JADA-2002-ROSE-37S-44S



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ABSTRACTI CARDIOVASCULAR DISEASE Cardiovascular diseases make up the most prevalent category of systemic disease in the United States and in many other countries, and increase in prevalence with age.2 IO N T A I n May 2000, the U.S. surgeon general’s office published its first report on oral health in America, emphasizing that oral health means much more than healthy teeth and that it is integral to general health.1 Included in the report is an extensive review of the burden that oral health problems place on vulnerable populations. The surgeon general confirmed that many systemic diseases and conditions have oral manifestations that may be the initial signs of clinical disease. In addition, the mouth is a portal of entry as well as the site of disease for microbial infections that affect general health status. Its functions can be affected adversely by many pharmaceuticals and other therapies commonly used to treat systemic conditions. “Oral Health in America: A Report of the Surgeon General” concluded with the recognition The patient that “the mouth is the center of vital tissues and functions that are critical to with total health and well-being across the cardiovascular life span.” The mouth serves as “a disease may mirror of health or disease, as a sentinel present a or early warning system, as an acceschallenge to sible model for the study of other tissues the dental and organs, and as a potential source of pathology affecting other systems and health care organs.”1 provider. T LOUIS F. ROSE, D.D.S., M.D.; BRIAN MEALEY, D.D.S., M.S.; LAURA MINSK, D.M.D.; D. WALTER COHEN, D.D.S. CON Oral care for patients with cardiovascular disease and stroke Background. The authors A D A J describe how oral disease, ✷ ✷  particularly periodontal disease, may place certain patients at increased risk N C of developing cardiovasA UING EDU 4 R cular disease and stroke. TICLE Results. Although the precise mechanisms of interaction are not clear, two biological mechanisms that may explain the relationship are presented. In addition, the authors describe the dental management issues that need to be understood in treating patients compromised by cardiovascular disease. Conclusions and Clinical Implications. The patient with cardiovascular disease may present a challenge to the dental health care provider, depending on the degree of hemodynamic compromise and the stability of his or her condition. Atherosclerosis is a progressive disease process that involves the large- to medium-sized muscular and large elastic arteries. It can lead to ischemic lesions of the brain, heart or extremities, and can result in thrombosis and infarction of affected vessels, leading to death. The impact of atherosclerosis on overall health is staggering. World Health Organization statistics indicate that in 1995, cardiovascular diseases were responsible for 20 percent of deaths worldwide (14 million people). In some developing countries, cardiovascular disease accounts for about 50 percent of deaths.3 For years, dentists have noticed that certain characteristics are common to patients with periodontitis and patients with cardiovascular disease (Figures 1 and 2). Both cardiovascular disease and periodontal disease are more likely to occur in people who are older, in men, in people of lower educational status with fewer financial resources, in those who smoke, in people who have stress and in those who are socially isolated. The classical risk factors for cardiovascular disease—hypertension, hyper- JADA, Vol. 133, June 2002 Copyright ©2002 American Dental Association. All rights reserved. 37S cholesterolemia and cigarette smoking—account for only about one-half to two-thirds of all cases of the disease. Vol. Grau and colleagues6 re-examined the Total Dental Index and found that only the periodontal component of the index was responsible for the association between oral infection and cerebrovascular ischemia (stroke). when Sir William Osler proposed that cardiovascular disease itself was an infection. Role of infections in atherosclerosis. diabetes. physical activity.760 subjects for 14 years. Since 1908. marital status. . Most of these studies4-7 have shown that there is an association between periodontal disease and cardiovascular disease. alcohol consumption and cigarette smoking. June 2002 Copyright ©2002 American Dental Association. Figure 2. 