurring in one to three minutes.11 For the reversal of sedative effects from benzodiazepine or Z drug administration, the recommended initial dose of flumazenil is 0.2 mg IV (2.0 mL of 0.1 mg/mL solution) over 15 seconds. If the desired level of consciousness is not obtained after 45 seconds, a second dose of 40
0.2 mg IV is delivered and repeated at 60-second intervals when necessary, up to a maximum dose of 1.0 mg. The dosage should be individualized based on the patient’s unique response.19 Delivery of sublingual injections of flumazenil in 0.2 mg aliquots has been observed by the authors to produce effective and rapid benzodiazepine reversal for situations when an IV port is not available. The effect of flumazenil administered by this route has not been well-studied (intramuscular, subcutaneous, and sublingual routes of flumazenil injection have been studied in dogs). There is some evidence that the onset of reversal by the sublingual or intramuscular route is sufficiently fast to manage acute emergencies.3,13 Initiation of convulsion is the most common serious adverse event associated with flumazenil reversal. This is frequently observed in patients relying on benzodiazepine effects to control seizures, if physically dependent on benzodiazepines, or those having ingested large doses of other drugs (mixed-drug overdose). Seizures are generally reversible with standard antiepileptic therapy, including benzodiazepines, phenytoin, or barbiturates. Severe adverse effects, including fatalities related to the development of cardiac arrhythmias, have been reported following reversal procedures in patients taking large quantities of tricyclic antidepressants. Withdrawal symptoms can occur following rapid injection of flumazenil in patients with long-term exposure to the benzodiazepines; withdrawal symptoms have been reported following flumazenil administration in patients receiving short-term benzodiazepines for sedative purposes. Withdrawal symptoms are generally mild and transient.19
After reversal, residual unmetabolized benzodiazepine in the circulation can re-engage GABA receptor sites as the effects of flumazenil wane, leading to the potential for resedation. In all reversal cases, the patient must be monitored during an extended in-office recovery period, and the transporting guardian/companion must be directed to observe the patient for resedation following discharge. The half-life for the benzodiazepine or Z drug used for AMOS must be known in order to anticipate the likelihood of resedation following reversal.11 Long-acting benzodiazepines could predispose certain patients to extended recovery periods and resedation after reversal. Selecting agents from the AMOS drug protocol will assist in avoiding oversedation by instead employing only those medications with short half-lives and inactive metabolites.
Discharge and postoperative management of the AMOS patient AMOS patients can present a challenge in determining when they have made sufficient recovery from sedation and are ready to be discharged. Assessing the patient’s alertness and orientation to person, place, and time is an important discharge criterion. Establishing that proper orientation existed at the time of discharge should be documented in the anesthesia record or progress notations. Some mentally challenged patients might not be aware of the answers to these classic questions, which can prompt the dentist to note that the patient was “alert, vital signs were stable, the patient was able to ambulate with assistance, with no apparent distress observed at the time of discharge to responsible guardian.” Some additional discharge criteria are:
• Patient exhibits normalization of vital signs; • Patient breathes unassisted, with no potential for airway obstruction; • Patient is fully responsive and alert, and is able to respond to normal questions and verbalize appropriately; • Following NPO, patient is able to drink small volumes of fluid in order to re-establish hydration with evidence of normal reflex swallowing patterns; • Patient acknowledges receipt of verbal postoperative instructions prior to departure and recognizes the responsible adult companion by name or relationship; • Patient prepares self for departure with little assistance into the care of the responsible adult companion for transportation.18 Occasionally, erratic gastric absorption can occur, possibly leading to delayed onset or prolonged recovery.13 Future technological advancements will allow for more objective measurement for assessing discharge readiness. Currently, the bispectral index could become such a tool by allowing for a continuous monitoring of the EEG and by computing a numerical value on a scale of 0–100 that correlates well to sedation depth.3 Ultimately, the treating dentist must be satisfied with the patient’s level of recovery prior to discharge. Patients, particularly the elderly, who have special needs are often unable to ambulate effectively after AMOS. These individuals should be assisted out of the office by wheelchair and delivered to a waiting vehicle. Per the preoperative arrangements, the patient is escorted and driven home by the responsible adult companion, who has already been properly informed of the postoperative care. The written
postoperative instructions should include the recommendation for all patients to avoid operation of cars or machinery for the remainder of the day following surgery.
