Complexities

Demystifying medical complexities

Although dentists often fear treating medically complex patients, in many cases this fear may be based not on scientific facts but rather on a "mythology" of the dangers of dentistry. Dentistry is a remarkably safe profession, even for most medically complex patients. The myths of endocarditis, artificial joint infections, local anesthetics and vasoconstrictors, dental surgery in anticoagulated patients and patients on antiplatelet drugs, and antibiotic interference with oral contraceptives are discussed. Although dental treatment is not usually a risk factor for endocarditis, practitioners should consult the 1997 American Heart Association statement for recommendations for endocarditis prevention. Most artificial joint patients should not receive antibiotic prophylaxis. Local anesthetics and vasoconstrictors can be used safely in most medically complex patients. Neither continuous anticoagulation nor antiplatelet medications should be withdrawn for dental surgery. Scientific studies have failed to document an interaction between antibiotics used in dentistry and oral contraceptives.

Many dentists, from those just out of school to experienced practitioners, approach dental treatment of medically complex patients with a mixture of two emotions: fear and paranoia. Fortunately, dentistry is not really as dangerous as many dentists are taught. Dental treatment has a remarkable safety record that is the envy of other health care professions.

Many things in dentistry that are done because they have always bee done. Many dentists may recommend certain types of materials, techniques, or treatments in patients because that was the way they were taught. Tradition is not necessarily a good way to practice dentistry.

Dentists are frequently taught that physician consultation can provide easy answers to the confusing questions of how to treat certain patients while also insulating the consulting dentist from liability in malpractice suits in the event of an unfavorable outcome. Actually, the dentist (not the physician) is ultimately responsible for the dental treatment.^1-3 Physician consultation, rather than insulating the dentist from liability in malpractice suits, can actually be a contributing factor in a malpractice suit, especially if the dentist relied on medical advice that the dentist knew or reasonably should have known to be erroneous.⁴

For example, a physician may recommend (unnecessary) antibiotic prophylaxis to prevent endocarditis for a patient undergoing a dental extraction because the patient had undergone heart bypass surgery (even though the American Heart Association does not recommend antibiotic prophylaxis in such a situation). If the dentist follows this advice, and the patient suffers a serious reaction to the antibiotic, then it is likely that both the dentist and the physician will be named in a subsequent malpractice action. "I did what the physician told me to do," is unlikely to be a valid legal defense. Although physician consultation can and should be a valuable adjunct to dental treatment decisions, it is no substitute for good clinical judgment based on current scientific studies and available national medical and dental group recommendations.

A dental license is not a license to defer dental treatment decisions to nondentists, even if the nondentists are physicians. Physicians are extremely well-trained in medicine, but usually not at all trained in dentistry. It is therefore not surprising, for example, that many physicians believe that root canal therapy carries a higher risk of hemorrhage than professional cleanings.⁵ Generally, if there is enough information from the patient’s medical history, then established scientific and national medical or dental group guidelines are sufficient to treat the patient. If there is information unknown to both the patient and the dentist, it may be appropriate to contact the physician for such information.

Well-meaning dentists and physicians often make dental treatment on medically complex patients more complex than it should be. Areas for which this can be the case include endocarditis, artificial joint infections, local anesthetics and vasoconstrictors, dental surgery in anticoagulated patients and patients on antiplatelet drugs, and antibiotic interference with oral contraceptives. Much of the thinking in these areas is not based on serious scientific thought but, rather, on tradition. In each area, a common myth will be presented, then the facts will be discussed. In each area, dentistry will be shown to be much safer than is commonly believed. Finally, the question of physician consultation and/or legal issues will be addressed in each area.

Myth 1

Dental procedures are a common cause of and antibiotics are an effective and harmless preventive of infective endocarditis.

Endocarditis is a rare heart infection that is caused by bacteremia, a bacterial invasion of the bloodstream. Although the bloodstream is usually sterile, most people have occasional bacteremias throughout the day. Usually, these bacteria quickly and harmlessly pass through the system; but, in rare cases, the bacteria can colonize on the heart valve, causing a heart infection known as infective endocarditis.⁶ Although endocarditis can occur in any patient, the principal risk factor is pre-existing heart valve abnormalities.^7,8

Roughly half of all cases of endocarditis are caused by the viridans streptococci,⁹ a group of microorganisms found abundantly in the mouth and gingival sulcus but also found on the skin, genitourinary tract, and eye. The initial flulike symptoms of streptococcal endocarditis usually occur within two weeks after the bacteremic incident.¹⁰ It is therefore difficult to determine definitively which bacteremic incident actually caused the subsequent infection, but it is not difficult to rule out any incidents that occurred more than two weeks before the initial symptoms.

Since some dental procedures can cause bacteremia by oral organisms, many cases of endocarditis have been blamed on the dentist. But several studies have shown that dental procedures cause very few, if any, cases of endocarditis of oral origin.^11-13 Most cases of endocarditis of oral origin are caused by frequent bacteremias from poor dental health and hygiene (bleeding gums and longstanding dental infections).¹² This is not surprising since in a typical month ending with an extraction, a patient with poor home care would have 5,000 more minutes of oral bactermia from "physiologic" sources (like brushing, chewing, and random bacteremias) than from the dental extraction.¹²

Still, it is possible that a dental procedure can cause a bacteremia that leads to endocarditis, and patients with pre-exisiting heart valve abnormalities are at greater risk of developing endocarditis than those without such abnormalities.¹⁴ The American Heart Association has issued statements on the prevention of endocarditis, most recently in 1997.¹⁵ This 1997 statement has been endorsed by the American Dental Association.¹⁶ Although it accurately points out that the most important preventive for endocarditis is good oral health and home care, the AHA also recommends that some patients with certain heart problems should receive antibiotic prophylaxis before certain dental procedures that cause significant bleeding.