133. In one such study.7 Potential biological mechanisms. dSystemic factors alter the immunoinflammatory process involved in both periodontal and cardiovascular diseases. Several longitudinal studies have followed a population of otherwise healthy people to determine what factors increase the risk of developing heart disease. serum lipid levels and diabetes. smoking. dental health (as measured by the Total Dental Index) was worse in subjects who had experienced an MI. the role of infection in cardiovascular disease has been discussed. with healthy control subjects. All rights reserved.72 relative risk compared with men without periodontitis. particularly in men younger than age 50 years. sex.5-7 38S JADA. total cholesterol level. These associations have been demonstrated across diverse populations and appear to be independent of traditional risk factors. He has not responded well to periodontal treatment and does not practice good oral hygiene. DeStefano and colleagues studied these data and found that people with periodontitis at baseline had a 25 percent increased risk of having coronary artery disease. or MI. the researchers found that men with periodontitis had a 1. Two biological mechanisms that may explain the relationship between cardiovascular disease and periodontal disease are discussed in this article: dBacteria from periodontal disease may enter the circulation and contribute directly to the atheromatous or thrombotic processes. systolic blood pressure. socioeconomic status. race.8 Infection is now recognized as a risk factor for atherogenesis and thromboembolic events. Research has shown that atherosclerosis is more common in patients with periodontitis. In another study by Mattila and colleagues. Some scientific studies have shown a link between infections of the mouth and coronary artery disease. education. poverty index. A 45-year-old man with coronary artery disease who smokes two packs of cigarettes per day. Mattila and colleagues4 compared patients who had experienced a myocardial infarction.5 a statistically significant association was found between dental infections and atheromatosis. The first National Health and Nutrition Examination Survey followed up 9. In examining the effects of different oral infections on the incidence of strokes. Histologic section of a coronary artery demonstrating atherosclerosis and thrombus formation. but do not provide for a biological rationale for the association.2 This suggests that periodontal disease and cardiovascular disease may have similar causative pathways. The authors concluded that dental disease was associated with an increased risk of cardiovascular disease. They found that after adjusting for age.Figure 1. body mass index.7 After adjusting for age. Certain people may be genetically predisposed to experience a hyperinflammatory response when stimulated by a bacterial challenge such as periodontal disease. prostaglandin E2) and tumor necrosis factor Figure 3. Common systemic factors involved in periodontal and cardiovascular diseases. There is evidence that infection with certain bacteria. such as Chlamydia pneumonae. Bacteroides forsythus and Actinobacillus actinomycetemcomitans) (Figure 310). These biological mediators can have a direct effect on the periodontal pocket. monocytes migrate through the endothelium into the underlying tissue. This is followed by inflammatory cell recruitment.10) (in particular.12 explains how inflammation relates to atherosclerosis. (Reprinted with permission of the publisher from Genco and colleagues. tumor necrosis factor-α).16 Consequently.14 Psychological and physiological stress during periodontal treatment has the potential to significantly alter hemodynamic stability. resulting in further damage and focal necrosis. Helicobacter pylori.13. Prospective interventional studies are needed to determine the exact link between periodontal disease and cardiovascular disease. these mediators cause vasodilation and increased vascular permeability. 39S . leading to thrombus formation. as well as to evaluate whether periodontal treatment may reduce the risk of developing cardiovascular disease. vascular fatty degeneration and intravascular coagulation. Vol. chemokines and growth factors are released as a result of activation of the monocytes (macrophages) into the blood vessel. connective-tissue degradation and bone destruction. cytokines. Haraszthy and colleagues9 studied 50 carotid atheromas via polymerase chain reaction. a stress-reduction protocol is frequently JADA. In the periodontal pocket. This is best achieved by minimizing any hemodynamic alterations during treatment (that is. June 2002 Copyright ©2002 American Dental Association. heart