Discussion Use of an approved drug in another dosage form, for another indication, at higher doses, in a different patient population, or for a use not mentioned in the original labeling is considered off-label use of the drug. The FDA, however, recognizes that the off-label use of drugs by practitioners is often appropriate and could represent the standard of practice.3,13 Incremental oral dosing, also known as titration, is an example of a commonly employed off-label practice that has grown in popularity. Quarnstrom and Donaldson employed oral triazolam in 270 cases over a course of 15 years in a dosage range of 0.125–0.5 mg and resorted to supplemental doses for only 17 (9.0%) of their 188 patients, yet they achieved a published success rate for a satisfactory level of sedation of 98.4%.14 They concluded that justification for using intravenous agents for patients requiring sedation was difficult when oral medication could provide such an excellent alternative, particularly in light of the increased cost of malpractice insurance and the difficulty and expense involved in obtaining IV sedation certification. Some controversy remains regarding titration when employing oral sedation. Repeated oral administration of a benzodiazepine like triazolam has been reported to result in the medication reaching a constant blood-level after it is administered over the course of three to five half-lives (achieving a steadystate condition), when the amount of drug that is accumulated equals the amount that is eliminated.3 Many www.agd.org
feel that this phenomenon produces the intrinsic safety mechanism of the benzodiazepine class and allows for the safer administration of two smaller doses over time based on the observation of patient response rather than one large dose at the onset. However, there is a delay in drug equilibration between the plasma and the effect site that can predict possible overdose if additional doses are administered only on the basis of periodic intraoperative reassessment of the patient’s anxiety level, since the plasma concentration could still be rising after the prior dose. Certain key attributes of the benzodiazepines suggest that administering additional amounts of the drug at time points of less than one hour on the basis of the patient’s sedative response can result in additional dosing while the central effects of the original dose are still increasing; this can lead to overdose.3 This consideration has caused the authors to teach their AMOS protocol to include a single supplemental intraoperative dose at hour 2 of the procedure, to limit operating time to four hours, and to avoid multiple incremental dosing techniques. There is fairly strong opinion that the oral route is inherently the safest and most practical route for drug administration.3,13 Protection is provided against foreign substances by the vomiting mechanism, first-pass elimination, and a muted anaphylactic response. The relatively slow absorption reduces distributional influences and allows for recognition of deleterious trends and the possibility of preventing further absorption. The oral route also avoids local damage associated with needle puncture, ischemia from intra-arterial injection, and venous irritation leading to thrombophlebitis. The use of an orally administered drug
Conscious Sedation Adult minimal oral sedation in the general practice setting
also avoids increasing anxiety in patients who are fearful of venipuncture. The cost of care is also substantially less for an orally administered agent compared to that of a parenterally administered sedative. When employing AMOS in the context of appropriate standards of care, the interests of the public and the profession are well-served by providing a costeffective service that can be made widely available. With respect to the risks and complications attendant with any form of drug administration, a survey of 7,740 oral sedation cases monitored with a pulse oximeter/ integrated blood pressure device noted that the most common physiologic change was a decrease in blood pressure; this was associated with anxiety reduction.13 Boynes et al reported on 202 consecutive anesthesia procedures in a special-needs clinic.20 The reported complication rate was 23.8%, with 95.8% of the complications considered mild. No reports of severe complications occurred, and no subjects required hospitalization. The highest percentage of complications occurred in patient groups that received IV sedation. Airway obstruction was the most common problem (11.4%), followed by nausea/vomiting (9.4%) and hypotension (3.0%). Pretreatment with anti-emetic medications did not predictably eliminate nausea and vomiting. Airway complications were observed most often in subjects with cerebral palsy.20 It is difficult to ignore the magnitude of need for AMOS procedures when analyzing certain segments of the dental patient demographic. Historically underserved, aged, physically disabled, and mentally challenged individuals have dental needs that are often treatable under 42
