PERSPECTIVES

Democracy and Dentistry

A Medical Profession within a Democracy

Robert P. Iovino, D.D.S.

AS AMERICAN DENTISTRY moves forward,driven by significant clinical advances that offer greater benefit to patients in form and function,it is appropriate to pause and reflect on the characteristics that define our profession. The publics desire for new, better, quicker care and its willingness to pay the requisite ever-greater fees have placed our profession in an enviable position. Too often our medical colleagues do not share in this prosperity. However, while many in our profession are benefiting from an unprecedented bull market, we must guard against letting this market define our profession. I am not suggesting that this prosperity is not hard earned or appropriate,just that in our modern, media-driven, market-based society, our allegiance must always be first to benefiting our patients over ourselves.Yes, the old-fashioned word virtueis applicable here. I would like to briefly review the origins of modern medicine/ dentistry, science, philosophy and the beginnings of our government to show the relatively concomitant birthing of all that has made American health care unique.A common theme throughout this article will be that of a profession, specifically, the dental profession. Remember, we are dental physicians, and dentistry arose from medicine. Indeed, the term medical profession is an inclusive heading for surgery,medicine,dentistry,pharmacy,nursing,etc.Paul Starr,author of The Social Transformation of American Medicine, defines a profession as an occupation that regulates itself through systematic, required training and collegial discipline; that has a base in technical specialized knowledge; and that has a service rather than profit orientation enshrined in its code of ethics.1
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An Open System

In the 17th and 18th centuries, the 13 American colonies essentially adopted the English open medical system,consisting of physicians, surgeons and apothecaries, in which no one group held a monopoly, and licensing served more to define guild distinctions than to keep unlearned persons from practicing. In a word, medicine had remained a largely open field. This situation blended well with the relatively free economy of the British Empire.2 A fee-for-service, profession-directed sliding scale system of remuneration remained in effect in most fields of medicine through the 1960s. Richard Harrison Shryock, in his work Medicine and Society in America 1660-1860, wrote: Dentistry was, in effect, the first full-time specialty in American medical practice; and the fact that it broke off from the medical profession may be ascribed in part to the latters disinclination as late as 1860 to recognize specialization of any sort. During the 1830s some dentists were M.D.s and some medical schools gave a little dental training. But, in the face of wide need for dental care, most medical colleges did little in this field. Hence, the better educated and more ambitious dentists established schools, societies, and journals of their own after 1840 and followed this by organizing a national association even before the advent of the A.M.A.. Dentists, by the very nature of their work, were always in danger of being relegated to the level of technicians. Yet, by 1860, they were acquiring a better status in this country than in Europe, and they represented the first medical field in which Americans attained pre-eminence.3

Free from Government Interference

The organized profession of dentistry in America continued to evolve over the next 80 years as nonprofit, university-based dental schools replaced for-profit diploma mills, and the skill and scientific training of their graduates improved correspondingly. Today, we have grown accustomed to the federal government playing a dominant role in health care. In comparison, one must remember that in the 19th century, the United States was a society where a national board of public health was instituted in 1875, but disbanded in 1882 because public health was not considered a province of the federal government.4 In accordance with our Constitution, it was left to the states to regulate the professions. But it was not until October 1895 that New York State began to license the practice of dentistry. Today, democracy seems pervasive. However, Yales Professor of History and Classics Donald Kagan reminds us,Although in our time democracy is taken for granted,it is in fact one of the rarest,most delicate and fragile flowers in the jungle of human experience.5 At the Constitutional Convention,the founding fathers combined elements of Athenian pure democracy and classical Roman mixed republic. Recognizing the Roman principle of dual citizenship6 and establishing our privilege as a voting citizen of both our state and nation, the founders were careful to always locate sovereignty in the people. Indeed, the roots of the word democracy are from the Greek demos, meaning people and krateein, meaning to rule. Our bicameral legislature, executive and judicial branches of government were instituted to maintain the checks and balances required to modify the passions of the majority and to protect the rights of the minority.
Popular Rule Prevails

No doubt the cost that America paid for this democracy was highwith its vulgarity, its materialism, its rootlessness, its antiintellectualism. But there is no denying the wonder of it and the real earthy benefits it brought to the hitherto neglected and despised masses of common laboring people. The American Revolution created this democracy, and we are living with its consequences still.11 By the Jacksonian Era, in this new egalitarian society, everyones opinion mattered, and the laymens was often valued above that of the expert. James Harvey Young reproduces the thoughts of a doctor in an interesting article titled American Medical Quackery in the Age of the Common Man:12 A New York doctor wrote The people regard it among their vested rights to buy and swallow such physick, as they in their sovereign will and pleasure shall determine; and in this free country, the democracy denounce all restrictions upon quackery as wicked monopolies for the benefit of physicians. legal restrictions on the right to practice medicine could not hold up. Pressure from voters who craved medical democracy jeopardized licensing laws that had been enacted by the various states between 1760 and 1830 By mid-century only three states made any pretense of trying to regulate who should and who should not practice the art of medicine. But countervailing forces were even then working against medical quackeryIn the year of Jacksons election, the New York State Medical Society, in adopting one of the first formal codes of medical ethics in America, expressed its

With the eclipse of the Federalists, any utopian hope that a disinterested, highly qualified natural aristocracy would evolve and be selected by the people to govern faded, as the classical Republican principles of popular rule prevailed. After the national election of 1800, partisan political parties and a plebiscitarian presidency were here to stay.7 Indeed, the American Revolution was only a part of the greater cultural change, as the structured hierarchical world of monarchy and aristocracy dissolved and the Enlightenment pushed the spread of science, liberty, republican government, trade and capitalismin other words, our modern civilization.8 Gordon Woods brilliant Pulitzer Prize-winning work, The Radicalism of the American Revolution, points to the American Revolution as bringing respectability and even dominance to ordinary people. He writes that it changed the culture of Americans and most important, it made the interests and prosperity of ordinary peopletheir pursuits of happinessthe goal of society and government.9 However, it was this dominance of the ordinary citizen that caused to happen in every realm of endeavorwhether art, language, medicine, or politicsconnoisseurs, professors, doctors, and statesmen had to give way before the power of the collective opinion of the people.10 Hence, we have what he termed our middling democracy. Gordon Wood closes his work with these words:
NYSDJ NOVEMBER 2006 19

opposition to the prevailing use of nostrums In New York State, doctorssought to make clear the distinctions in professional conduct between the reputable practitioner and the quack.
Pride and Self Respect

This adolescent America exhibited optimism and pride.As reflected in the poetry of Walt Whitman and the theory of philosopher and educator John Dewey,many citizens of this young democracy shared a Periclian enthusiasm for the potential greatness of their country and its common man. Richard Rorty writes, National pride is to countries what self-respect is to individuals: a necessary condition for self improvement.13 Health care manifested this pride in its forward drive, as the scientific foundation behind it advanced and the utilitarian benefits of effective medical care, on both a community and individual basis, by qualified professionals made a difference. Hobbs argued that society is formed primarily to guarantee the most basic natural right, the individuals right to self-preservation.14 In the last half of the 18th century, the founding fathers were profoundly influenced by Locke and Hobbs and their political theory of modern natural right. Thus, it was not philosophically inconsistent for late-19th-century America to abandon its unregulated health care system and to replace it with the formalized, albeit, less democratic, highly regulated one that has evolved today. The states boards of regents, working in conjunction with their resident professional societies and the strict standards they enforce, insulate health care from direct popular control, and together they are entrusted to protect the public health and the common good. However, our current, formalized health care system still reflects unique characteristics attributable to its more free-wheeling past. American conceptions of government authority and the realities of constituent politics tell us why the United States stands alone (among the worlds industrialized nations) in its failure to enact national health insurance.15 As long as some form of freedom of choice exists via an affordable private health care system,the middle class will likely resist being dictated to by a nationalized one-tier form of public care. As the traditional avenues guaranteeing access to such private care become less accessible, Americans may finally be ready to embrace national health insurance.
A Valued Commodity