Although it is widely agreed upon that antibiotics can be a valuable adjunct in treating infections, there is still controversy as to whether antibiotics are effective in preventing infections.^7,17. Although antibiotic prophylaxis has been shown to prevent experimental endocarditis in animals, there have been "apparent failures" of antibiotic prophylaxis to prevent endocarditis in humans.¹⁸ Case/control studies have shown that antibiotic prophylaxis is effective less than half the time.^19,20 Risk/benefit studies have shown that in some scenarios, the small risk of serious reactions (e.g., gastrointestinal upset, hearing loss, allergy, anaphylaxis, and even death) to antibiotics actually can be greater than the even smaller risk that a patient would develop endocarditis.^21,22 Durack has stated it may be time to scale back on antibiotic prophylaxis and eliminate it altogether except for the highest risk patients having the highest risk procedures (e.g., patients with artificial heart valves or previous history of endocarditis having extractions or gingival surgery).²³

Practitioners usually have neither the time nor the interest to become expert in the area of endocarditis prevention. The 1997 AHA statement, written by a prominent group of experts in endocarditis, is a simple and useful guide for the practicing dentist. It provides a list of patients and dental procedures for which antibiotic prophylaxis is recommended and those for which it is not recommended. Although it is not meant to be a standard of care in all cases, it is a virtual certitude that in a malpractice case involving endocarditis, the AHA statement will be consulted. Since it will not be reprinted here, readers are urged to consult a copy of the statement and related articles.^24,25

Physician Consultation

Physician consultation is often an excellent tool for information on a patient’s heart condition. Consultation is generally not recommended for deciding whether or not to administer antibiotic prophylaxis for a specific dental procedure or the choice, dosage, or timing of the antibiotic. Instead, the latest (1997) AHA statement should be consulted.

Myth 2

Dental treatment is a common cause of and antibiotics are a harmless and effective preventive of artificial joint infections.

As the population ages, there are more joint replacement surgeries being performed, including hips, knees, and shoulders. These artificial joints can become infected from bacteremias; and such infections can be very serious, leading to further surgeries, disfigurement, and even death. In the past, dentists were urged to prescribe antibiotic prophylaxis for these patients to prevent such infections. It is now clear that most dental patients should not receive antibiotic prophylaxis to prevent artificial joint infections.^26-28

Although there have been many documented artificial joint infections, only a few of these have been blamed on dental treatment. But after examining these few cases carefully, several authorities came to the same conclusion: in none of these cases was the dental treatment the probable cause of the subsequent joint infection.^29-31

The American Dental Association and the American Academy of Orthopaedic Surgeons issued a statement in 1997 concluding that antibiotic prophylaxis was not indicated for most patients with artificial joints. The only patients for whom antibiotic prophylaxis should even be considered is a small number of high risk artificial joint patients (e.g., patients with previous artificial joint infections, insulin-dependent diabetes, and radiation-induced immunosuppression).² Even among these increased-risk patients, it is still within the standard of care not to recommend antibiotic prophylaxis to prevent artificial joint infections: "Practitioners must exercise their own clinical judgment in determining whether or not antibiotic prophylaxis is appropriate."² Other groups have issued similar statements. The American Academy of Oral Medicine has stated that "there is insufficient scientific evidence to support routine antibiotic prophylaxis for patients with prosthetic joints who are receiving dental care."³² The British Society for Antimicrobial Chemotherapy recommends against any antibiotic prophylaxis before dental treatment in these patients.³³

Some authorities have noted that because there is good evidence that artificial heart valve patients are at risk of endocarditis from dental treatment, so artificial joint patients must be at risk of artificial joint infections from dental treatment.³⁴ But while the single leading cause of prosthetic valve endocarditis is streptococcus, found abundantly in the mouth, the single leading cause of prosthetic joint infections is staphylococcus.^7,26 Staphylococci are ubiquitous on the skin, but are not commonly found in the blood after dental procedures.^35,36 Also, unlike cases of endocarditis, with an incubation period of a few days to two weeks, late artificial joint infections have been associated with much longer incubation periods, from four months to almost nine years.^30,37-39

After placing artificial knee joints in 23 rabbits, Blomgren injected staphylococci into each rabbit. Four of the 10 surviving rabbits had artificial joint infections.^40,41 This experiment has been called the best evidence supporting antibiotic prophylaxis to prevent prosthetic joint infection after dental treatment.⁴² But there were serious flaws in this small study, and it has little relevance to dental treatment. The organism used was a staphylococcus, which is rarely, if ever, found in the blood after dental treatment. In addition, the inocula were more like septicemias than transient bacteremias after dental treatment: More than half of the rabbits died from these massive inocula. Animal experimentation has therefore failed to show that dental treatment causes artificial joint infections.

Risk/benefit and cost/benefit analyses have shown that the risks and costs of antibiotic prophylaxis outweigh the potential benefits:^43-47 Because of the risks of serious reactions to certain antibiotics, when all prosthetic joint patients receive antibiotic prophylaxis for dental treatment, there may actually be a net loss of life as compared to no use of prophylaxis.