rate. Ross’ hypothesis suggests that injury to the epithelium causes the initial lesion. People who are genetically predisposed to this proinflammatory response may be at a higher risk of developing periodontal disease and cardiovascular disease. particularly interleukin-1. A major feature of this process is lipid accumulation. DENTAL MANAGEMENT OF PATIENTS WITH CARDIOVASCULAR DISEASE The primary management goal for the patient with cardiovascular disease during dental therapy is to ensure that any hemodynamic change produced by dental treatment does not exceed the cardiovascular reserve of the patient. Seventy-two percent of the surgical specimens indicated bacterial content and 44 percent of the atheromas contained at least one of the periodontal microorganisms studied (Porphyromonas gingivalis. as well as on the vascular endothelium and smooth muscle. by maintaining the patient’s optimum blood pressure. The result of recruitment of inflammatory cells into the major blood vessels is the proliferation of vascular smooth muscles. which is also known as the Ross “Responseto-Injury Hypothesis. cytomegalovirus and other periodontopathic bacteria are associated with heart disease. arterial occlusion and infarction. Prevotella intermedia. This fibrous cap also may erode and rupture. All rights reserved. and the atheromatous plaque can become covered with a fibrous cap over the focal necrotic area in the later stages of this process.15. Considerable evidence has identified atherosclerosis as an inflammatory disease. 133. leading to a chronic arterial inflammatory process.”11. These people also have the greatest amounts of pathogenic bacteria and systemic factors that may contribute to an altered immunoinflammatory response.Infectious agents may cause injury directly to the epithelium and partially activate the inflammatory response seen with atherosclerosis. prostaglandins (in particular. heart rhythm. During this inflammatory process. cardiac output and myocardial oxygen demand). where there is a proliferation of smooth muscle cells.13. People with severe periodontitis have the strongest link to cardiovascular disease. This hypothesis. Carotid artery atheroma. Hydrolytic enzymes. These people may produce higher levels of proinflammatory cytokines. including unstable outcome in regard to cardiovascular complications angina. All rights reserved.18 Stable angina generally is caused by atherosclerotic narrowing of coronary vessels and presents with infrequent episodes of pain. unstable and variant (Prinzmetal’s angina). is the major cause of sudden death in the United States.22.000 epinephrine have found no significant changes in mean arterial pressure. artery bypass surgery.to 40-fold during stress.24 It usually is caused by decreased coronary blood flow. with aspiration permorning when the patient is well-rested and has formed to prevent intravascular injection.22 So it is recommended that patients with mild-to40S epinephrine injection. use of a stressreduction protocol and profound anesthesia is an integral part of periodontal therapy for these patients. observed after intravenous concentration in dental anesthetics is fivefold greater (that is. patients with cardiovascular disease may be at greater risk of experiencing massive endogenous epinephrine release secondary to poor local anesthesia than they are from the small amount of vasoconstrictor used in local anesthetics. cular disease. usually precipitated by physical exertion or emotional stress.23 Ischemic heart disease. Patients receiving local anesthetic without vasoconstrictor often have significantly impaired pain control compared with those receiving local anesthetic with epinephrine. The two most commonly with vasoconstrictors generally is contraindicated in used vasoconstrictors are patients with significant cardiovasin patients with epinephrine and levonordefrin.13. severe hypertension and local anesthetic agents with vasosevere congestive heart failure.4 milliliters of 2 percent lidocaine with 1:100. It is clear from the literature that psychological or physiological stress may exacerbate ischemic symptoms. uncontrolled dysrhythAnesthetic agents. The use of mias. minimize endogenous release of epinephrine may dpreoperative or intraoperative conscious sedabe a more important factor in ensuring hemodytion or both.16. namic stability in patients with cardiovascular dexcellent postoperative analgesia. assumption that such a protocol will minimize Although small amounts of vasoconstrictor proadverse hemodynamic alterations. blood pressure or heart rate in healthy patients or in those with mild-tomoderate cardiovascular disease.suggested for patients with significant cardiovasmoderate cardiovascular disease receive the cular compromise. Normal epinephrine release from the adrenal medulla can increase 20. 