democracy.17 The best interest of the patient must always remain the primary goal of the American health care system, and success here should be allowed to secondarily fulfill the best interest of the provider. Maintenance of this equation is basic in order for this sector of our liberal democracy to stand any chance of surviving. Liberal pragmatist Richard Rorty cautions his brethren on the left against forming a politically useless unconscious by adopting ideals which nobody is yet able to imagine being actualized Among these ideals are participatory democracy and the end of capitalism.18 In 1997, Rorty wrote, The public, sensibly, has no interest in getting rid of capitalism until it is offered details about the alternatives.19 Rorty is unimpressed with the prospects of socialism. Nor does he embrace the classical Athenian pure democracys near total avoidance of professionalism.Technocrats, often referred to as professionals, are needed. The economist Paul Krugman views health care as a public responsibility. He points out that health care seems to be heading back to the top of the political agendait turns out that even in America, with its faith in the free market, people dont trust forprofit corporations to make decisions about their health.20 In 2006,it remains to be seen if health professionals can continue to behave in a democracy,if the citizens within the democracy can remain independent and optimistic,and if access to high quality,affordable care can be maintained; only then can the delivery of medical/dental care in the United States conceivably continue in its current form. Can American dentistry cope with its success? The forthcoming public debate on the desirability of overhauling our health care delivery system could well write the next chapter on health care in our society. Democracy and dentistry may never be the same. REFERENCES
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. Starr, P. The Social Transformation of American Medicine. Basic Books. 1982, p. 15. Shryock RH.Medicine in America 1660-1860.New York:New York University Press.1960,p.20. Ibid. pps. 151-152. Oatman EF. Medical Care in the United States. The H.W. Wilson Co. 1978, p. 18. Kagan D.Pericles of Athens and the Birth of Democracy.New York:The Free Press.1991, p.2. Millar F. The Roman Republic in Political Thought. Hanover & London:University Press of New England. 2002, p. 2. Ackerman B. The Failure of the Founding Fathers. Cambridge, MA & London, England: The Belknap Press of Harvard University Press. 2005, p. 5. Wood GS.The Radicalism of the American Revolution.New York:Vintage Books.1991,p.192. Ibid. p. 8. Ibid. p. 364. Ibid. p. 369. Young JH. American medical quackery in the age of the common man. The Mississippi Valley Historical Review 1961;47(4):579-593. Rorty R. Achieving Our Country. Cambridge, MA, & London, England: Harvard University Press. 1998, p. 2. Strauss, L. Natural Right and History. Chicago & London: The University of Chicago Press. 1950, p. 181. Rothman DJ. A Century of Failure: Class Barriers to Reform. In Morone & Belkin, The Politics of Health Care Reform. Durham & London: Duke University Press. 1994, p. 13. ADA Newsletter. Jan. 23, 2006. Zakaria F. The Future of Freedom. New York & London: W.W. Norton & Co. 2003, pps.199-238. Rorty R. Achieving Our Country. Cambridge, MA, & London, England: Harvard University Press. 1998, p. 102. Ibid. p. 104. Krugman P. Medicine: who decides. New York Times Dec. 26 2005.

While access to dental care often remains an individual choice,with an out-of-pocket expense, it demonstrates the publics willingness to pay for what it perceives to be a valued commodity. However, the $81.5billion portion of the gross national budget spent on dentistry pales in comparison to the $1.9 trillion allocated to total health care.16 Indeed, it is this disparity that has relegated medicine to the realm of managed care, with significant impact on our fellow physicians autonomy. Fareed Zakaria points to the development of an illiberal democracy, where an all-consuming desire for profits has allowed traditional professional elites to abdicate their responsibilities, along with the compounded loss of their stabilizing influence within our
20 NYSDJ NOVEMBER 2006

Dental Management of the Gravid Patient

Michael D. Turner, D.D.S., M.D.; Fiza Singh; Robert S. Glickman, D.M.D.
Abstract Gravidity is defined as the development of the young in utero. It initiates hormonal, psychological and physiological changes in the female patient, providing the dentist with many questions about the management of these patients. These physiologic alterations, as well as the embryologic development of the fetus, will be discussed along with the treatment alterations that should be considered. The changes are often subtle, but can lead to disastrous complications if proper precautions are not taken. Conversely, appropriate management of routine and dental emergencies can be denied by the practitioner because of misconceptions about pregnancy and fetal tolerance. Anesthetic and pharmacology of agents used in dentistry in treating the pregnant patient will be reviewed.

as the embryologic development of the fetus, are often subtle, but they can lead to disastrous complications if proper precautions are not taken. Conversely, appropriate management of routine and dental emergencies can be denied by the practitioner because of misconceptions about pregnancy and fetal tolerance. Anesthetic and pharmacology of agents used in dentistry in treating the pregnant patients will be reviewed.While medications are commonly used in dentistry when treating a pregnant patient, careful attention must be given to their effect on maternal and fetal health.
Local Anesthetics

GRAVIDITY IS DEFINED as the development of the young in utero. It initiates hormonal, psychological and physiological changes in the female patient, providing the dentist with many questions about the management of these patients. These physiologic alterations, as well
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Local anesthetics freely cross the placental barrier, so the issue of fetal toxicity must be considered in administering these agents. The majority of amide type agents,that is,lidocaine,mepivicaine,etc.,are bound to serum proteins,specifically,alpha1-acid glycoprotein.In the pregnant patient, there is a decreased concentration of alpha1-acid glycoprotein levels,which results in an increase of the free local anesthetic plasma concentration. Does this increase in the plasma concentration create a potential for toxic reactions, especially in more potent agents like bupivacaine?1 In general, the direct effects of local anesthesia on the neonate seem to be minimal, even at higher doses. The Collaborative Perinatal Project (CPP) was a multicenter, government-funded study that prospectively reviewed 60,000 pregnancies between 1959 and 1965, with the final subjects being

examined at age 8, in 1975. The data was reviewed for a vast amount of potential causes of fetal morbidity and mortality. Data that was reviewed and published in 1971 did not show that the administration of benzocaine, procaine, tetracaine and lidocaine during pregnancy resulted in an increased rate of fetal complications.2,3 Since 1971, there has not been a report of any teratogenic event from the use of any local anesthetic agent. When local anesthesia is administered in dentistry, it is most commonly dispensed with a 1:100,000 epinephrine concentration for vasoconstriction. There has been a tentativeness to use epinephrine with local anesthesia in the pregnant patient.The concern is that the accidental intravascular injection of epinephrine will cause uterine artery vasoconstriction and decreased uterine blood flow. In animal models, the decrease in the uterine blood flow occurs transiently, although the magnitude and duration of this decrease are equivalent to the decrease in uterine blood flow caused by a single uterine contraction.4 However, clinically large doses of vasoconstrictive agents should probably be avoided to preserve placental perfusion.In general, there does not appear to be any significant contraindication to the use of lidocaine and epinephrine in the gravid patient.
Antibiotics

TA B L E 1
FDA Categories for Medication Use in Pregnant Patients Controlled studies in women fail to demonstrate risk to fetus in first trimester, and possibility of fetal harm appears remote. Animal studies do not indicate risk to fetus; there are no controlled human studies, or animal studies do show an adverse effect on fetus, but well controlled studies in pregnant women have failed to demonstrate risk to fetus. Studies have shown drug to have animal teratogenic or embryocidal effects, but no controlled studies are available in women, or no studies are available in either animals or women. Positive evidence of human fetal risk exists, but benefits in certain situations (e.g., life-threatening situations or serious diseases for which safer drugs cannot be used or are ineffective) may make use of drug acceptable despite its risks. Studies in animals or humans have demonstrated fetal abnormalities, or evidence demonstrates fetal risk based on human experience, or both, and risk clearly outweighs any possible benefit.

Blood volume increases in the pregnant patient by approximately 40%. This hypervolemia also protects the mother and fetus from hypoxia and hypovolemia during the birth process. The increase in blood volume increases creatinine clearance, leading to a lower serum concentration of bound antibiotics in the pregnant patient compared to a nonpregnant patient. This may alter the effective dosage of the antibiotic, but this fact has not been studied. Most antibiotics do cross the placenta and, thus, have the potential to affect the fetus. Penicillin, a -lactam-structured cell wall inhibitor, has been used in clinical practice since the 1940s. Of more than 3,500 fetuses studied in the CPP, there was no increase in congenital anomalies or other adverse effects after exposure to penicillin in the first trimester.5 Penicillin remains the antibiotic of choice in treating the gravid patient with an oral infection.Clavulanate is added to penicillin derivatives to broaden their antibacterial spectrum. Of 556 infants exposed in the first trimester, no increased risk of birth defects was observed.6 Cephalosporins are the most commonly prescribed antibiotic in general use today. Although there have been no large studies of the safety of cephalosporin use in pregnancy, there have been no teratogenic effects reported. All cephalosporins, regardless of their generation, have a Food and Drug Administration (FDA) classification B: presumed safe based on animal models. The macrolide family of antibiotics, that is, erythromycin, clindamycin, azithromycin and clarithromycin, cross the placenta only minimally. Erythromycin and clindamycin are used extensively for oral infections in patients with allergies to penicillin or with resistant bacteria. All the macrolides, except clarithromycin, are FDA Class B. Clarithromycin is a Class C medication, which implies

uncertain safety to date. No teratogenic risk of erythromycin has been reported. In 79 patients in the CPP7 and 6972 patients in the Michigan Medicaid data, no increased risk of birth defects was noted.6 In one study of 122 first trimester exposures to clarithromycin (Biaxin), no increased risk of birth defects was noted.8 The use of metronidazole (flagyl) in pregnancy is controversial. The reduced form of the drug is teratogenic, but humans are not capable of reducing metronidazole and so should not be at risk.9 It has not been reported as teratogenic in animal models. Although it has not been associated with adverse fetal effects, it is currently recommended for use in the second and third trimesters only, with an FDA category B rating.9 There are no large epidemiologic studies of the use of flouroquinolones,that is,Ciprofloxacin or Levofloxacin,in pregnancy.These agents have been reported to cause irreversible arthropathy in immature animals, but their safety during pregnancy is not established. Tetracyclines are bacteriostatic antibiotics that reversibly bind the 30S ribosome and inhibit bacterial protein synthesis. They have a very broad spectrum of coverage. Tetracyclines cross the placenta and deposit in fetal teeth and bone, causing yellow-brown discoloration if given after five months gestation.13 Despite earlier reports, tetracycline does not cause enamel hypoplasia and does not inhibit fibula growth in the preterm infant.14 In summary, Tetracycline has an FDA classification of D and should be avoided in pregnant patients to prevent intrinsic staining of the teeth.
Analgesics