Physician Consultation

It may be prudent to consult the patient’s physician if there is a discrepancy between what the physician recommends and what the American Academy of Orthopaedic Surgeons/American Dental Association 1997 statement recommends to find out if the physician has information about the patient’s medical history that is unknown to the dentist.

If the patient or the patient’s physician insists on antibiotic prophylaxis, then it is still acceptable to treat the patient. Jacobsen summed it up well: "Let the physician prescribe the medicine; the dentist can then do the dentistry."⁴⁸ This way the dentist may not be faced with a legal problem from potential harm from an unnecessarily prescribed drug.

Myth 3

Dental patients on continuous anticoagulant or antiplatelet drugs should have these drugs withdrawn before dental surgery.

Anticoagulant medications such as warfarin sodium (coumadin) are often administered continuously (daily) to patients to prevent complications such as stroke and thromboembolisms.^49,50 Although these medications are often lifesaving, they can also increase the risk of hemorrhage after medical or dental procedures. Anticoagulation is measured by the International Normalized Ratio or Prothrombin Time Ratio. The American Heart Association⁵¹ and the American College of Chest Physicians⁵² recommend a therapeutic level of anticoagulation of no higher than INR 3.5 or about PTR 2.0 (although some authorities⁵³ have stated no higher than INR 4.0, or about PTR 2.2). Although 73 percent of physicians surveyed in 1996 recommend withdrawing coumadin before some or all dental procedures, more physicians recommended withdrawing coumadin for root canal therapy than for professional cleanings, even though root canal therapy carries little or no risk of hemorrhage.⁵

In extensive reviews of the literature, it was shown that in more than 950 patients on continuous anticoagulant therapy (many at higher than currently recommended therapeutic levels) receiving more than 2,400 surgical dental procedures, only 12 patients (<1.3 percent) needed more than local measures (e.g., biting on gauze or tea bags, suturing, or application of cellulose sponges) to control hemorrhage.^54,55 Only three of these patients (<0.31 percent) were anticoagulated within or below currently recommended therapeutic levels, but these were not well-documented. In other words, there has never been a well-documented case of hemorrhage uncontrolled by local measures after dental surgery in a continuously anticoagulated patient. On the other hand, of 526 patients having 575 interruptions of continuous anticoagulation, five (0.95 percent) suffered serious emobolic complications; four of these patients died. There is no difference in blood loss between dental extraction patients continuing anticoagulation and those in whom anticoagulation is withdrawn.⁵⁶

Continuous (daily) antiplatelet medications (aspirin) are often used to prevent a heart attack. Many physicians recommend withdrawing aspirin before dental surgery.⁵ Although there have been case reports of postoperative hemorrhage after dental surgery,^57-59 controlled studies have not indicated a risk in patients taking low-dose (100 mg/day) aspirin. In an interesting study of patients taking aspirin undergoing unexpected (emergency) major operations (including appendectomy, cholecystectomy, intestinal resection, or mastectomy), there was no difference in perioperative blood loss between the study group and a control group of patients not taking aspirin undergoing the same procedures.⁶⁰ The aspirin group also had no postoperative bleeding problems. In a similar study of patients undergoing dental extractions, the aspirin group was no different than the placebo (acetaminophen) group.⁶¹ A recent study came to the same conclusion: There is no need to stop aspirin before oral surgery.⁶²

Anticoagulants and antiplatelet drugs are often lifesaving; dental surgery is almost never life-threatening. When used at currently recommended therapeutic levels, these medications should not be withdrawn for dental surgery.

Physician Consultation

Physician consultation or consultation with the patient’s medical laboratory is often helpful for the anticoagulated patient’s latest level of anticoagulation (INR). Consultation is generally not recommended on the question of whether or not to withdraw anticoagulation once the dentist knows that the patient is at therapeutic levels of anticoagulation. For patients on continuous antiplatelet medications such as aspirin, physician consultation is usually not necessary unless there are other areas of concern in the medical history, especially those that affect bleeding time.

Myth 4

Local anesthetics and vasoconstrictors should be used with special caution in most medically compromised patients.

Although the safety of local anesthetics and vasoconstrictors has often been questioned, the reality is that they should be used the same in most medically compromised patients as they are in otherwise healthy patients.⁶³ For example, in spite of drug manufacturer warnings that there may be a severe hypertensive or hypotensive reaction between MAO inhibitors and vasoconstrictors in anesthetics,⁶⁴ animal,⁶⁵ and human^66,67 studies indicate there is no such interaction.