1:20. increased myocardial oxygen demand or both. β-andrenergic blocking agents and calcium channel blockers.000). preferably in the vide profound anesthesia. exogenous vasoconstrictors is required for the majority of patients with carmay be contraindicated in patients with severe diovascular disease.15. Most human studies examining hemodynamic variables after dental injection of 1. however. its remains controversial.15 Periodontal treatment planning may be altered in these patients by the need for shorter appoint- JADA.19 since the hemodycardiovascular disease Levonordefrin is only 20 percent as namic effects are similar to those potent as epinephrine. There is little duce little risk for the average patient with carobjective evidence.19 The use of local constrictors in patients with cardioIntraligamentary injection of local anesthetic agents vascular disease remains controanesthetics with vasoconstrictor versial. a greater physical reserve.16.000) than the most common concentration of epinephrine (1:100.17. Researchers have suggested that the use of conduse of profound local anesthesia to minimize scious sedation to decrease stress and therefore discomfort.20 For this reason.18 disease than are attempts to avoid the small We should note that almost all references sugamount of epinephrine used in local anesthetic gesting a stress-reduction protocol do so on the injections. Therefore.21. recent myocardial infarction or coronary associated with periodontal therapy. There are three types of angina: stable. that such a protocol diovascular disease.8 to 5. therefore. . Vol. most commonly manifested as angina or myocardial infarction.17. Ischemic heart disease.19.19 Such stress may be induced by pain during dental treatment. The medications most commonly used to treat patients with stable angina include nitrates such as nitroglycerin. 133. June 2002 Copyright ©2002 American Dental Association. which includes the following: smallest amount of local anesthetic needed to prodshorter appointments. or that it produces a better cardiovascular compromise. and the health care The use of local anesthetics with vasoconstrictors provider also may place nitroglycerin tablets in may be contraindicated in patients with refracthe emergency medical kit. June 2002 Copyright ©2002 American Dental Association.19. and consultation with the patient’s physiexisting cardiovascular disease. angina generally are not candidates for elective implantable pacemakers or automatic defibrilladental therapy. nasal canal may help prevent intraoperative Dysrhythmias. need alteration of the drug regimen before JADA. since continued pain tion of blood flow to the brain.15. including relations for preoperative or intraoperative conscious tively short appointments and a stress-reduction sedation.24 A protocol simensuing functional deficit depend on the type of ilar to that described above for unstable angina stroke and the extent of the lesion.30 Patients with may provide the best means of managing acute stroke frequently are treated with oral anticoagudental needs. 133. or CVA. The dental health care routine dental care for at least six months after provider must be aware of this potential during experiencing a myocardial infarction. tablets to each appointment.18.25 tromagnetic fields created by The other major category of dental equipment. which may cause myocardial infarction.17 The drugs of choice for treating rhythmias may require special precautions an acute anginal attack are 100 percent oxygen during dental therapy. dental treatment may best Unstable angina occurs when there is a drabe accomplished in a controlled medical setting matic increase in the frequency or severity of with careful cardiac monitoring. use of only small amounts of vasocontreated with techniques similar to those used for strictor in local anesthetics and possible indicathe patient with stable angina. and electrocautery units.24 Patients with unstable Some dysrhythmias are treated with patient is at rest.18 The patient may commonly are used.27 accident. ischemic heart disease frequently Automatic defibrillators often encountered by oral health care providers is activated without warning. Most require special Variant angina (that is.24 anginal attacks or when angina appears while the 15.17 After the six-month postmyocarlants and may. tion