Obstetricians have discouraged pregnant women from taking analgesic doses of aspirin and other NSAIDs because of the potential affect on platelet aggregation and the availability of suitable and safe substitutes like acetamenophen.15 Prolonged bleeding time is caused by the inhibition of the production of the prostaglandin thromboxNYSDJ NOVEMBER 2006 23

TABLE 2
Summary of Commonly Used Medications in Oral and Maxillofacial Surgery Practice and their Use in Pregnancy Drug Local anesthetics Lidocaine Mepivicaine Prilocaine Bupivacaine Analgesia Aspirin Acetaminophen Ibuprofen COX-2 inhibitor Codeine FDA Category B C B C C/D B B/C C C Use During Pregnancy Yes Yes Yes No, may cause hypotension No, associated with IUGR Yes Avoid in third trimester; may close PDA Avoid in third trimester; may close PDA Associated with first trimester malformations; can use in second or third trimester Yes Yes Yes Yes Yes Yes Yes No During Breastfeeding Yes Yes Yes Yes No Yes Yes Yes Yes

Oxycodone Morphine Fentanyl Antibiotics Penicillins Erythromycin Clindamycin Cephalosporins Tetracycline Sedatives Hypnotics Benzodiazepines Barbiturates Nitrous oxide

B/C B B B B B B D

Yes Yes Yes Yes Yes Yes Yes No

general, chronic NSAIDS usage should be avoided in the pregnant patient because of the concerns of bleeding and possible, although unlikely, premature closure of the ductus arteriosum. Morphine, meperidine and oxycodone are considered safe analgesic agents for use any time during pregnancy. Codeine, a common postsurgical analgesia, has been associated with decreased fetal body weight resulting from maternal toxic doses in mice and hamster models. It should be noted that codeine did not induce any increase in structural malformations in mice.19 In the CPP, no increased relative risk of malformations was observed in 563 codeine users.7 In general, the use of codeine, and, specifically, oxycodone, should be considered safe to administer to the pregnant patient, although chronic use can precipitate neonatal withdrawal symptoms.20
Hypnotics

D D Not assigned

No, risk for fetal craniofacial anomalies No, risk for fetal craniofacial anomalies Controversial

ane, an important component of platelet aggregation. In a metanalysis done by Kozer, no increase in fetal or neonatal bleeding was found to be significant.16 These fears were largely derived from studies of patients taking large doses of aspirin and extrapolations from other NSAIDS. Inhibition of prostaglandin synthesis by NSAIDs also increases concerns about premature fetal ductus arteriosus constricture,a vital component of the fetal circulatory system that will induce primary pulmonary hypertension and closure. Most of the reported cases of premature ductus arteriosus closure occurred secondary to indomethicin administration for tocolysis, the slowing or halting of labor. Indomethacin, like all NSAIDS, is a reversible inhibitor of cyclooxygenase and blocks the enzymatic conversion of arachidonic acid to prostaglandin G2, a precursor of prostaglandin E2 and F2 alpha.17 Premature ductal closure occurs as a result of the inhibition of the production of prostacyclin and prostaglandin E2, which are necessary for continued ductal patency.18 Ibuprofen, the most widely used NSAID, had no published reports linking its use to congenital defects.Cyclooxygenase (COX)-2 inhibitors (celecoxib and rofecoxib) are classified as category C medications based on animal studies. In
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The use of benzodiazepines, that is, valium or versed, has been associated with an increase in the incidences of cleft palate, central nervous system dysfunction, and dysmorphism after in utero exposure.21 Neurotransmitters regulate palate shelf reorientation during development. GammaNo aminobutyric acid (GABA) acts as an inhibitory neurotransmitter. No One theory is that benzodiazepines, diazepam Controversial specifically, may mimic GABA, thus causing incomplete palatal closure.22 Unfortunately, the data for these studies are not reliable,because of a secondary drug exposure variable in the patient pool. Barbiturates have been found to cause congenital anomalies in animals,but teratogenic human effects have not been reported.23 In general, benzodiazepams and barbiturates should be avoided in the pregnant patient because of the concerns over teratogenic effects.
Inhalational Agents

The use of inhalational agents in the pregnant patient, regardless of the agent used, presents three major issues. The first is fetal oxygenation; the second is avoidance of teratogenic agents; and the third is the prevention of premature labor. Fetal oxygenation is controlled by maintenance of normal maternal PaCO2 and PaO2, uterine vascular resistance and maternal blood pressure.24 Concerns have been expressed because of the possibility of premature closure of the ductus arteriosus secondary to high oxygen saturation. Short-term administration of high levels of oxygen present no risk to the fetus; even with a maternal PaO2 of 600 mm Hg, the fetal PaO2 does not rise above 50 to 60 mm Hg. Thus, there is no risk of retroplacental fibroplasia or premature closure of

TABLE 3 Development Milestones of Fetal Development

the ductus arteriosus in utero secondary to increased maternal oxygen content. The normal state of uterine vasculature is wide dilation, but under certain conditions, a severe constriction can occur. Maternal alkalosis, which can commonly result from hyperventilation, will cause direct vasoconstriction that will reduce placental blood flow. Of the inhalation agents in use today in dentistry, the most common, and potentially the most teratogenic, is nitrous oxide. The potential teratogenic effects of N2O are related to its ability to inactivate methionine synthetase. Methionine synthetase is responsible for the conversion of homocystiene and methyltetrahydrofolate to methionine and tetrahydrofolate. Methionine is an essential amino acid and tetrahydrofolate is needed for the synthesis of DNA.25 In animal studies, a higher level of spontaneous abortion and birth defects was seen with nitrous oxide exposure in Sprague-Dawley rats.26 The effect has not proved to be clinically significant in humans, but it has been suggested that all patients undergoing anesthesia with N2O receive prophylactic doses of folic acid, methionine and vitamin B12. Two studies, following chronic nitrous oxide gas exposure, were reviewed. The first study followed Swedish midwives who were exposed to nitrous oxide. It concluded that night work and high workload increase the risk of spontaneous abortion, not nitrous oxide.27 The second study followed female dental assistants. An elevation in risk of spontaneous abortion was seen among women who worked with nonscavenged nitrous oxide for three or more hours per week.28 The use of nitrous oxide remains controversial, but consideration in its use is thought to be acceptable in the pregnant patient as long as it is less than 50% of the inhalant, with the other part being oxygen. In addition, the patient should be given supplemental vitamins, specifically to replace methionine, as a precaution.29
Management

Month 1

Week 1 2

Development Patient not actually pregnant. Ovary releases egg and is fertilized by sperm, and is termed zygote and is implanted into uterine lining. It consists of spherical mass of cells with central cavity (the blastocyst). Two distinct layers, endoderm and ectoderm and is termed embryo. Three distinct layers with third primary germ layer (mesoderm) differentiation. Initial formation of neural tube, infolding on ectodermal surface (future nervous system). Also initial formation of heart, digestive tract, sensory organs and arm and leg buds. Completion of embryonic period, paired heart tubes have begun to pump and bone starts to replace cartilage. Lateral folding of embryologic plate, followed by growth at cranial and caudal ends and budding of arms and legs. Branchial arches that will form mandible, maxilla, palate, external ear, and other head and neck structures. Lens placodes appear, marking site of future eyes. Three main subdivisions of forebrain, midbrain and hindbrain are apparent. Dorsal and ventral horns of spinal cord have begun to form, along with peripheral motor and sensory nerves. On cellular level, growth of axons and den drites and elaboration of synaptic connections continue at rapid pace, making CNS vulnerable to teratogenic or hypoxic influences throughout gestation. Average embryo weighs 9g and has crown-rump length of 5cm. Several organ systems increase in cell number and size; circulatory, hepatic and urinary systems are operating; and reproductive organs are developed. By third month, is now called fetus, and is approximately 7.5cm long and 14g. Sucking, swallowing and extremities reflexes are developed. Nourishment is supplied by placenta. Tooth buds appear, fingers and toes are well defined. Rate of body growth outpaces cranial growth and fetus is 10cm long. Movement apparent to palpation. Soft downy lanugo covers body, and hair begins to grow on head, brows and eyelashes. Inner ear bones have calcified and auditory input can be detected by fetus. Fetuss skin is thin and shiny with no underlying fat, finger and toe prints visible. Eyelids begin to part and eyes are variably open. Weight is 800g and length is 35cm. Fat deposition begins and retinal development is complete. Fetus is very reactive to stimuli from light and sound and is able to suck thumb, hiccup and cry. Placental function begins to diminish. Fetal length is 30cm and weight is 1.36kg. Significant acceleration in growth Most systems are well developed, although lungs are typically immature. Fetal length is 45cm and 2.25kg Lungs are fully mature, weight triples and length doubles as body stores protein, fat, iron, and calcium.
NYSDJ NOVEMBER 2006 25