the influence of oral sedation; it has been noted that profoundly challenged persons cannot always be managed with AMOS.21 The elderly are an increasing segment of the population in the U.S. and represent the fastest growing segment of the population in the world, with U.S. estimates of more than 51 million people in the over-65 age group by 2020.14 High malpractice insurance costs, government regulations that dictate when hospitalization is indicated, and the threat of litigation have caused many dentists to avoid treating elderly special-needs cases, deferring to the most cooperative and easily managed patients.14 Safe and effective in-office sedation techniques can expand access to routine dental care for many elderly patients and have a significant impact on their quality of life. Unfortunately, avoidance of dental care remains a reality for dental-phobic special needs patients. A phobia is a persistent or irrational fear that results in a compulsion to avoid a specific object, activity, or situation; it can impede daily function. Smith and Heaton reviewed 19 studies and concluded that anxiety toward dentistry has remained stable over the past 50 years, despite obvious improvements in pain control, dental materials, and less-invasive procedures.21 The 1998 and 2006 U.S. surveys by Dionne et al found that 18–55% of adults would visit the dentist more frequently if they were given a drug to make them less nervous.3 Assuming a current population of 300 million, using a median estimate of 35% would yield 105 million U.S. adults who might be avoiding dental treatment due to fear and apprehension. The vast majority of these individuals could benefit from AMOS.
Summary In the U.S., 80% of dentists are generalists; less than 10% are either oral surgeons or dental anesthesiologists. These statistics indicate that there are not enough anesthesia-trained dentists to treat all of the patients who desire to receive treatment under sedation.6,13 General dentists should strive to incorporate an efficacious in-office sedative technique in order to assist this underserved portion of the population. A growing volume of research and clinical experience has shown that the administration of AMOS by properly trained providers can provide a safe and effective means for treating many patients with special needs in an outpatient dental setting. This approach would allow a population that has historically had limited or no routine dental care a much-needed opportunity to access treatment that will improve their health and quality of life.
Acknowledgements The following individuals made contributions to this article: Anne B. Knox, DMD; J. Hunter Hicklin, DMD; Ramy Majid, DDS; Jeffrey W. Taylor, DMD; and Michael T. Williams, DMD.
Disclaimer The authors have no proprietary, financial, economic, commercial, professional, or other personal interest of any nature or kind in any product, service, and/or company that could be construed as influencing the position presented in this article.
Author information Dr. Stillwell is an associate professor and assistant director, University Hospital General Dentistry Residency, University of Alabama at Birmingham, where Dr. Anderson is adjunct clinical faculty.
1. American Society of Anesthesiologists. Continuum of depth of sedation: Definition of general anesthesia and levels of sedation/analgesia. Amended October 21, 2009. Available online at http://www.asahq.org/For-Members/ClinicalInformation/~/media/For%2520Members/ documents/Standards%2520Guidelines%2520 Stmts/Continuum%2520of%2520Depth%2520 of%2520Sedation.ashx. Accessed January 11, 2011. 2. Guidelines for the use of sedation and general anesthesia by dentists. Chicago: American Dental Association;2007:47-55. Available at: http:// www.ada.org/sections/educationAndCareers/ pdfs/doc_policies.pdf. Accessed January 11, 2011. 3. Dionne RA, Yagiela JA, Cote CJ, Donaldson M, Edwards M, Greenblatt DJ, Haas D, Malviya S, Milgrom P, Moore PA, Shampaine G, Silverman M, Williams RL, Wilson S. Balancing efficacy and safety in the use of oral sedation in dental outpatients. J Am Dent Assoc 2006;137(4):502513. 4. Coke JM, Edwards MD. Minimal and moderate oral sedation in the adult special needs patient. Dent Clin North Am 2009;53(2):221-230. 5. Feck AD, Goodchild JH. The use of anxiolytic medications to supplement local anesthesia in