Although drug manufacturers still state that amide local anesthetics may cause severe hyperthermic reactions in patients susceptible to malignant hyperthermia,⁶⁴ animal and human studies show amide local anesthetics do not pose a special risk in such patients.^68-71 This is fortunate because the only injectable anesthetics in single-use dental cartridges manufactured in the United States for dental use (and virtually the only injectable anesthetics used by dentists) are amides such as lidocaine, mepivacaine, prilocaine, etidocaine, and bupivacaine. The ester anesthetic procaine (Novocain) is no longer manufactured in dental cartridges in the United States.⁷²

Although the anesthetic preservative methylparaben has been banned by the Food and Drug Administration in the United States for single-use dental cartridges,⁷³ there are small quantities of sulfite antioxidant preservatives for vasoconstrictors added to anesthetics with vasoconstrictors. Sulfites are also used in beer, wine, and much restaurant food. Restaurant meals typically contain about 25 to 200 mg of sulfites, which is at least 27 times the amount of sulfite in a single cartridge of lidocaine with 1:100,000 epinephrine (0.9 mg).⁷⁴ Again, in spite of drug manufacturers’ warnings to the contrary, the vast majority of asthmatic patients can safely receive anesthetics with sulfite-containing vasoconstrictors.^75,76 Although a few steroid-dependent asthmatic patients may be sensitive to low doses of sulfites, a general rule is that if a patient can drink beer or wine or eat a restaurant meal, then the patient can safely have sulfite-containing local anesthetics.^74,77

Allergy to amide local anesthetics is extremely rare, and there are few if any well-documented cases of true allergy to amide local anesthetics.⁷² Some patients claim they are allergic to Novocain, but further questioning often reveals their symptoms more consistent with a psychosomatic reaction or an intravascular injection of vasoconstrictor-containing anesthetic.

To prevent lip mutilation after dental procedures, some dentists administer anesthetics without vasoconstrictors, thinking that the lip anesthesia will not last as long when using anesthetics with vasoconstrictors. Scientific studies, however, have shown that although pulpal anesthesia may last longer when vasoconstrictors are added to local anesthetics, the duration of lip anesthesia is the same with or without vasoconstrictors.^78,79 But anesthetics with vasoconstrictors have less anesthetic per cartridge. Mepivacaine 3 percent plain has 50 percent more anesthetic per cartridge (54 mg) than lidocaine 2 percent with epinephrine (36 mg). Lidocaine has a significantly higher maximum recommended dose (13.9 cartridges in a 150-pound adult; 4.4 cartridges in a 50-pound child) than does mepivacaine plain (7.4 cartridges in a 150-pound adult; 2.8 cartridges in a 50-pound child). There have been several unfortunate case reports of overdoses of mepivacaine plain during dental appointments, leading to the death of small children.^80,81 Inclusion of a vasoconstrictor might have slowed the anesthetic absorption rate and reduced its toxicity.

When a vasoconstrictor is necessary, epinephrine is often preferred over levonordefrin in medically compromised patients.⁸² Because epinephrine is a more potent vasoconstrictor than levonordefrin, mepivacaine with 1:20,000 levonordefrin has five times as much vasoconstrictor (90 mcg levonordefrin per cartridge) as does lidocaine with 1:100,000 epinephrine (18 mcg epinephrine per cartridge). The effects of epinephrine may be potentiated by tricyclic antidepressants. Anesthetics with epinephrine should therefore be used cautiously in patients taking tricyclic antidepressants, but levonordefrin-containing anesthetics should not be used at all in such patients because its effects are potentiated even more.^66,83

Physician Consultation

Generally a physician consultation is not necessary unless more information is needed about the patient’s medical history.

Myth 5

Antibiotics used in dentistry interfere with oral contraceptives, thereby contributing to unwanted pregnancies.

Dentists have long been indoctrinated with the fear of wrongful death lawsuits for negligence in prescribing medications. Now, there are even warnings about "wrongful birth" lawsuits. A wrongful birth or unwanted pregnancy, it is said, can be caused by a dentist failing to warn a woman of a possible interaction between her birth control pills and an antibiotic that the dentist prescribes. The dentist could then legally be liable for damages, including child support payments. Since many women of childbearing age are taking oral contraceptives and since dentists frequently prescribe antibiotics, this issue can be of great concern to practicing dentists. Some have advised that women who are prescribed antibiotics should be warned of a potential interaction and advised to use an additional birth control method.^84-86 At least one dermatologist has gone so far as to withhold needed antibiotics from any women on birth control pills.⁸⁷

This concern came to a climax in the lay media: A tabloid newspaper addressed the issue under the headline "A dental visit can make you pregnant!" Fortunately, after reviewing the scientific and medical literature, it appears that the fears of antibiotic interference with oral contraceptives are not based on scientific evidence but instead on irrational myths.

There have been case reports of unwanted pregnancy after administration of antibiotics, including many of the antibiotics used in dentistry. These case reports have led many to conclude that the antibiotics caused the oral contraceptive to fail. This type of reasoning has been called "post hoc, ergo propter hoc" (after this, therefore on account of this). But simply because a pregnancy occurred after antibiotic ingestion does not prove that the antibiotic helped cause the pregnancy. From 1968 to 1984 there were 63 pregnancies reported in England in women on oral contraceptives who were concurrently receiving antibiotics (not including rifampin, which has been scientifically shown to decrease oral contraceptive efficacy).⁸⁸ From 1973 to 1984, there were more than 300 million prescriptions for antibiotics (not including rifampin) in England. In a landmark article questioning the interaction between antibiotics and oral contraceptives for the first time in the dental literature, Becker pointed out that such statistics introduce the likelihood of mere chance correlation between unwanted pregnancies and antibiotics.⁸⁹

Many of the case reports of unwanted pregnancy blaming antibiotics occurred in women also taking other medications known to decrease contraceptive efficacy. In addition, some of these reports may be related to the known 1 percent failure rate of oral contraceptives. Finally, many women may skip doses of the contraceptive, which may lead to unwanted pregnancy. For example, it is estimated that up to 50 percent of teenage girls on oral contraceptives miss doses. The average teenager misses three pills during a 28-day cycle, and the failure rate among teenagers is eight times (8 percent) the failure rate among all women (1 percent).⁹⁰

The American Dental Association reported on possible antibiotic interference with oral contraceptives in 1991.⁹¹ Although it is now doubtful that any antibiotics used in dentistry are truly responsible for oral contraceptive failure, those listed by the American Dental Association were only the penicillins, tetracyclines, sulfonamides, erythromycin, metronidazole, griseofulvin, and cephalosporin. Clindamycin was not implicated in oral contraceptive failure.