3 4

Treatment of the female patient should always include a comprehensive review of the patients medical and surgical history. If the patients pregnancy is not confirmed, treatment, unless emergent, should be deferred until a definitive documentation of the patients status is obtained, usually by the patients primary care physician. Minor procedures should follow basic guidelines. The supine position should be avoided in late pregnancy to avoid the development of the supine hypotensive syndrome, in which a spine position causes a decrease in cardiac output, resulting in hypotension, syncope and decreased placental perfusion. In addition, the supine position may cause a decrease in arterial oxygen tension (PaO2) and increase the incidence of dyspepsia, a nondescript, nonspecific sensation from gastoresophageal reflux secondary to an incompetent lower esophageal sphincter. Finally, the supine position poses an increased risk of developing deep vein thrombosis (DVT) by compression of the inferior vena cava, leading to venous stasis and clot formation. The ideal position of the gravid patient in the dental chair is

the left lateral decubitus position, with the right buttock and hip versus open reduction with internal fixation is complex. Open elevated 15 degrees. reduction allows for the quick restoration of adequate nutrition and Dental radiographs should also be kept to a minimum,with approfunction. If maxillomandibular fixation is necessary, parenteral priate patient shielding and collimation.Animal and human studies nutrition supplementation is recommended. The mucosa of the have shown that greater than 10 cGy total exposure to radiation,or more oropharynx is also friable and easily susceptible to edema; therethan 5 cGy during the first trimester, is associated with intrauterine fore, the airway must be closely monitored for obstruction and subgrowth retardation and congenital fetal abnormalities.A full-mouth sequent intubation. radiographic examination exposes .27cGy,33 so the If endotracheal intubation is not feasible, acceptable maximum amount of periapical X-rays It is important to remember tracheotomy may be considered. Fetal monitoring must also be followed to ensure uterousing these numbers could theoretically be 50 to placental perfusion and fetal well-being. 100 in number, based upon the trimester of the that treatment is being Maxillofacial infections in the pregnant patient.Thus,minimal and necessary use of dental rendered to two patients: patient should be addressed immediately. The radiographs is recommended during pregnancy. gravid patient is more susceptible to infection Hujoel, in 2004, did find an association mother and fetus. for a variety of reasons. Mild infections should between low-term birth weights and dental be managed via incision/drainage under local radiography.34 The modern panoramic radianesthetic with appropriate antibiotic coverage. It is essential to ograph typically has a 0.1 cGy exposure,with appropriate lead shieldaggressively treat the gravid patient to minimize the risk of infecing. Older machines can give higher doses but only to the head and tion spreading. neck region. The American College of Obstetric and Gynecology recFascial space infection should be handled in a standard fashommends that pregnant women be counseled that diagnostic radiion: airway assessment, imaging (computed tomography scan), ographs of less than 5 rads have not been associated with an increase and to the operating room for adequate incision and drainage. in fetal anomalies or pregnancy loss.35 One rad equals one cGy. Postoperatively, if the patient is unable to maintain oral intake, If maxillofacial trauma occurs in the gravid patient, head and parenteral nutritional support must be instituted. Until the results neck computed tomography scans or plain films are acceptable of the culture/sensitivity are returned, empirical antibiotic theragiven the minimal radiation exposure (with a lead shield) to rule py is appropriate. out facial fractures. The question of maxillomandibular fixation

26 NYSDJ NOVEMBER 2006

More severe infections should be managed in the operating room under general anesthesia with intravenous antibiotics and incision and drainage.Other issues with the gravid patient who is hospitalized for an extended period of time include avoiding bladder catheterization to minimize the risk of urinary tract infections and the use of subcutaneous heparin for deep vein thrombosis prophylaxis. It is important to remember that treatment is being rendered to two patients:mother and fetus.The American College of Obstetricians recommends obstetric consult prior to any treatment.36 If there is uncertainty about the diagnosis of pregnancy, all treatment (unless emergent) should be postponed unless a definitive determination of pregnancy can be obtained. Patients may be unsure of their pregnancy status. In a study of 12- to 21-year-old females in a day surgery visit, 1 in 200 tested pregnant after universal screening.37 With these findings, it is best to avoid drugs and therapy that would put a fetus at risk in all women of child-bearing age for whom a negative pregnancy test has not been ensured.
Conclusion

Many fallacies exist regarding the management of the gravid patient. It is incumbent upon the health care provider to accurately assess each patient, provide optimal care and never defer appropriate treatment unless factually supported. REFERENCES
1. Denson DD, Coyie DE, Thompson GA. Bupivicaine protein binding in the term parturient: effect of lactic acidosis. Clin Pharmacol Ther 1984;35:702. 2. Caplan B, Montgomery LA.Results of vision screening at seven years in the Johns Hopkins Collaborative Perinatal Project. Johns Hopkins Medical Journal 1971;128(5):261-4. 3. Yellich GM. Perioperative considerations in the pregnant patient. Oral Maxillofac Surg Clin North Am 1992;4:651. 4. Hood DD, Dewan DM, James FM III. Maternal and fetal effects of epinephrine in gravid ewes. Anesthesiology 1986;64:585. 5. Weinstein AJ, Gibbs RS, Gallagher M. Placental transfer of clindamycin and gentamicin in term pregnancy. Obstet Gynecol 1976;124:688. 6. Briggs GG, Freeman RK, Yaffe SJ. Drugs in Pregnancy and Lactation. 6th Ed. Baltimore: Williams & Wilkins. 2002:284. 7. Heinonen PO, Slone D, Shapiro S. Birth Defects and Drugs in Pregnancy. Littleton: Publishing Sciences Group. 1977:296-313. 8. Einarson A, Phillips E, Mawji F. A prospective controlled multicentre study of clarithromycin in pregnancy. Am J Perinatol 1998;15:523-525. 9. Dashe JS,Gilstrap LC.Antibiotic use in pregnancy.Obstet Gynecol Clin North Am 1997;24:617. 10. Reyes MP, Ostrea EM, Cabinian AE. Vancomycin during pregnancy: does it cause hearing loss or nephrotoxicity in the infant? Am J Obstet Gynecol 1989;161:977. 11. Niebyl J. Antibiotics and other anti-infective agents in pregnancy and lactation. Amer J Perinatol 2003; 20:405-414. 12. Baskin CG, Law S, Wenger NK. Sulfadiazine rheumatic fever prophylaxis during pregnancy: does it increase the risk of kernicterus in the newborn? Cardiology 1980;65:222. 13. Kline AH, Blattner RJ, Lunin M. Transplacental effects of tetracyclines on teeth. JAMA 1964;188:178. 14. Porter PJ, Sweeney EA, Golan H. Controlled study of the effect of prenatal tetracyline on primary dentition. Proceedings of the 5th Interscience Conference on Antimicrobial Agents and Chemotherapy, Washington, DC, 1965;668. 15. Schoenfeld A, Bar Y, Merlob P. NSAIDS: Maternal and fetal considerations. Am J Reprod Immunol 1992;28:141. 16. Kozer E, Costei A M, Boskovic R, Nulman I, Nikfar S, Koren G. Effects of aspirin consumption during pregnancy on pregnancy outcomes: meta-analysis. Birth Defects Research Part B, Developmental and Reproductive Toxicology 2003;68(1):70-84. 17. Niebyl JR, Blake DA, White RD, Kumor KM, Dubin NH, Robinson JC. The inhibition of premature labor with indomethacin. Am J Obstet Gynecol 1980;136:1014-9. 18. Moise K. Effect of advancing gestational age on the frequency of fetal ductal constriction in association with maternal indomethacin use. Am J Obstet Gynecol 1993;168:1350-3. 19. Williams J, Price CJ, Sleet RB. Codeine: developmental toxicity in hamsters and mice. Fundam App Toxicol 1991;16:401.

20. Khan K, Chang J. Neonatal abstinence syndrome due to codeine. Arch Dis Child Fetal Neonatal Ed 1997;76:F59-F60. 21. Laegreid L, Olegard R, Wahlstrom J. Abnormalities in children exposed to benzodiazepines in utero. Lancet 1987;1:108. 22. Zimmerman EF,Venkatasubramanian K, Wee EL. Role of neurotransmitters and teratogens on palate development. Progr Clin Biol Res 1985;163C:404. 23. James FM.Anesthesia for nonobstetric surgery during pregnancy.Clin Obstet Gynecol 1987;30:621. 24. Hawkins, J. Anesthesia for the pregnant patient undergoing nonobstetric surgery. In: Schwartz, ed. American Society of Anesthesiologist 2005;33:137-144. 25. Nunn JF, Chanarin I. Nitrous oxide inactivates methionine synthetase. In: Eger EI II, ed. Nitrous Oxide 1985. 26. Mazze RI, Fujinaga M, Badin JM. Halothane prevents nitrous oxide teratogenicity in Sprague-Dawley rats; folinic acid does not. Teratology 1988. 38:121-7. 27. Axelson G, Ahlborg G, Bodin L. Shift work, nitrous oxide exposure, and spontaneous abortion among Swedish midwives. Occup Environ Med 1996;53:374. 28. Rowland AS, Baird DD, Shore DL. Nitrous oxide and spontaneous abortion in female dental assistants. Am J Epidemiol 1995;141:531. 29. Christensen B.Preoperative methionine loading enhances restoration of the cobalamin-dependent enzyme methionine synthase after nitrous oxide anesthesia,Anesthesiology 1994;80:1046-1056. 30. Shnider SM, Webster GM. Maternal and fetal hazards of surgery during pregnancy. Am J Obstet Gynecol 1965;92:891. 31. Brodsky JB, Cohen EM, Brown BW. Surgery during pregnancy and fetal outcome. Am J Obstet Gynecol 1980;138:1165. 32. Pederson,H,Finster M.Anesthetic risk in the pregnant surgical patient.Anesthesiology 1979;51:439. 33. Anonymous. US Department of Health and Human Services, Public Health Service, Food and Drug Administration. Nationwide Evaluation of X-ray Trends (NEXT). Washington, DC: US Dept of Health and Human Services; 1993. 34. Hujoel P, Bollen A, Noonan C, del Aguila M. Antepartum Dental Radiography and Infant Low Birth Weight. JAMA 2004;291:19871993. 35. ACOG Committee on Obstetric Practice. Guidelines for Diagnostic Imaging During Pregnancy. Obstet Gynocol 2004; 104:647-651. 36. ACOG Committee on Obstetric Practice. Non-obstetric surgery in pregnancy. Obstet Gynocol 2003; 102: 431. 37. Pierren N, Moy L, Redd S. Evaluation of a pregnancy testing protocol in adolescents undergoing surgery. J Pediatr Adolesc Gynecol 1998;11:139.