the anxious patient. Compend Contin Educ Dent 2005;26(3):183-190. 6. Donaldson M, Goodchild JH. Maximum cumulative doses of sedation medications for in-office use. Gen Dent 2007;55(2);143-148. 7. ASA physical classification system. Available at: http://my.clevelandclinic.org/services/ anesthesia/hic_asa_physical_classification_ system.aspx. Accessed January 11, 2011. 8. American Society of Anesthesiologists. ASA physical status classification system. Available at: http://www.asahq.org/clinical/physicalstatus. htm. Accessed January 11, 2011. 9. Wynn RL, Bergman SA. Reported adverse effects and drug interactions of triazolam (Halcion). Gen Dent 2004;52(5):378-381. 10. Goodchild JH, Donaldson M. Calculating and justifying total anxiolytic doses of medications for in-office use. Gen Dent 2006;54(1):54-57. 11. Yagiela JA, Neidle EA, Dowd FJ. Pharmacology and therapeutics for dentistry, ed. 4. St. Louis: Mosby;1998. 12. Donaldson M, Gizzarelli G, Chanpong B. Oral sedation: A primer on anxiolysis for the adult patient. Anesth Prog 2007;54(3):118-129. 13. Berthold C. Enteral sedation: Safety, efficacy, and controversy. Compend Contin Educ Dent 2007;28(5):264-271.
14. Quarnstrom FW, Donaldson M. Triazolam use in the dental setting: A report of 270 uses over 15 years. Gen Dent 2004;52(6):496-501. 15. Wynn RL, Bergman SA. The new Z-drugs as sedatives and hypnotics. Gen Dent 2005;53(3):174177. 16. Terzano MG, Rossi M, Palomba V, Smerieri A, Parrino L. New drugs for insomnia: Comparative tolerability of zopiclone, zolpidem, and zaleplon. Drug Saf 2003;26(4):261-282. 17. Malamed SF. Sedation: A guide to patient management, ed. 3. St. Louis: Mosby;2003. 18. Goodchild JH, Dickinson SC. Anxiolysis in dental practice: A report of three cases. Gen Dent 2004;52(3):264-269. 19. Romazicon side effects. Available at: http:// www.drugs.com/sfx/ romazicon-side-effects. html?printable=1. Accessed January 11, 2011. 20. Boynes SG, Moore PA, Lewis CL, Zovko J, Close JM. Complications associated with anesthesia administration for dental treatment in a special needs clinic. Spec Care Dentist 2010;30(1):3-7. 21. Smith TA, Heaton LJ. Fear of dental care: Are we making any progress? J Am Dent Assoc 2003; 134(8):1101-1108.
self CDE 2 HOURS instruction CREDIT
Exercise No. 298
Conscious Sedation Subject Code 163 The 15 questions for this exercise are based on the article “Adult minimal oral sedation in the general practice setting” on pages 31-43. This exercise was developed by Steven E. Holbrook, DMD, MAGD, in association with the General Dentistry Self-Instruction committee. Reading the article and successfully completing the exercise will enable you to: • recognize the need for adult minimal oral sedation in general dentistry; • differentiate between agents available for adult minimal oral sedation; and • understand how adult minimal oral sedation can be used to effectively manage phobic, elderly, mentally impaired, or physically disabled patients
1. A patient undergoing adult minimal oral sedation (AMOS) should exhibit which of the following reactions? A. Normal response to verbal commands B. No response to tactile stimulation C. Depressed respiratory function D. Depressed cardiovascular function
2. AMOS is routinely offered to patients that are classified as ASA I or II. Patients who are classified as ASA III or IV should not be considered for AMOS. A. Both statements are true. B. The first statement is true; the second is false. C. The first statement is false; the second is true. D. Both statements are false.
3. Advantages of hydroxyzine as an oral sedative include all but which of the following? A. Antisialogogue action B. Antiemetic action C. Reduces seizure threshold D. Useful for asthmatic patients
5. The mechanism of action of benzodiazepines resides in their ability to A. slow the uptake of gamma amino butyric acid. B. suppress hypothalamic nuclei. C. bind to neural transmembrane chloride channel subunits. D. stimulate serotonin release.