Rifampin was first implicated in decreased contraceptive efficacy in 1971.⁹² Since then, other antibiotics have been blamed, including the penicillins (amoxicillin, ampicillin, and penicillin), metronidazole, the macrolide antibiotics (including erythromycin and roxithromycin), cotrimoxazole, and the tetracyclines. Rifampin, a potent enzyme-inducing antituberculosis drug generally not used in dentistry, has been scientifically shown to decrease the levels of oral contraceptives.^93,94 Similar studies on ampicillin,^95,96 metronidazole,⁹⁷ tetracycline,⁹⁸ roxithromycin,⁹⁹ cotrimoxazole,¹⁰⁰ temafloxacin,¹⁰¹ and doxycycline¹⁰² have consistently failed to show decreased contraceptive levels in women taking these antibiotics concurrently. One antibiotic, cotrimoxazole, has been shown to increase levels of estrogen and progesterone.⁹⁹ Unlike rifampin, none of these antibiotics are enzyme inducers.

To prevent wrongful birth lawsuits from unwanted pregnancies, dentists prescribing antibiotics are trained to recommend additional forms of contraception to women taking oral contraceptives. But giving such advice can unnecessarily upset women and could theoretically lead to lawsuits for emotional distress and/or loss of consortium. Also, because of receiving this advice, many women may refuse to take antibiotics at all, which may lead to greater infection, another potential lawsuit. In addition to exhaustively reviewing the literature, Hersh¹⁰³ analyzed a California legal proceeding in which a woman and her husband sued her gynecologist for the "wrongful life" of their child allegedly caused by an interaction between her oral contraceptive medication and the penicillin V that the dentist prescribed.¹⁰⁴ The plaintiffs lost the case because they were unable to show scientific studies that documented a significant interaction or that she became pregnant while taking the penicillin. In addition, under California law, practitioners are not required to discuss risks of very low incidences. Hersh pointed out that the failure rate would have to exceed double the expected failure rate for a practitioner to be required to discuss the potential risk.

Antibiotics used in dentistry have not been shown to decrease oral contraceptive efficacy. Of all antibiotics studied, only rifampin has been scientifically shown to decrease oral contraceptive efficacy. On the other hand, diarrhea or breakthrough bleeding from any cause (including antibiotics) can be a sign of decreased absorption of oral contraceptives, and patients in these situations should use additional birth control methods.¹⁰⁵ Since oral contraceptives are not 100 percent effective, many patients may wish to use additional methods of contraception anyway.

Conclusion

Dental treatment on many medically complex patients may not be so complex. Although dental treatment generally does not cause endocarditis, it can. Dentists should consult the 1997 American Heart Association statement for recommendations on antibiotic prophylaxis in patients at risk for endocarditis. Most patients with artificial joints should not have antibiotic prophylaxis -- the only ones for whom antibiotic prophylaxis should even be considered are patients at high risk. Neither continuous anticoagulation nor continuous antiplatelet medications should be withdrawn for dental surgery unless patients are at higher than therapeutic levels or they have other medical considerations. In spite of many admonishments to the contrary, local anesthetics and vasoconstrictors can be used without special reservation in virtually all medically complex patients. Local anesthetics with vasoconstrictors should be preferred over plain anesthetics in children. Scientific studies have failed to document an interaction between antibiotics used in dentistry and oral contraceptives. Physician consultation can be a valuable adjunct to dental treatment but should not be a substitute for the dentist’s clinical judgment based on current scientific literature and available national medical and dental group guidelines.

Author

Michael J. Wahl, DDS, is an assistant attending dentist at Christiana Care Health Services in Wilmington, Del., and a clinical assistant professor of surgery at Allegheny University Hospitals. He is also in private practice in Wilmington, Del.

References

1. Todd KM, A legal perspective on antibiotic prophylaxis. J Am Dent Assoc 128:1007, 1997.

2. American Dental Association, American Academy of Orthopaedic Surgeons, Antibiotic prophylaxis for dental patients with total joint replacements. J Am Dent Assoc 128:1004-7, 1997.

3. Jacobson JJ, Prosthetic joint patients [letter]. J Am Dent Assoc 125:1432-4, 1994.

4. Wahl MJ, Prosthetic joint patients [letter]. J Am Dent Assoc 125:664-6, 1994.

5. Wahl MJ, Howell J, Altering anticoagulation therapy: a survey of physicians. J Am Dent Assoc 127:625-38, 1996.

6. Pallasch TJ, A critical appraisal of antibiotic prophylaxis. Int Dent J 39:183-96, 1989.

7. Pallasch TJ, Slots J, Antibiotic prophylaxis and the medically compromised patient. Periodontol 2000 10:107-38, 1996.

8. Little JW, Antibiotic prophylaxis for prevention of bacterial endocarditis and infectious major joint prostheses. Oral Maxillof Surg Infec 2(3):93-101, 1992.