NYSDJ NOVEMBER 2006 27

ECTODERMAL DYSPLASIA
A Seven-Year Case Report
Janet Gruber, R.D.H., M.S.; Glen Kreitzberg, D.D.S.
Abstract This case report describes the manifestations of ectodermal dysplasia and tracks the seven-year management of a male ED patient. It demonstrates the benefits of early intervention, describes restorative and orthodontic treatment rendered, and a range of future treatment options available when early intervention is employed.

ECTODERMAL DYSPLASIA (ED) is defined as a genetic disorder in which two or more ectodermal structures are abnormal in development. This congenital birth defect affects the ectoderm, which is one of the three germinal cell layers that form the early embryo. The structures most commonly affected include teeth, skin, hair, nails, sweat glands, parts of the eye and ear, adrenal tissue, facial structures and nerve tissue. Specifically, poor or absent sweat and sebaceous gland formation, poor or absent hair, teeth and nail formation, and deficient lacrimal, pharyngeal, conjunctive and salivary gland formation may be evident with varying degrees of severity.1,2 Kidney and bladder involvement might also be a mani28 NYSDJ NOVEMBER 2006

festation of this disorder.3-5 Altered genes may be inherited from a parent, or normal genes may become mutated. The inherited version can be autosomal dominant, autosomal recessive or xlinked, the most common being the latter. Although this genetic disorder is considered relatively rare, occurring once in every 10,000 to 100,000 births,6 dental professionals need to be aware of the clinical manifestations, as often the initial diagnosis is made when expected tooth formation, both primary and permanent, fails to occur or occurs abnormally. Appropriate interventions, instituted at an early age, will help to maintain a healthy oral cavity and allow the patient to develop socially, physically and emotionally.
Craniofacial and Oral Manifestations

The craniofacial manifestations of ED are numerous and may include ears that are obliquely set and prominent; mid-face depression, with the lower third appearing small because of a lack of alveolar bone development; protuberant lips resulting from reduced vertical dimension;7 small head height; high set orbits; frontal bossing, pointed chin; high, broad cheek bones;8 narrow, short maxillary width and palatal

depth dimension; small and retrusive malar and maxillary regions; and clefting of the lip and/or palate.9 Other reported conditions include deficiencies of lacrimal and salivary glands, atrophic rhinitis, and hypoplasia of the oral, pharyngeal and tracheobronchial glands, which make the patient susceptible to bronchitis and pneumonia in addition to hoarseness and dysphonia (loss of voice).10 Of the approximate 150 variations of ED, 111 present with oral manifestations. The oral manifestations include an abnormality in the number, shape, calcification of enamel, eruption patterns, alveolar ridge height and width and salivary secretions.11 Common tooth abnormalities observed include conical crown forms in the anterior dentition and microdonts and/or taurodonts in the posterior sextants, with globe-shaped crowns that lack normal occlusal morphology. The microdonts and conical shaped crowns are a result of hypoplastic enamel that rids the teeth of their usual bulky enamel contours.2,12 The most frequent oral characteristic of ED is hypodontia or anodontia,due to a suppression of dental ectoderm. Approximately 25% of ectodermal dysplasia children present with anodontia and 75% with hypodontia.11 In cases of hypodontia, affected enamel may be hypoplastic, hypocalci-

fied or hypomature since the enamel is the part of the tooth derived from ectoderm. More than one type of enamel dysplasia may be evident in an individual.12 Delayed eruption, abnormal eruption patterns, tooth positions and malocclusions, generally Class III in nature, with maxillary retrusion and mandibular protrusion, are also common in ED syndromes. Because of the absence of teeth, a decreased alveolar ridge volume, especially in length, resulting in a loss of vertical dimension, has been well documented in several studies presented in the literature.11,12 The various oral manifestations may affect speech, mastication and swallowing, all of which will have an impact on the physical, social and emotional well-being of the patient.
Case Report

Figure 1. Panoramic film exposed at 5 1/2 years of age revealing 11 permanent tooth buds, hypocalcification of enamel and microdontia.

Figure 2. Patient profile and dentition photographed at 6 years of age, prior to intervention.

Restorative Treatment A 4-year-old male presented for dental treatment in our general dentistry office in May of 1998.His mother,a dental hygienist,was aware of his ED diagnosis.Upon initial examination, we noted a healthy young man exhibiting several characteristics of ED. He had fine blond hair, somewhat dry lips and eyes, 20 conicalshaped deciduous teeth, microdontic in size, and amelogenesis imperfecta. A panoramic film showed the buds of 11 permanent teeth, once again, hypocalcified, microdonts and conically shaped (Figure 1).His medical history revealed kidney and bladder abnormalities present upon birth, as well as right-hand syndactly of the first and second digits and third and fourth digits.Our initial examination went well, as the patient was extremely cooperative. He was placed in our recall system for continued treatment and observation. At age 6, we noted the need for dental sealants.Teeth 19,30,L,K,S and T were treated. The visit was uneventful. Upon clinical examination, we noted a disparity in the growth and development of the dental arches, as the patient exhibited a Class III occlusion (Figures 2,3). We began considering techniques to enhance maxillary growth to reestablish the proper alveolar relationship and encourage alveolar growth,to provide for support of the face and allow for bone to sup-

Figure 3. Cephalometric radiograph exposed at 6 years of age, prior to intervention.

Figure 4. Removable headgear worn 14 hours a day.

port his teeth.We also contemplated implants in the future. The patient was referred to an orthodontist for additional treatment. When the patient reached age 7, we again sealed appropriate teeth, this time, employing a flowable composite in the areas of the teeth that appeared most vulnerable. Prior radiographs revealed that many of the deciduous teeth had unusually long roots, which, perhaps, would be sufficient to provide future abutments for restorative procedures. At this time, our patient began the early stages of his orthodontic treatment. Orthodontic Treatment The patient first presented for an orthodontic evaluation on May 11, 2000, at 6 years of age, with an anterior crossbite, severe Class III malocclusion, maxillary retrusion, and deficient maxillary and mandibular alveolar height. Our goal was to enhance alveolar growth and development and establish a Class I occlusion, while preserving the dentition as best we could. Early orthodontic treatment was our method of choice, as it has been clearly established that bone follows teeth. Given our very cooperative patient, combined with very cooperative

parents, we were ready to begin. Treatment was initiated on February 2, 2001,with the insertion of a palatal expander and the cementation of protraction headgear. Headgear was worn approximately 14 hours a day, and on June 19, 2001, a 2 mm overjet was noted (Figures 4-7). Six weeks later, the patient presented with a 3 mm to 4 mm overjet, which was maintained until the removal of the appliance in September 2001 (Figure 8). Upon removal of the appliance, retainers were rendered, and, despite conscientious home care throughout the treatment, areas of severe decalcification were noted. The young patient returned to our office for restorative procedures. We employed a combination of flowable and filled resins to restore the decalcified areas and to restore wear patterns on the occlusal surfaces during treatment. In addition, we built the occlusal surfaces up to continue to gain vertical dimension (Figure 9). In January 2002, after restorative procedures were completed, new retainers with springs were fitted to labialize the front teeth. A reevaluation in September 2002, at 8 years of age, revealed that protraction headNYSDJ NOVEMBER 2006 29

Figure 5. Patient with headgear engaged.

Figure 6. Patient with headgear engaged.

Figure 7. Patient with headgear engaged.

Figure 8. Cephalometric radiograph exposed at 7 3/4 years of age.

Figure 9. Panoramic radiograph exposed at 8 years of age.