6. Which drug can reverse all benzodiazepines? A. Benzadrine B. Flumazenil C. Naloxone D. Physostigmine
7. Precautions that should be used with benzodiazepines include all but which of the following? A. Sedative clearance time increases with concurrent use of proton pump inhibitors. B. Anterograde amnesia could affect recall of postoperative instructions. C. They are contraindicated in patients with narrow angle glaucoma. D. Dosage should be increased by 50% in patients over the age of 65.
8. Which of the following agents could be most effectively utilized as an oral sedative for a short crown delivery appointment? A. Zaleplon B. Lorazepam C. Zolpidem D. Triazolam
9. Which of the following agents could be utilized most effectively for a long dental appointment? A. Zaleplon B. Lorazepam C. Zolpidem D. Triazolam
4. What are the most commonly used medications for adult oral sedation? A. Antihistamines B. Benzodiazepines C. Barbituates D. Non-benzodiazapine hypnotics
10. What is the recommended mode of administration of flumazenil? A. Subcutaneous B. Intramuscular C. Sublingual D. Intravenous
13. Midazolam is administered as an oral cocktail with all but which of the following? A. Grapefruit juice B. Apple juice C. Liquid Tylenol D. Liquid Advil
11. Advantages of oral administration of sedatives include all but which of the following? A. A delay in drug equilibration between plasma and the effect site occurs. B. Slow absorption reduces distributional influences. C. Anxiety is exacerbated in patients fearful of venipuncture. D. Cost of care is substantially less than parenteral administration.
14. Which of the following would be an excellent sedative agent for use in a patient who was a heavy smoker? A. Triazolam B. Midazolam C. Hydroxyzine D. Zolpidem
12. What is the most common serious adverse effect of benzodiazepine reversal with flumazenil? A. Vomiting B. Arrhythmias C. Convulsions D. Withdrawal
15. Which of the following sedative agents would not be contraindicated in patients who are pregnant or who have narrow angle glaucoma? A. Triazolam B. Midazolam C. Hydroxyzine D. Zolpidem
Answer form and Instructions are on pages 79-80. Answers for this exercise must be received by December 31, 2012. To enroll in Self-Instruction, click here.
Shear bond strength of seventh generation bonding agents on dentin of primary teeth— An in vitro study Geoffrey Gonzales, DMD
Alfred P. Rich, DMD, MDS
Matthew D. Finkelman, PhD
This controlled, randomized, in vitro study evaluated the shear bond strength of several seventh generation bonding agents on the dentin of primary teeth. Six different adhesives were used: Xeno IV, Clearfil S3 Bond, Adper Prompt-L-Pop, AdheSE One, Bond Force, and Optibond (control). Ninety primary teeth were prepared by wet grinding with a 320-grit silicon carbide paper on a polishing wheel running at 110 RPM. After 24 hours of storage in water, shear bond strengths of each group were determined. The mean shear bond strength of the tested adhesive systems to primary dentin was 12.27 MPa. One-way ANOVA testing showed a statistically significant difference between adhesive products
dhesive systems in dentistry have improved significantly from decade to decade, especially with the advancement of seventh generation adhesive systems, available since the early 2000s. Newer seventh generation adhesive systems have simplified bonding techniques, allow for a reduced number of applications, produce fewer technical errors, and eliminate the need for rinsing etching products prior to bonding.1,2 These seventh generation adhesive systems benefit both clinicians and pediatric patients by decreasing chairtime and producing less postoperative tooth sensitivity compared to totaletch adhesive systems.3 Seventh generation systems have also allowed increased bond strengths without the need for excessive mechanical retention, creating more conservative tooth preparations.4 Initially, adhesive systems involved the mixing of multiple liquids prior to application of the bonding 46
(P < 0.001). Tukey HSD post hoc tests were used to assess which means were significantly different from one another. There was no statistically significant difference between the fifth generation adhesive system (Optibond) and the two seventh generation systems (Xeno IV and Bond Force), with Optibond exhibiting a lower mean shear bond strength compared to Bond Force. Within the limitations of this study, there is a significant difference between seventh generation bonding materials. Bond Force and Optibond appear to exhibit higher shear bond strengths than the other products. Received: December 15, 2010 Accepted: March 10, 2011
agent.5 These earlier bonding systems utilized the “total-etch” technique that removed the smear layer, creating microporosities for a micromechanical bond. The totaletch step, requiring a separate etch and rinse procedure, causes demineralization of both enamel and dentin, allowing the substrate of dentinal tubules to be penetrated by the separate primer and adhesive solutions.6 Fourth generation adhesive systems (total-etch systems) required a separate etch of 30–40% phosphoric acid, a hydrophilic monomer primer, and a final application of bonding resin. Fifth generation bonding systems simplified procedures by combining the primer and adhesive. Newer sixth and seventh generation systems operate with the all-in-one “self-etch” method. This approach eliminates the total-etch step, foregoing the etch and rinse steps of the earlier generations. It also combines the acid etchant, primer, and adhesive.