occurs during the first year. many of which have side effects such as gingival overgrowth or xerostomia be instructed to bring his or her own nitroglycerin that may impact the dentition or periodontium. Although stroke resulting from the increased electrical instability is a cerebrovascular disorder or cerebrovascular of the myocardium after the infarction. most patients may be cians. The survival rate and severity of the gerous cardiac dysrhythmias. tory dysrhythmias19. in consultation with their physidial infarction period. preoperative anxiinfective endocarditis and do not require prophyolytic agents may be indicated for stress reduction lactic antibiotic coverage before dental therapy. Patients with cardiac dysanginal attacks. pacemakers placed within the last Prinzmetal’s angina) usually occurs 30 years are bipolar and generally precautions during at rest and probably is caused by are not affected by the small elecdental therapy.24 This treatment.29 and to minimize endogenous epinephrine release.15. Antidysrhythmic drugs and sublingual nitroglycerin. dental treatment tion entitled “Cardiovascular Disease. If emerautomatic defibrillators present a low risk of gency dental care is needed. especially hypercian may be needed. A stroke results from sudden interrupare addressed definitively.ments. and may need to stabilize the operrecommendation is based on the fact that the ating field through use of a bite-block or other peak mortality rate following myocardial infarcsuch devices. Vol. Older pacemaker models were unipolar and could The dentist should closely monitor be disrupted by equipment that the patient’s hemodynamic status generates an electromagnetic field. Patients with cardiac and oxygen saturation before and such as ultrasonic instruments dysrhythmias may during treatment. it is discussed in the above secDuring this six-month period. which deprives it of may potentiate hemodynamic alterations or danoxygen.28 Acute dental needs usually tension.26 primarily Cerebrovascular accident. and consultation with the tors in addition to drug therapy. 41S . Pacemakers and patient’s physician usually is indicated. coronary artery spasm. Researchers and clinicians sudden movement and endanger the patient in commonly recommend that patients not receive the dental setting. Supplemental oxygen delivered via a protocol where indicated. All rights reserved.17.16.” because generally is limited to managing acute dental CVAs occur most frequently in patients with needs. which may require appointment. 38 percent and 25 percent of patients. if possible. numerous procedures by dental disease. method. or INR. also brushing than it was from a dental extraction. The most important adjunct to systemic antibiotic prophylaxis. Vol. therapy. nutrition and body weight. which may result in endocarditis. It may be mastication and oral particular attention during dental prudent to allow at least seven hygiene procedures. The dental health care provider tion through professional therapy and oral should counsel the patient about the importance hygiene instruction. but by dental disease.31 Dysphasia may be present in the tions stress the importance of establishing and patient with stroke and can cause changes in diet. CVA or thromabnormal or damaged cardiac tissue.0 times that of the laboratory oral microorganisms probably are caused not by control PT. respecThis PT ratio method of reporting PT is no longer tively. such centage of patients with endocarditis who have as dicumarol and warfarin.18. especially boembolism frequently receive anticoagulant valves.000 the United States by the International Normaltimes greater from routine chewing and tooth ized Ratio. clinicians an increased incidence of bacteremia.0 times the tion and oral hygiene procedures. . caries and increased risk of the dentist in reducing periodontal inflammaof infection. increasing the risk of microorganisms term regimen of chlorhexidine establishing resistant strains. Inability reduce potential sources of bacterial seeding. Because dental procedures of thorough oral hygiene. The patient’s head position days to elapse between appointcan be adjusted if needed. the PT has been expressed as the teremia in 40 percent of patients.”32 ments for ease of use. Dental procedures often cause a Anticoagulant therapy. 