Figure 10. Panoramic exposed at approximately 10 years of age.

gear was again required because of rapid growth of the mandible and a current edgeto-edge anterior bite relationship. The enamel hypoplasia present on the deciduous teeth, as well as on the few erupted permanent teeth, along with the patients history of severe decalcification, prevented the use of a cemented appliance.As a result,a non-traditional hard trutain material was used to fabricate a removable protraction appliance. Because of the morphology of the teeth, we needed to add retention for our appliance. The patient was referred to the general dentist for the bonding of composite retention additions to the buccal surfaces of the maxillary posterior teeth to aid in retention of the removable protraction appliance. In November, the appliance was inserted; it was to be worn 14 hours a day with elastics totaling 400 grams of pressure per side. The removable appliance proved successful. In February, the patient returned with a 2 mm overjet. Interestingly, occasional negative sequelae to extensive tooth movement are often fenestrations and/or dehiscence on the buccal surfaces as a
30 NYSDJ NOVEMBER 2006

result of treatment. We did not experience this in the maxilla. However, severe gingival recession on the facial of deciduous n was noted. We had not advanced the mandible at all. The dehiscence was possibly due to a mouthguard, worn at night to prevent attrition. The mouthguard was reduced in thickness and height to relieve possible irritation in that area. A referral was made to a periodontist for a surgical procedure to create as healthy an environment as possible, as current radiographs revealed a permanent dentition microdont in torso version, apical to n. We wanted to establish a healthy environment for the eventual eruption of the adult toothbud. In May 2003, a successful periodontal pedicle graft surgery was performed buccal to n to increase the band of attached gingiva. Again, the combination of a cooperative patient, along with cooperative parents, were key to our success. In January 2004, at 10 years of age, the patient was reduced to 10 hours of headgear wear a day for maintenance of the acquired 4 mm overjet (Figure 10,11). Denture adhe-

sive was being used to aid in retention. The appliance was remade in June 2004 for retention purposes. As of June 2005, 4 mm of overjet is being maintained with 400 grams of pressure applied approximately eight to nine hours a day, with denture adhesive being used for retention. At 11 years of age, our patient exhibits a well formed maxillary/mandibular relationship. He looks good from front and in profile, and his occlusion is virtually a Class I relationship. He is maintaining his overjet of 4 mm, does not appear to be in danger of regression and functions well (Figures 12-17). Future Treatment We now have in effect a Class I relationship in this young man, with enough tooth buds present between his deciduous and succedaneous teeth to aid us in our quest to preserve his alveolus. He is afforded treatment options. Consultation with a pediatric prosthodontist provided the treatment plan, which consisted of continuing to build up occlusals with composite to maintain vertical dimen-

Figure 11. Cephalometric radiograph exposed at 10 years of age.

Figure 12. Patient at 11 years of age.

Figure 13. Patient profile at 11 years of age.

Figure 14. Patient occlusion at 11 years of age.

Figure 15. Patient occlusion at 11 years of age.

Figure 16. Patient occlusion at 11 years of age.

sion, with the possibility of eventual removable overdentures. This is the most common treatment rendered for this type of situation.It appears,though,that because of early intervention, there may be more options for us. Because of his currently successful Class I relationship and functionally adequate dentition, we would like to preserve his teeth as long as possible. This will help us maintain bone quality and volume, clearing the way for possible dental implants in the future, if needed. We plan to continue to keep the vertical dimension established through occlusal restorations and build ups, either directly or with indirect onlay type restorations. In addition, we will maintain esthetics and function in the anterior region by employing direct composite veneers, or, possibly, porcelain veneers. These teeth may be splinted for strength after our young man has stopped growing. Home care and regular treatment will be critical to success. If implants are ever needed, we hope that our treatment has preserved alveolus, though we always could employ the many

grafting techniques that are available to us. In addition, distraction ontogenesis has a clearly defined successful track record and could be employed in this instance to regain completely new, natural bone growth. This would give us the bone needed for successful implant restoration. Dentistry marches on, and who knows what will be available to us in the future for this fine young man? It is an exciting thought. REFERENCES
1. National Foundation for Ectodermal Dysplasias Scientific Advisory Board.A Family Guide to Ectodermal Dysplasias. Mascoutah,IL: NFED; 2003. 2. Ibsen O,Phelan J.Oral Pathology for the Dental Hygienist. 2nd Ed. Philadelphia: W.B. Saunders Co.; 1996. 3. London R, Heredia RM, Israel J. Urinary tract involvement in EEC Syndrome. AJDC. 1985;139:1191-1193. 4. Mass S, de Jong T, Buss P, Hennekam RCM. EEC syndrome and genitourinary anomalies: An update. American J of Medical Genetics. 1996;63:472-478. 5. Nardi AC, et al. Urinary tract involvement in EEC syndrome: A clinical study in 25 Brazilian patients. American J of Medical Genetics. 1992;44:803-806. 6. Abadi,B,Herren,C.Clinical treatment of ectodermal dysplasia: A case report. Quintessence Int. 2001;32:743-5. 7. Vasan N. Management of ectodermal dysplasia in childrenan overview. Annals of Royal Australasian College of Dental Surgeons. 2000;15:218-222.

Figure 17. Patient occlusion at 11 years of age.

8. Bixler D, Saksena SS, Ward RE. Characterization of the face in hypohidrotic analysis. Birth Defects. 1988; 24:197-203. 9. Saksena SS, Bixler D. Facial morphometrics in the identification of gene carriers of x-linked hypohidrotic ectodermal dysplasia. American J. Med. Genetics. 1990;35:105-14. 10. Itthagarun A, King NM. Ectodermal dysplasia: A review and case report. Quintessence Int. 1997;28:595-602. 11. Ruhin B, et al.Pure ectodermal dysplasia: Retrospective study of 16 cases and literature review. Cleft Palate Craniofacial Journal. 2001;58:504-518. 12. National Foundation for Ectodermal Dysplasias Scientific Advisory Board. Parameters of Oral Health Care for Individuals Affected by Ectodermal Dysplasia Syndromes. Mascoutah, IL: NFED; 2003

NYSDJ NOVEMBER 2006 31

Conventional Root Canal Therapy of C-Shaped Mandibular Second Molar

A CA S E R E P O RT
Evan A. Lynn, D.D.S.
Abstract The C-shaped root canal system and treatment implications were first described by Cooke and Cox in 1979.1 C-shaped canals are most frequently found in mandibular second molars, but they can occur in any mandibular molar, and they have been reported in maxillary molars as well.2 C-shaped mandibular molars are characterized by a C-shaped groove that connects one or more root canals. This groove can occur anywhere along the root canal system, making it difficult to diagnose and treat. A C-shaped root canal system may appear completely normal at the level of the pulp chamber but can begin to manifest itself in the middle or apical one-third.1,3 Furthermore, C-shaped canals are challenging if not impossible to predict radiographically.1 C-shaped canals in mandibular second molars are found most frequently in the Chinese population, with reports showing up to a 31.5% incidence, 4 as compared to an approximate 7% incidence in the general population.1 This case report demonstrates an incidence of a Cshaped canal that was unable to be detected radiographically and which contained three separate root canals that communicated in the apical one-third of the root canal sys32 NYSDJ NOVEMBER 2006

tem. Canal orifices were located approximately 2 mm below the level of the CEJ, which is in agreement with a recent micro-computed tomography study of C-shaped mandibular molars that found 98% of all C-shaped molars studied had orifices located 1 mm to 3 mm below the CEJ.3 The CT study also found that all C-shaped canals contained fused roots and confirmed previous findings that the C-shape configuration varies greatly throughout the length of the canal.

A 26-YEAR-OLD FEMALE presented complaining of lingering pain to cold associated with tooth #18. The patient had been referred by her restorative dentist for root canal therapy on the tooth.A temporary filling material had been placed in the tooth after caries excavation by the general dentist. The patient reported no significant medical history. An intraoral exam confirmed the presence of an IRM temporary restoration in the occlusal of tooth #18. A cold test conducted with ethyl chloride yielded a prolonged and exaggerated response from the tooth. A periapical digital radiograph (Figure 1) revealed the presence of a restorative material in the coronal aspect of the pulp chamber. The periapical area appeared normal. The periodontal ligament space appeared normal radiographically. Tooth #18 had percussion sensitivity, but there was no pain to palpation in the mucobuccal fold. Adjacent and opposing teeth responded within normal limits to vitality and percussion tests. The tooth was diagnosed as having an irreversible pulpitis. Conventional root canal therapy was recommended.