The major difference between sixth and seventh generation bonding systems is that sixth generation systems require more than one liquid to be mixed before application on the tooth surface. Unlike earlier generations, both sixth and seventh generations utilize the smear layer as the bonding substrate. This smear layer is then demineralized by the acidic primer, whereupon the exposed collagen can be copolymerized with hydrophilic monomers. The self-etch adhesive is then incorporated into a hybrid layer that includes dentinal substrate with exposed dentinal tubules. There is limited research concerning seventh generation adhesive systems utilizing the dentin of primary teeth. Cadroy et al and da Costa et al both evaluated bond strengths and interfacial morphology differences between permanent and primary teeth.7,8 Their efforts concluded that self-etching systems must be used cautiously because
bond integrity is related to the quality of the hybrid layer formed; this feature is entirely different in permanent and primary samples. Studies show that permanent teeth have superior bond strength when compared to primary teeth in seventh generation bonding systems, possibly due to the differences in dentinal anatomy between permanent and primary teeth.6,7 A major difference between permanent and primary teeth is that primary teeth have thinner dentin than permanent teeth, whereas dentinal tissue follows the anatomical shape of funneling. This dentin funneling in primary teeth shows increased tubule diameter formation toward the pulp as the depth of the cavity preparation increases. Research indicates lower bond strengths from deeper dentin compared to those of superficial dentin.9 In addition, evidence also demonstrates that dentin bonding in permanent teeth tends to be more successful than in primary teeth, possibly due to hybrid layer thickness.10 Much of the literature on bonding and microleakage studies utilizing primary teeth show that the weakest link in the failures of bond interfaces is in the gingival and gingivoproximal areas.11 A study by Owens and Johnson suggested that microleakage is present in all areas but might be more demonstrable at the dentin interface.12 As the proximal box in mesial or distal preparations of primary teeth migrates gingivally, there is less enamel margin to ensure favorable enamel-bond strength. At the cervical extent of the crown, the enamel margin in primary teeth diminishes rapidly, and the bond strength of the dentin ensures or destroys the bond integrity of primary teeth. Current seventh generation materials are being advocated for use as
liners, thereby improving overall bond strengths in teeth.13
Materials and methods The experimental design was a controlled, randomized, in vitro study. This project was reviewed by the authors’ Institutional Review Board and was expedited as a project that involved no human subjects. All tissue samples were nonpatient identified, and all samples were handled and disposed of according to the Tufts Protocol for Human Specimens Disposal. Six different dental adhesives were used. Ninety exfoliated or extracted human primary teeth were collected from different dental clinics. All teeth had intact coronal structure and caries-free surfaces. Teeth were debrided with a rubber cup and pumice prior to use and stored in a 0.2% sodium azide solution. It has been suggested that sodium azide interferes less with bonding studies compared with other available mediums, such as formalin, thymol, chloramines, sodium hypochloride, and ethanol.14-17 Although definitive evidence is not yet possible due to many variables, collection of tooth samples and timing of bonding application to stored teeth can prove important to bond strength studies.18
polishing wheel at 110 RPM using an Ecomet 3 (Buehler). A random number generator randomized the bonding agent assignment to each of the six test groups. Bonding of primary teeth