30 probably are caused rinses to aid in plaque control. All rights reserved. gag reflex may be diminished after may be accomplished at the same a CVA as well. a goal of dental therapy in patients with valvular chlorhexidine mouthrinse has been recommended heart disease is the need to prevent infective before dental procedures. June 2002 Copyright ©2002 American Dental Association.5 to 2. masticagreater levels of anticoagulation (> 2.32 Guntheroth34 control time). endocarditis.36 had recent dental treatment varies widely in the Most patients maintain a therapeutic level of literature from 3 to 40 percent. is the PT value 42S JADA. since implicit in the American Heart Association. although some patients may require dental treatment.37 The INR. the AHA recommends antibiotic prophyhygiene procedures extremely difficult. The alternatively. recommendations in regard to the prevenand trigger thrombus formation and ensuing ceretion of bacterial endocarditis.”32 to completely clear the mouth of food particles The recommendations further emphasize the role may result in halitosis. known as the “corrected” PT ratio. resulting in a prothrombin time.32-35 anticoagulation. maintaining “the best possible oral health to mastication. Patients with prostransient bacteremia that rarely lasts longer than thetic heart valves. Periodontal disease may predispose patients to To prevent a subsequent stroke. Most cases of infective endocarditis involving or PT. found that while dental extractions induced bacHistorically.32 but the bacteria may lodge on history of myocardial infarction.30 and the laxis prior to “dental procedures known to induce dental health care provider may gingival or mucosal bleeding. or a 15 minutes. a fact must treat active infections aggressively.30 ments within this one-week period. perhaps in Patients at risk of developing Most cases of consultation with an occupational infective endocarditis may undergo infective endocarditis therapist. 133. The pertherapy consisting of coumadin derivatives. or even minor infection may alter blood coagulation AHA. and is being replaced in bacteremias during a one-month period was 1. of 1. other valvular disorders.undergoing periodontal therapy. need to modify oral hygiene instruincluding professional cleaning. These recommendabral infarction.34 He concluded that the exposure time to used in most countries. Weakness of the facial that involve bleeding may induce a transient bacarea or paralysis of extremities may make oral teremia.32 As a local Valvular heart disease. normal mastiratio of the patient’s actual PT (in seconds) to a cation and tooth brushing induced bacteremias in control value that varies between laboratories. multiple courses of antibiotic involving oral The dentist may initiate a longtherapy. while ments or to select an alternate thorough and constant evacuation antibiotic regimen for appointwill help prevent aspiration of foreign matter. 2. e-mail “[email protected]. Geneva: World Health Organization. 19110. University of Pennsylvania School of Dental Medicine. Nagao M. All rights reserved. The World Health Report 1995: bridging the gaps. 7. Nieminen MS. 43S . since some people are more at risk of developing thrombus formation or hemorrhage than are others. an international reference thromboplastin. while penicillin may counteract coumadin’s effect. Buggle F. Few of the treatment approaches are founded on controlled clinical trials that have assessed the effect of different treatment modalities on well-defined outcome criteria. Philadelphia: Lea & Febiger. Philadelphia. the public health community was alerted to the need to promote oral health by the first surgeon general’s report on oral health. Dr. et al. Dr. Stroke 1997. Rose.298:779-81. 1995. often is used to prevent thrombosis formation. Diseases of the arteries. Valtonen VV. Philadelphia. In addition. Mealey is chief of periodontics and chief of Dental Professional Services. BMJ 1989.41. 5. In many instances. and these must be considered. dean-emeritus. CONCLUSION In May 2000. depending on the degree of hemodynamic compromise and the stability of his or her condition. Cohen is chancellor-emeritus. Minsk is an assistant professor of surgery and medicine.39. interfere with formation of prothrombin and increase anticoagulation. 133. Philadelphia. 1. Zeid M.43 Aspirin. Pa.S. potentiating its anticoagulant effect. Osler W. For these patients. Umino M. Identifi- JADA. aspirin therapy may be discontinued for several days before the dental procedure if treatment is expected to induce significant bleeding. Although the precise mechanisms of interaction are not clear. an inhibitor of platelet aggregation.40 Tetracyclines may decrease vitamin K production. Atherosclerosis 1993. Williamson DF. and in private practice in periodontics. 4. 