9. Yagiela JA, Prophylactic antibiotics: cardiac and prosthetic considerations. J Calif Dent Assoc 23(10):29-40, 1995.

10. Starkebaum M, Durack D, Beeson P, The "incubation period" of subacute bacterial endocarditis. Yale J Biol Med 50:49-58, 1977.

11. Bayliss R, Clarke C, et al, The teeth and infective endocarditis. Br Heart J 50:506-12, 1983.

12. Guntheroth WG, How important are dental procedures as a cause of infective endocarditis? Am J Cardiol 54:797-801, 1984.

13. Strom BL, Abrutyn E, et al, Dental and cardiac risk factors for infective endocarditis. A population-based, case-control study. Ann Intern Med 129:761-9, 1998.

14. Steckelberg JM, Wilson WR, Risk factors for infective endocarditis. Infect Dis Clin North Amer 7(1):9-19, 1993.

15. Dajani AS, Taubert KA, et al, Prevention of bacterial endocarditis: recommendations by the American Heart Association. J Am Med Assoc 277:1794-1801, 1997.

16. Dajani AS, Taubert KA, et al, Prevention of bacterial endocarditis: recommendations by the American Heart Association. J Am Dent Assoc 128:1142-51, 1997.

17. Wahl MJ, Myths of dental-induced endocarditis. Arch Intern Med 154:137-44, 1994.

18. Durack DT, Kaplan EL, Bisno AL, Apparent failures of endocarditis prophylaxis: analysis of 52 cases submitted to a national registry. J Am Med Assoc 250:2318-22, 1983.

19. van der Meer JTM, van Wijk W, et al, Efficacy of antibiotic prophylaxis for prevention of native-valve endocarditis. Lancet 339:135-9, 1992.

20. Lacassin F, Hoen B, et al, Procedures associated with infective endocarditis in adults: a case control study. Eur Heart J 16:1968-74, 1995.

21. Bor DH, Himmelstein DU, Endocarditis prophylaxis for patients with mitral valve prolapse: a quantitative analysis. Am J Med 76:711-17, 1984.

22. Clemens JD, Ransohoff DF, A quantitative assessment of pre-dental antibiotic prophylaxis for patients with mitral-valve prolapse. J Chron Dis 37:531-44, 1984.

23. Durack DT, Antibiotics for prevention of endocarditis during dentistry: time to scale back? Ann Intern Med 129:829-31, 1998.

24. Pallasch TJ, Gage TW, Taubert KA, The 1997 prevention of bacterial endocarditis recommendations by the American Heart Association: questions and answers. J Calif Dent Assoc 27(5):393-9, 1999.

25. Pallasch TJ, Antibiotic prophylaxis: significance of its recent evolution. J Calif Dent Assoc 25(9):619-32, 1997.

26. Wahl MJ, Myths of dental-induced prosthetic joint infections. Clin Infect Dis 20:1420-5, 1995.

27. Wahl MJ, Clinical issues in the prevention of dental-induced endocarditis and prosthetic joint infection. Pract Perio Aesth Dent 6(6):25-32, 1994.

28. Little JW, Managing dental patients with joint prostheses. J Am Dent Assoc 125:1374-8, 1994.

29. Council on Dental Therapeutics, American Dental Association. Management of dental patients with prosthetic joints. J Am Dent Assoc 121:537-38, 1990.

30. McGowan DA, Hendrey ML, Is antibiotic prophylaxis required for dental patients with joint replacements? Br Dent J 158:336-8, 1985.

31. Thyne GM, Ferguson JW, Antibiotic prophylaxis during dental treatment in patients with prosthetic joints. J Bone Joint Surg [Br] 73B:191-4, 1991.

32. Eskinazi D, Rathbun W, Is systematic antimicrobial prophylaxis justified in dental patients with prosthetic joints? Oral Surg Oral Med Oral Pathol 66:430-1, 1988.

33. Simmons NA, Ball AP, et al, Case against antibiotic prophylaxis for dental treatment of patients with joint prostheses. Lancet 339:301, 1992.

34. Rubin R, Salvati EA, Lewis R, Infected total hip replacement after dental procedures. Oral Surg 41:18-23, 1976.

35. Hall G, Hedström SÅ, et al, Prophylactic administration of penicillins for endocarditis does not reduce the incidence of postextraction bacteremia. Clin Infect Dis 17:188-94, 1993.

36. Heimdahl A, Hall G, et al, Detection and quantitation by lysis-filtration of bacteremia after different oral surgical procedures. J Clin Microbiol 28:2205-9, 1990.

37. Maniloff G, Greenwald R, et al, Delayed postbacteremic prosthetic joint infection. Clin Orthop Rel Res 223:194-7, 1987.

38. Poss R, Thornhill TS, et al, Factors influencing the incidence and outcome of infection following total joint arthroplasty. Clin Orthop 182:117-26, 1984.

39. McCarthy J, Stingemore N, Clostridium difficile infection of a prosthetic joint presenting 12 months after antibiotic-associated diarrhoea. J Infect 39:94-6, 1999.

40. Blomgren G, Hematogenous infection of total joint replacement: an experimental study in the rabbit. Acta Orthop Scand 52(suppl 187):1-64, 1981.