Informed consent was obtained for endodontic therapy on tooth #18. We administered 3.6 mg of lidocaine with 1:100,000 parts of epinephrine as an inferior alveolar nerve block and a supplemental long buccal infiltration. Ten minutes later, the tooth was again tested with ethyl chloride to confirm anesthesia. Rubber dam isolation was obtained. Access of the pulp chamber on tooth #18 was initiated using a sterile, tapered diamond bur in a high-speed handpiece. Extensive bleeding was noted upon pulpal access, confirming the diagnosis of an irreversible pulpitis. Coronal pulp chamber tissue was excised with a #8 latch angle bur, followed by irrigation with 5.25% sodium hypochlorite; hemostasis was obtained. The distal canal orifice was identified 2 mm below the CEJ and was found to have a C-shaped configuration extending from the distolingual aspect of tooth #18 toward the mesiobuccal. A separate mesiolingual and mesiobuccal orifice was located (Figure 2). Multiple radiographs were taken with K-files in the separate canals. They confirmed the joining of the three canals upon apical exit, as is commonly found in a C-shaped canal configuration.1,2 The working lengths of all three canals were found to be identical, as indicated by an apex locator and radiographs. Preparation of the distal canal required rotary instrumentation to a final taper of .08 mm in a crown-down fashion. The mesiobuccal and mesiolingual canals were instrumented with a .06 tapered rotary file to the point where the three canals joined (2.5 mm short of the working length). The final 2.5 mm of the mesial canals were instrumented with conventional K-files. Each mesial canal was opened to a 50K file at the apex and stepped back to a 70K file to the point where the three canals join. Copious irrigation using sodium hypochlorite was used to facilitate tissue dissolution and removal. Following complete instrumentation, the canals were dried. A final one-minute rinse with 18% EDTA, followed by sodium hypochlorite, was conducted to remove the smear layer. The canals were dried and obturated using the warm vertical condensation technique as first described by Dr. Herbert Schilder in 1967.5 A final periapical radiograph was taken perpendicular to tooth #18 (Figure 3). It revealed complete obturation of the three communicating canals.A second radiograph taken from a mesial angulation (Figure 4) revealed the C-shape of the distal canal in the coronal and middle one-third. The patient was referred back to her restorative dentist with instructions to use the mesial canals if a post was required because of the unusual C-shaped configuration of the distal canal. The restorative dentist opted to restore tooth #18 with a bonded resin restoration. The patient was recalled for a six-month follow-up. She reported that she was completely asymptomatic. A periapical radiograph taken from an extreme distal angulation (Figure 5) revealed the buccal-lingual complexity of the C-shaped distal canal.

Figure 1. Pre-op.

Figure 2. C-shaped distal.

Figure 3. Straight final.

NYSDJ NOVEMBER 2006 33

Discussion

Figure 4. Mesial angle.

This case represents common characteristics of many C-shaped canals: Radiographic detection of the C-shaped canal was not possible; three separate canals were represented by three separate orifices found 2 mm below the level of the CEJ; the three canals communicated in the apical one-third of the root canal system; and excessive hemorrhage was noted upon instrumentation of the distal canal. The practitioner should keep these findings in mind when treating any second mandibular molar, as these findings are common among C-shaped teeth.1,3 Magnification and illumination can help identify these hard-todetect C-shaped canal configurations. Greater canal enlargement, along with copious irrigation with sodium hypochlorite, can facilitate complete tissue removal. Warm vertical obturation will allow GuttaPercha to flow into the difficult-to-reach anatomical variants. Mesial roots (if present) may be considered for post placement because of the difficulty in preparing a C-shaped canal to receive a round post. As with any tooth requiring root canal therapy, access is still the key. If the practitioner has straight line visual access of all the orifices, complete debridement and obturation can be accomplished. REFERENCES
1. Cooke HG, Cox FL. C-shaped canal configuration in mandibular molars. J Am Dent Assoc 1979:99:836-9. 2. Sidow SJ, West LA, Liewehr FR, Loushine RJ. Root canal morphology of human maxillary and mandibular molars. J Endod 2000;26:675-8. 3. Fan B, Cheung G, et al. C-shaped canal system in mandibular second molars: Part IAnatomic features. J Endod 2004:30:899-902. 4. Yang ZP,Yang SF, Lin YL. C-shaped root canals in mandibular second molars in Chinese population. Endod Dent Traumatol 1988;4:160-3. 5. Schilder H. Filling root canals in three dimension. Dent Clin North Amer 1967;723-44.

Figure 5. Six-month follow-up.

34 NYSDJ NOVEMBER 2006

Diagnosing Bulimia Nervosa with Parotid Swelling

C A S E R E PORT
Mimi J.Y. Park, D.D.S.; Louis Mandel, D.D.S.
Abstract Patients with bulimia nervosa (BN) may show dental erosion, resulting from the effect of acid regurgitation. Asymptomatic bilateral parotid swellings may also be present. Other signs include serum electrolyte imbalance and Russells sign. The authors describe the case of a 26-year-old woman with BN, whose only clinical manifestation of BN was her bilateral parotid swellings. Because patients with BN tend to be secretive about their purging, it is important that the clinician consider BN as part of a differential diagnosis when faced with such painless parotid gland swellings.

BULIMIA NERVOSA (BN) is an eating disorder that usually affects young females and involves approximately l% to 4% of the general female population,1 with an incidence of 5% to 10% in female college students.2 The peak age of onset is 18 years, while the female-to-male ratio ranges from 10:1 to 20:1.1 Several factors play an important role in the development of BN and include genetics,3 physiology,1,4,5 psychologic considerations and societal pressure. Psychologically, patients with BN have a perception that a certain range of weight and eating habit is necessary to gain approval from others. Rigid self-control is fundamental to ones self-worth and is manifested in a BN patient as an obsessive regulation of body weight. The BN patient is usually extremely sensitive to perceived criticism, rejection and blame, and has a diminished selfesteem.6 In todays culture, where there is a very narrow range in the standard of physical attractiveness, societys attitude also is a significant factor.7
36 NYSDJ NOVEMBER 2006

BN is characterized by recurrent cycles of binge eating. Individuals may consume an average of 3,500 calories per sitting and as much as 50,000 calories in a 24-hour period.8 A compensatory forced purging follows in an effort to rid the body of the excessive caloric intake. Purging behavior usually involves self-induced vomiting, but patients also abuse laxatives and use diuretics.1 Bulimics may induce vomiting twice a week or as many as 140 times a week8,9 and often have another eating disorder, anorexia nervosa (AN). BN patients are characterized by a body weight, normal to slightly above normal, that is maintained by a constant cycle of bingeing and purging. AN patients are characterized by a weight that is less than 85% of the normal value, brought about by a significant and prolonged restriction of caloric intake.1 When assessing a BN patient, it is important to perform a thorough examination. In the early stages of bulimia, the eyes may have tiny conjunctival hemorrhages, caused by the increased intrathoracic pressure associated with vomiting.10 Frequent vomiting can also lead to gastroesophageal reflux disease.1 Furthermore, the repeated contact of incisors to the dorsum of the hand during selfinduced vomiting results in skin abrasions, lacerations and calluses, known as Russells sign11 (Figure 1). The oral manifestations of BN can include bilateral parotid gland swellings,with reports of such occurrences in 10% to 66% of patients.12-15 The swellings, which are infrequently present in the submandibular glands, are diffuse, soft and asymptomatic in nature. They tend to vary in size in direct proportion to the frequency of the emetic episodes. Typically, the patient is extremely concerned about the cosmetic deformity caused by the swellings. The swellings result from hypertrophy of the gland, which may be initiated by the constant cholinergic stimulus associated with emesis serving to activate the salivary glands16 or, alternatively, from increased zymogen retention.13,17 Dental enamel erosion, particularly of the lingual surfaces, is the classic sign of BN and results from constant exposure of

Figure 1. Callused knuckles (arrows) in BN patient.

Figure 2. Extensive erosions noted on palatal surfaces of maxillary teeth.

enamel to the erosive effect of the regurgitated gastric acids18,19 (Figure 2). Exposed dentinal tubules lead to increased sensitivity and caries. Patients who participate in prolonged and frequent emetic episodes may develop a Bartter-like syndrome (BS), characterized by a serum electrolyte pattern demonstrating a triad of hypokalemia, hypochloremia and a metabolic alkalosis. A significant increase in morbidity related to the electrolyte imbalance can result in electrocardiographic changes.20, 21 Furthermore, dehydration from fluid loss may develop from vomiting, diarrhea caused by laxatives or increased urination from diuretic use.
Case Report

A 26-year-old female patient was referred to the Salivary Gland Center of Columbia University College of Dental Medicine with bilateral parotid swellings that had been present for four months (Figure 3). The patient had no pain and said there was no fluctuation in gland size in relation to meals. Since the initial onset of the swellings, there has been no significant glandular enlargement. The patient was in excellent health and was taking no medications. Upon palpation, the bilateral parotid swellings were found to be soft and non-tender. Intraorally, no signs of enamel erosion were evident. The oral hygiene was excellent. The mucous membrane was moist, and normal amounts of clear saliva were visible exiting from the parotid ducts orifices when the glands were aggressively milked. An examination of the hands revealed no calluses or lacerations. Upon questioning, the patient admitted to vomiting four to six times a day for the past 18 months. A CT scan with contrast clearly showed enlargement and increased density of both parotid glands (Figure 4). In addition, both glands were enhanced by an increased presence of vascular structures containing contrast.

Figure 3. Clinical view of BN patient with bilateral parotid gland swelling (arrows) most noticeable on patients right side.