3. Mattila KJ. sufficient evidence exists to conclude that oral lesions. Dental infections and coronary atherosclerosis. It generally is used in small doses of 325 milligrams or less and usually will not alter bleeding time significantly at this dose. University of Texas Health Science Center. June 2002 Copyright ©2002 American Dental Association. Oral health in America: a report of the surgeon general: executive summary. Grau AJ. Valtonen VV. Dr. and in private practice in periodontics.37 Clinicians should alter anticoagulant therapy only in consultation with the patient’s physician. ed. In addition. University of Pennsylvania School of Dental Medicine.16:377-85. Philadelphia. Russell CM. drug interactions with warfarin and other similar agents are numerous. 100 S. Kahn HS. Rockville. place certain patients at increased risk of developing cardiovascular disease and stroke. Eglin Air Force Base.103:205-11. Rose is a professor of surgery and medicine. Air Force Hospital. Philadelphia. Ziegler C. a clinical assistant professor of periodontics. World Health Organization.43:213-8. Trevisan M. University of Pennsylvania School of Dental Medicine. However. Md. and a clinical assistant professor of periodontics. Hietaniemi KL. DeStefano F. MCP Hahnemann School of Medicine. Mattila KJ. In: Osler W. Address reprint requests to Dr.that would have been determined had the test been done using the World Health Organization’s standard thromboplastin. Nieminen MS. MCP Hahnemann School of Medicine. 8. Int Dent J 1993. Systemic diseases in elderly dental patients. The dental health care provider may consult with the patient’s physician before treatment (which can induce bleeding) to determine whether modification of anticoagulant therapy is indicated. the effect of aspirin lasts at least four to seven days. Anda RF. Zambon JJ. Association between acute cerebrovascular ischemia and chronic and recurrent infection. Broad St. a greater burden is being placed on the dental community to become more familiar with oral microbiology and the pharmacological approaches available to treat oral diseases that may have systemic implications. These observations are leading dentists and physicians to interact more closely in caring for patients. Dental disease and risk of coronary heart disease and mortality. The patient with cardiovascular disease may present a challenge to the dental health care provider. Aspirin and other nonsteroidal antiinflammatory drugs may dramatically increase the risk of warfarin-associated bleeding. 2020 Land Title Building. Genco RJ. Modern medicine: Its practice and theory. a clinical professor of periodontics. 1908:429-47.44 Because of its irreversible binding to platelets.42 Metronidazole may inhibit coumadin’s metabolism. Association between dental health and acute myocardial infarction. Philadelphia. especially advanced periodontic pathologies. Florida. net”. BMJ 1993. 9. 2000. higher doses may increase bleeding time and predispose the patient to develop postoperative bleeding. Many of the dental treatment approaches used for these patients are based on consensus opinion established through years of experience and informed clinical judgment. U. Valle MS. Philadelphia.: National Institute of Dental and Craniofacial Research. Research also may be limited by the difficulty in obtaining study populations of adequate size for relatively rare disorders such as infective endocarditis. such studies are limited by ethical or medicolegal considerations involved with placing patients at risk of developing systemic complications.306:688-91.. Haraszthy VI. " Dr. San Antonio.28:1724-9. MCP Hahnemann School of Medicine.38 The major source of variability in reporting (due to differences in calculating) is the PT ratio to the international reference standard. Philadelphia. et al. 6. and in private practice in periodontics. Vol. 133. 33. Weinber JB.38:525-36. 20. Felder RS. 37.15(1):58-66. Int J Oral Maxillofac Surg 1987. Weinblatt E. Hirsh J. Repeated 1-hour electrocardiographic monitoring of survivors of myocardial infarction at six-month intervals: arrhythmia detection and relation to prognosis. Safe treatment of the post-heart-attack patient. 35. Dent Clin North Am 1994. Ross R. Zambon JJ. O’Neal R. Tzukert AA. Martinowitz U. Hersh EV Angina pectoris: diagnosis and treatment in the outpatient setting. 36. Scheitler LE. Am J Cardiol 1981. 10. Dalen JE. The pathogenesis of atherosclerosis (second of two parts).146:2203-4. 