41. Blomgren G, Lindgren U, Late hematogenous infection in total joint replacement: studies of gentamicin and bone cement in the rabbit. Clin Orthop 155:244-8, 1981.

42. Cioffi GA, Terezhalmy GT, Taybos GM, Total joint replacement: a consideration for antimicrobial prophylaxis. Oral Surg Oral Med Oral Pathol 66:124-9, 1988.

43. Jacobson JJ, Schweitzer SO, Kowalski CJ, Chemoprophylaxis of prosthetic joint patients during dental treatment: a decision-utility analysis. Oral Surg Oral Med Oral Pathol 72:167-77, 1991.

44. Little JW, The need for antibiotic coverage for dental treatment of patients with joint replacements. Oral Surg Oral Med Oral Pathol 55:20-3, 1983.

45. Tsevat J, Durand-Zaleski I, Pauker SG, Cost-effectiveness of antibiotic prophylaxis for dental procedures in patients with artificial joints. Am J Public Health 79:739-43, 1989.

46. Jacobson JJ, Schweitzer S, et al, Chemoprophylaxis of dental patients with prosthetic joints: a simulation model. J Dent Educ 52:599-604, 1988.

47. Jacobson JJ, Schweitzer S, et al, Antibiotic prophylaxis for dental patients with joint prostheses? A decision analysis. Inter J Tech Assess Health Care 6:569-87, 1990.

48. Jacobsen PL. Guidelines stressed [letter]. J Am Dent Assoc 125:798, 1994.

49. Herman WW, Konzelman JL, Sutley SH, Current perspectives on dental patients receiving coumarin anticoagulant therapy. J Am Dent Assoc 128:327-35, 1997.

50. Beirne OR, Koehler JR, Surgical management of patients on warfarin sodium. J Oral Maxillofac Surg 54:1115-8, 1996.

51. Hirsh J, Fuster V, Guide to anticoagulant therapy. Part 2: oral anticoagulants. Circulation 89:1469-80, 1994.

52. Hirsh J, Dalen JE, et al, Oral anticoagulants: mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 102 (suppl):312S-26S, 1992.

53. Cannegieter SC, Rosendaal FR, et al. Optimal oral anticoagulant therapy in patients with mechanical heart valves. N Engl J Med 333:11-7, 1995.

54. Wahl MJ, Dental surgery in anticoagulated patients. Arch Intern Med 158:1610-16, 1998.

55. Wahl MJ, Myths of dental surgery in patients receiving anticoagulant therapy. J Am Dent Assoc 131:77-81, 2000.

56. Campbell JH, Alvarado F, Murray RA, Anticoagulation and minor oral surgery: Should the anticoagulation regimen be altered? J Oral Maxillofac Surg 58:131-5, 2000.

57. Thomason JM, Seymour RA, et al, Aspirin-induced post-gingivectomy haemorrhage: a timely reminder. J Clin Periodontol 24:136-8, 1997.

58. Davis MJ, Aspirin-induced prolonged bleeding: report of case. J Dent Child 43:350, 1976.

59. McGaul T, Postoperative bleeding caused by aspirin. J Dent 6:207-9, 1978.

60. Ferraris VA, Swanson E, Aspirin usage and perioperative blood loss in patients undergoing unexpected operations. Surg Gynecol Obstet 156:439-42, 1983.

61. Pawalk DF, Itkin AB, et al, Clinical effects of aspirin and acetaminophen on hemostasis after exodontics. J Oral Surg 36:944-7, 1978.

62. Ardekian L, Gaspar R, et al, Does low-dose aspirin therapy complicate oral surgical procedures? J Am Dent Assoc 131:331-5, 2000.

63. Wahl MJ, Local anesthetics and vasoconstrictors: myths and facts. Pract Periodont Aesth Dent 9:649-52, 1997.

64. 1997 Physicians’ Desk Reference. Medical Economics, Montvale, NJ, p 563.

65. Yagiela JA, Duffin SR, Hunt LM, Drug interactions and vasoconstrictors used in local anesthetic solutions. Oral Surg Oral Med Oral Pathol 59:565-71, 1985.

66. Boakes AJ, Laurence DR, et al, Interactions between sympathomimetic amines and antidepressant agents in man. Br Med J 1:311-15, 1973.

67. Elis J, Laurence DR, et al, Modification by monoamine oxidase inhibitors of the effect of some sympathomimetics on blood pressure. Br Med J 2:75-8, 1967.

68. Wingard DW, Bobko S, Failure of lidocaine to trigger porcine malignant hyperthermia. Anesth Analg 58:99-103, 1979.

69. Harrison GG, Morrell DF, Response of MHS swine to IV infusion of lignocaine and bupivacaine. Br J Anaesth 52:385-7, 1980.

70. Steelman R, Holmes D, Outpatient dental treatment of pediatric patients with malignant hyperthermia: report of three cases. J Dent Child 59:62-5, 1992.

71. Gielen M, Viering W, 3-in-1 lumbar plexus block for muscle biopsy in malignant hyperthermia patients. Amide local anaesthetics may be used safely. Acta Anaesthesiol Scand 30:581-3, 1986.

72. Clinical action of specific agents. In, Malamed SF, Handbook of Local Anesthesia, 4th ed. Mosby, St. Louis, 1997, pp 49-73.