Six different systems were evaluated: Xeno IV (Dentsply Caulk), Optibond (Kerr Corporation), Clearfil S3 Bond (Kuraray America, Inc.), Adper Prompt-L-Pop (3M ESPE), AdheSE One (Ivoclar Vivadent Inc.), and Bond Force (Tokuyama Dental America Inc.). The adhesive systems were applied to dentin according to each manufacturer’s instructions. The restorative material (Estelite Sigma, Tokuyama Dental America Inc.) was applied to the prepared dentin surface using a bonding jig (Ultradent Products, Inc.); then, both the bonding agent and restorative material were photocured using a Optilux 500 (Kerr Corporation) with an 11 mm tip. The control group (Optibond) required photocuring after the application of the bonding agent and after placement of the restoration. Each specimen was stored in distilled water for 24 hours at 37°C after application of the bonding agent and the composite material.19
Shear bond strength test
Sample models were made with a model holder 25 mm deep and 25 mm in diameter, as acrylic resin was poured into the model holder with a stabilized tooth specimen. Two millimeters of the buccal or lingual clinical crown was exposed, and the model was trimmed to an acceptable size. To obtain flat dentin samples, each sound specimen was cut parallel to its long axis on the buccal or lingual surfaces with an Isomet 1000 (Buehler). Dentin surfaces were prepared by wet grinding with a 320-grit silicon carbide paper on a
After 24 hours of storage in water, shear bond strengths for each group were determined by using a model 5566A universal testing machine (UTM) (Instron Corp.) at 0.5 mm/ minute crosshead speed. The notched blade of the UTM was placed flush against the resin sample so that the force would break the sample in the apical to occlusal direction.
One-way ANOVA and a Tukey HSD test were used to assess whether differences were statistically
Dental Materials Shear bond strength of bonding agents on dentin of primary teeth
Table 1. Descriptive statistics by bonding agent (all values in MPa).
Mean bond strength
Clearfil S3 Bond
95% confidence interval for mean Lower bound
Chart 1. Side-by-side error bars of MPa. 25
Mean ±1 SD value
0 1 2 3 4 5 6 Group Group 1 = Xeno IV Group 2 = Clearfil S3 Bond
Group 3 = Adper Prompt-L-Pop Group 4 = AdheSE One
significant. SPSS statistical software (version 17) was used to conduct all analyses.
Results Mean shear bond strength values and standard deviations of the adhesive products are shown in Table 1. The mean shear bond strength of the adhesive systems to primary dentin was 12.27 48
Group 5 = Bond Force Group 6 = Optibond (control)
MPa. One-way ANOVA tests highlighted a statistically significant difference between adhesive products (P < 0.001). Post hoc tests using a Tukey HSD test assessed which means were significantly different from one another. Significant differences were found between multiple products. The bonding system with the lowest average bond strength (8.27 MPa)
was AdheSE One, which was significantly different from all systems except Adper Prompt-L-Pop (9.86 MPa) and Clearfil S3 (11.57 MPa). The superior bond systems were Xeno IV (12.96 MPa), Optibond (14.26 MPa), and Bond Force (16.70 MPa). Charts 1 and 2 display side-by-side error bars and box plots to compare the six products. Table 2 illustrates which products exhibited statistically significant differences. A Levene test was used to test the assumption of equal standard deviations. Results were not statistically significant (P = 0.663), indicating that the ANOVA assumption of equal standard deviations was tenable. Quantile-quantile plots showed that the data were approximately normally distributed. No statistically significant difference was found between the fifth generation adhesive system (Optibond) and the two seventh generation systems (Xeno IV and Bond Force), with Optibond exhibiting a lower mean shear bond strength than Bond Force.
Discussion Anatomical studies have determined that primary teeth have a greater
Table 2. Results of post-hoc tests using a Tukey HSD test. Bonding agent
Mean bond strength (MPa)
Significantly different from
P values of statistically significant differences
Clearfil S3 Bond
Bond Force Optibond