29. McCarthy FM. Oral Surg Oral Med Oral Pathol 1992. Garrett S. Compend Contin Educ Dent 1999.295:420-5. N Engl J Med 1976. Shuman SK. Institutional.145:1592-5. Cardiovascular effects and safety of dental anesthesia and dental interventions in patients with recent uncomplicated myocardial infarction. 44. Kaste M. Mason RB. 1989. Oral Surg Oral Med Oral Pathol 1984. 42. Perusse R. Acetylsalicylic acid and acetominophen. Wilson W. Goldberg JD.295:369-77. ventricular arrhythmias. Anesth Pain Control Dent 1993. part I: cardiovascular diseases. Review of very high-risk cardiac patients in the dental setting. Frequency of bacteremia following different modalities of periodontal treatment (abstract 842). 21. Haraszthy V. Dental extraction for patients on oral anticoagulant therapy. Minaker KL.102:312S-26S. 44S 27. How important are dental procedures as a cause of infective endocarditis? Am J Cardiol 1984. 41. Oral Surg Oral Med Oral Pathol 1992. Syrjanen J. Galili D. Reynolds H. Spec Care Dentist 1992. Dental treatment in very high risk patients with active ischemic heart disease. Knoll-Kohler E.70:274-7. Dajani AS. Dental management of anticoagulated patients. and Medical Affairs. Heart Dis Stroke 1993. Compendium 1989. Luria MH. A physician’s guide to coordinating oral health and primary care. Kasco G. Matsuura H.54:797-801. Arch Intern Med 1985. 18. Peltola J. et al.71:1554-60. Periodontal ligament injection: evaluation of systemic effects. Genco. Miller SB. Arch Intern Med 1986. The pathogenesis of atherosclerosis (first of two parts). 12. and sudden death. Stroke and the dental patient. Reyes AA. Gilbert GH. Dental care of the polymedication patient. Chisdak B. and optimal therapeutic range. J Periodontol 2000. Galili D. June 2002 Copyright ©2002 American Dental Association. 17. Smith GN. Lyman G. J Oral Maxillofac Surg 1990. Valtonen V. Pulpal anesthesia dependent on epinephrine dose in 2% lidocaine: a randomized controlled double-blind crossover study.66:680-2. Ruberman W. J Can Dent Assoc 1992.76:298-300. Compendium 1993. 15. clinical effectiveness. J Can Dent Assoc 1992. Assessing the risk of angina for dental therapy. Iivanainen M.225(3):179-84.2:388-92. Dent Clin North Am 1994. Taicher S. N Engl J Med 1976. Glomset J. 32. Garfunkel AA. 22.48:972-9. Council on Community Health.56:571-4. Findler M. Grossi SG. Hematologic and surgical management of the dental patient with plasminogen activator deficiency. All rights reserved. Cintron G. The systemic management of cardiovascular risk patients in dentistry. Oral Surg Oral Med Oral Pathol 1990. 40. Poller L. Yakirevitch V. Debanne SM. Prevention of bacterial endocarditis: recommendations by the American Heart Association. Glomset J. Wynn RL.58:253-6. Fortsch G. part one.40(1):18-20. Osman MI.38:633-44. Ross R. J Dent Res 2001. JADA 1994. 23. Hypertension update: a survey of the literature of interest to dentists. Bussey HI. Mosseri M. Hospital. 11. 28. 19. Compendium 1994. 43. Guntheroth WG. Dental infections in association with cerebral infarction in young and middle-aged men. 26. Haemodynamic changes under emotional stress following a minor surgical procedure under local anesthesia.125:721-7. Taubert KA. Pashley DH.80:141. Findler M. Ho A. Turcotte JY. Overview of risk factors for periodontal disease and implications for diabetes and cardiovascular disease. Meidan Z. 16. Genco RJ. Oral Surg Oral Med Oral Pathol 1993.47:1197-204. Dental responsibility for the medically compromised patient. 34.58:838-44. Oral Surg Oral Med Oral Pathol 1983. JADA. 30. Creighton JM. Meyer FU. Dental nonsteroidal anti-inflammatory drugs and prostaglandin-based drug interactions. Mazar AL. 13.19(1 supplement):40-5.73:537-40. Fay JT. How to monitor the dosage of warfarin. Dental care for the pediatric cardiac patient. 31.cation of pathogens in atheromatous plaques. Shapiro S.2:49-57.45(8):47-57. Geriatrics 1990. Vol. Frank CW. Carr MM. Oral anticoagulants: mechanism of action. MacAfee KA 2nd. 25. Goebel WM. Hart N.118:645-6. Goulet JP.74:687-91.14:892-900. et al. RJ. J Intern Med 1989. Phillips G.58:201-7. 39. Chest 1992. Levine E. 38. . J Oral Med 1984. Principles of surgical risk assessment of the elderly patient.39:218-45. Oral Surg Oral Med Oral Pathol 1988. Glurich I.10:598-604. Gen Dent 1992. Farkas JA. Perioperative hemodynamic changes in ischemic heart disease patients undergoing dental treatment. Long-term follow-up after recovery from acute myocardial infarction: observations on survival. Ostuni E. 24. 14. Contraindications to vasoconstrictors in dentistry.277:1794-801. Huttunen JK. et al.12(2):84-8. Deykin D. JAMA 1997. Terzhalmy GT. Medina R. Garfundel AA.16:688-94.
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