73. The cartridge. In, Malamed SF, Handbook of Local Anesthesia, 4th ed. Mosby, St. Louis,1997, pp 91-9.

74. Simon RA, Sulfite sensitivity. Ann Allerg 56:281-8, 1986.

75. Bush RK, Taylor SL, et al, Prevalence of sensitivity to sulfiting agents in asthmatic patients. Am J Med 81:816-20, 1986.

76. Goldfarb G, Simon R, Provocation of sulfite sensitive asthma. J Allergy Clin Immunol 73:135 [Abstr 107], 1984.

77. Pérusse R, Goulet J-P, Turcotte J-Y, Contraindications to vasoconstrictors in dentistry, Part II. Oral Surg Oral Med Oral Pathol 74:687-91, 1992.

78. Hersh EV, Hermann DG, et al. Assessing the duration of mandibular soft tissue anesthesia. J Am Dent Assoc 126:1531-6, 1995.

79. Yagiela JA, Local anesthetics: a century of progress. Anesth Progr 32:47-56, 1985.

80. Moore PA, Preventing local anesthesia toxicity. J Am Dent Assoc 123(9):60-4, 1992.

81. Hersh EV, Helpin ML, Evans OB, Local anesthetic mortality: report of case. J Dent Child 58:489-91, 1991.

82. Robertson VJ, Taylor SE, Gage TW, Quantitative and qualitative analysis of the pressor effects of levonordefrin. J Cardiovasc Pharm 6:929-35, 1984.

83. Patient evaluation. In, Jastak JT, Yagiela JA, Donaldson D, Local Anesthesia of the Oral Cavity. WB Saunders, Philadelphia, 127-44, 1995.

84. Donley TG, Smith RF, Reduced oral contraceptive effectiveness with concurrent antibiotic use: a protocol for prescribing antibiotics to women of childbearing age. Compend Contin Educ Dent 11:392-5, 1990.

85. Gibson J, McGowan DA, Oral contraceptives and antibiotics: important considerations for dental practice. Br Dent J 177:419-22, 1994.

86. Bainton R, Interaction between antibiotic therapy and contraceptive medication. Oral Surg Oral Med Oral Pathol 453-5, 1986.

87. Coskey RJ, Tetracycline and oral contraceptives [letter]. J Am Acad Dermatol 5:222, 1981.

88. Back DJ, Grimmer SFM, et al, Evaluation of Committee on Safety of Medicines yellow card reports on oral contraceptive-drug interactions with anticonvulsants and antibiotics. Br J Clin Pharmac 25:527-32, 1988.

89. Becker DE, Drug interactions in dental practice: a summary of facts and controversies. Compend Contin Educ Dent 15:1228-42, 1994.

90. Sondheimer SJ, Update on oral contraceptive pills and postcoital contraception. Curr Opin Obstet Gynecol 4:502-5, 1992.

91. ADA Health Foundation Research Institute, Department of Toxicology. Antibiotic interference with oral contraceptives. J Am Dent Assoc 122(12):79, 1991.

92. Orme ML’E, Back DJ, Breckenridge AM, Clinical pharmacokinetics of oral contraceptive steroids. Clin Pharmacokin 8:95-136, 1983.

93. Back DJ, Breckenridge AM, et al, The effect of rifampicin on norethisterone pharmacokinetics. Eur J Clin Pharmacol 15:193-7, 1979.

94. Back DJ, Breckenridge AM, et al, The effect of rifampicin on the pharmacokinetics of ethinylestradiol in women. Contraception 21:135-43, 1980.

95. Back DJ, Breckenridge AM, et al, The effects of ampicillin on oral contraceptive steroids in women. Br J Clin Pharmac 14:43-8, 1982.

96. Friedman CI, Huneke AL, et al, The effect of ampicillin on oral contraceptive effectiveness. Obstetr Gynecol 55:33-7, 1980.

97. Joshi JV, Joshi UM, et al, A study of interaction of low-dose combination oral contraceptive with ampicillin and metronidazole. Contraception 22:643-52, 1980.

98. Murphy AA, Zacur HA, et al, The effect of tetracycline on levels of oral contraceptives. Am J Obstet Gynecol 164:28-33, 1991.

99. Meyer B, Müller F, et al, A model to detect interactions between roxithromycin and oral contraceptives. Clin Pharmacol Ther 47:671-4, 1990.

100. Grimmer SFM, Allen WL, et al, The effect of cotrimoxazole on oral contraceptive steroids in women. Contraception 28:53-9, 1983.

101. Back DJ, Tjia J, et al, The lack of interaction between temafloxacin and combined oral contraceptive steroids. Contraception 43:317-23, 1991.

102. Neely JL, Abate M, et al, The effect of doxycycline on serum levels of ethinyl estradiol, norethindrone, and endogenous progesterone. Obstet Gynecol 77:416-20, 1991.

103. Hersh EV, Adverse drug interactions in dental practice: interactions involving antibiotics, Part II of a series. J Am Dent Assoc 130:236-51, 1999.

104. LaCasa C, California court denies wrongful birth claim. J Law Med Ethics 24(3):273-4, 1996.

105. Miller DM, Helms SE, Brodell RT, A practical approach to antibiotic treatment in women taking oral contraceptives. J Am Acad Dermatol 30:1008-11, 1994.

To request a printed copy of this article, please contact: Michael J. Wahl, DDS, 1601 Concord Pike, Wilmington, DE 19803 or at WahlMichaelJ@aol.com.