Figure 4. CT scan (axial view) with enlarged and enhanced parotid glands (arrows). NYSDJ NOVEMBER 2006 37

Discussion

Although the exact mechanism has not been determined, it is thought that multiple emetic episodes cause an autonomic neuropathy.13,17,22,23 The sympathetic nerve supply to the secreting acinar cell is related to the production and secretion of zymogen, the precursor of amylase. With sympathetic nerve dysfunction, there is an increase in zymogen storage in the cell from an increase in production, decreased zymogen secretion or a combination of both. A cellular hypertrophy from cellular engorgement by zymogen results and causes clinical enlargement of the parotid gland. Substantiation was derived from the CT scan of the parotid glands, which demonstrated glandular enlargement and increased density (Figure 2). Normally, parotid glands appear lucent on a CT scan due to high fat content. In our patients case, the normally present intraparotid fat was replaced with acinar hypertrophy, which caused the increased density. Although electrolyte studies were not performed, the finding of abnormally low or low normal serum electrolyte levels has been observed in BN patients with parotid swellings.24 These serum electrolyte abnormalities can serve as an important adjunct in the diagnosis of BN by offering an objective test.24 BN patients often deny participating in bulimic practices when confronted. Two supportive signs of BN, dental erosion and Russells sign, point to a diagnosis of BN (Figures 1,2). Typically, persistent vomiting produces a very characteristic pattern of erosion, referred

to as perimylolysis.25 Enamel loss is first noted on the lingual surfaces of the maxillary central and lateral incisors, the surfaces directly in the path of the gastric acid contained in vomitus. Dental erosion in the bulimic patient usually becomes obvious within three years, but not all patients develop such erosions.26 Rinsing with water or a bicarbonate mixture that neutralizes the acidic environment that follows each emetic episode, and the regular use of fluorides will reduce or prevent dental erosion. Russells sign may also be absent because, while vomiting is commonly induced by the use of a finger to stimulate the pharynx, other narrow objects such as a toothbrush have been used. Some patients become so proficient at inducing vomiting that they do not need an external stimulus. They can vomit simply by contracting the abdominal muscles.27
Treatment

Although parotidectomy has been performed on bulimic patients for cosmetic reasons,28 no treatment is the most reasonable option. Cessation of emesis with the gradual return of normal body electrolyte levels has resulted in a reduction of the swellings.17,18,22,23 In a minority of cases, swellings persist for long periods of time and may not resolve.29 Treatment of eating disorders often involves a multidisciplinary team of medical, dental, nutritional and mental health specialists.30 The patient should also have access to individual, group, family and behavioral therapeutic approaches. Early identification of BN by the dental clinician demands prompt referral to medical

38 NYSDJ NOVEMBER 2006

and psychiatric therapists. The risk of further metabolic damage to the body from abnormal levels of serum electrolytes will be reduced and the need for hospitalization avoided.
Conclusion

Bilateral asymptomatic parotid enlargement, in conjunction with dental erosion, Russells sign, and serum electrolyte imbalance can be used as tools for the diagnosis of BN. Early detection can prevent further deterioration and the onset of serious medical complications. REFERENCES
1. Mehler P. Bulimia nervosa. N Engl J Med 2003;349:875-81. 2. Nevos S. Bulimic symptoms: prevalence and ethnic differences among college women. Int J Eat Disord 1985;4:151-68. 3. Bulik CM, Devlin B, Bacanu SA, et al. Significant linkage on chromosome 10p in families with bulimia nervosa. Am J Hum Genet 2003;72:200-7. 4. Monteleone P, Martiadis V, Colurcio B, Maj M. Leptin secretion is related to chronicity and severity of the illness in bulimia nervosa. Psychosom Med 2002;64:874-9. 5. Bruce KR, Steiger H, Koerner NM, Israel M, Young SN. Bulimia nervosa with co-morbid avoidant personality disorder: behavioral characteristics and serotonergic function. Psychol Med 2004;34:113-24. 6. Gongora VC, Derkson J.I, Van der Staak CP. Role of core beliefs in the specific cognition of bulimic patients. J Nerv Ment Dis 2004;192:297-303. 7. Orbanic S. Understanding bulimia: signs, symptoms, and the human experience. Am J Nurs 2001;101:35-42. 8. Humphries LL. Bulimia: diagnosis and treatment. Compr Ther 1987;13:12-15. 9. Casper R. The pathophysiology of anorexia nervosa and bulimia nervosa. Annu Rev Nutr 1986;6:299-316. 10. Siddiqui A, Ramsay B, Leonard J. The cutaneous signs of eating disorders. Acta Derm Venereal 1994;74:68-9. 11. Daluiski A, Rahbar B, Meals R. Russells sign: subtle hand changes in patients with bulimia nervosa. Clin Orthop 1997;343:107-9. 12. Mitchell JE, Seim HC, Colon E, Pomeroy C. Medical complications and medical management of bulimia. Ann Intern Med 1987;107:71-7. 13. Vavrina J, Muller W, Gebbers JO. Enlargement of salivary glands in bulimia. J Laryngol Otol 1994;108:516-8. 14. Riad M, Barton JR,Wilson TA, Freeman CPL, Marais AGD. Parotid salivary secretory pattern in bulimia nervosa. Acta Otolaryngol 1991;11:392-5. 15. Kinzl J, Biebl W, Herold M. Significance of vomiting for hyperamylaselmia and sialadenosis in patients with eating disorders. Int J Eat Disord 1993;13:117-24. 16. Mandel L, Kaynar A. Bulimia and parotid swelling: a review and case report. J Oral Maxillofac Surg 1992;50:1122-5. 17. Mandel L, Arai S. Diagnosing bulimia nervosa with parotid gland swelling. J Am Dent Assoc 2004;135:613-6. 18. Valena V, Young WG. Dental erosion pattern from intrinsic acid regurgitation and vomiting. Aust Dent J 2002;47:106-15. 19. Little JW. Eating disorders: dental Implication. Oral Surg Oral Med Oral Pathol Oral Radio Endod. 2002;93:138-43. 20. Edwards KI. Obesity, anorexia, and bulimia. Med Clin North Am 1993;77:899-909. 21. Sharp CW, Freeman CPL. The medical complications of anorexia nervosa. Br J Psychiatry 1993;162:452-62. 22. Mandel L, Hamele-Bena D. Alcoholic parotid sialadenosis. J Am Dent Assoc 1997;21:95-8. 23. Coleman H, Altini M, Nayler S, Richards A. Sialadenosis: a presenting sign in bulimia. Head Neck 1998;20:758-62. 24. Mandel L. Serum electrolytes in bulimic patient with parotid swellings. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003; 96:414-9. 25. Hurst PS, Lacey JH, Crisp AW. Teeth, vomiting and diet: a study of the dental characteristics of seventeen anorexia nervosa patients. Postgrad Med J 1977;53:298-305. 26. Scheutzel P. Etiology of dental erosionintrinsic factors. Eur J Oral Sci 1996;104: 178190. 27. McGilley BM, Pryor TL. Assessment and treatment of bulimia nervosa. Am Fam Physician 1998;57:2743-50. 28. Wilson T, Price T. Revisiting a controversial surgical technique in the treatment of bulimic parotid hypertrophy. Am J Otolaryngol 2003;24:85-8. 29. Brotman AW, Rigotti N, Herzog DR. Medical complication of eating disorders: outpatient evaluation and management. Compr Psychiatry 1985;26:258-72. 30. Rosenblum J, Forman S. Evidence-based treatment of eating disorders. Curr Opin Pediatr 2002;14:379-83.
NYSDJ NOVEMBER 2006 39

Cavernous Hemangioma of the Palate

A REVIEW OF ETIOLOGY, PATHOGENESIS AND TREATMENT OPTIONS
Michael R. Markiewicz, B.S.; Joseph E. Margarone III, D.D.S.; Alfredo Aguirre, D.D.S., M.S.; Lakshmannan Suresh, B.D.S., M.S., F.D.S.R.C.P.S.
Abstract Cavernous hemangiomas of the palate are a rare but not infrequent sighting in the oral and maxillofacial region. The etiology and pathogenesis of these lesions are not definitively understood and are currently being explored. Treatment options usually include, but are not limited to, surgical excision of the lesion. Alternative management paradigms should be considered when dealing with this type of lesion. Precaution should be taken before any surgical intervention.

buccal mucosa and the lateral borders of the tongue, but can occur at any oropharyngeal location. Palatal hemangiomas are uncommon, with an occurrence of less than 3%.5-8 When observed in the dental patient, multiple treatment paradigms can be employed. Microscopically, oral hemangiomas can be classified as capillary or cavernous, based on the size of the vascular spaces.9 Cavernous hemangiomas of the palate are rare, with only a few cases reported in the English literature.10,11 The purpose of this article is to report an additional case of cavernous hemangioma of the palate, to review the etiology and pathogenesis of hemangiomas, and to discuss the possible alternatives to surgery when managing hemangiomas in the oral and maxillofacial region.
Case report

HEMANGIOMAS ARE AMONG the most common tumors of infancy. They are characterized by rapid endothelial proliferation of the blood vessel.1,2 More than 60% of cases of hemangiomas are found in the head and neck region. Hemangiomas of the oral cavity are common and represent 14% of all hemangiomas occurring in the head and neck region.3 Oral hemangiomas are usually diagnosed between the second and fourth decades of life, in comparison to hemangiomas of the head and neck, which are usually diagnosed in the first and second decades. Based on epidemiological studies, there is a male predilection of 2:1. Oral hemangiomas appear clinically as small, well-circumscribed, red-blue swellings, and are usually painless.4 They often arise from frequently traumatized mucosal sites, such as the lip, the
40 NYSDJ NOVEMBER 2006

A 58-year-old white female was referred by her dentist for evaluation of a lesion in the palate. The patient was not aware of the lesion. Past medical and surgical history was non-contributory. On examination, a raised, purple-blue colored lesion was noted at the midline of the palate, approximating the junction of the hard and soft palate (Figure 1). The lesion measured 0.5 cm x 0.5 cm. It was non-tender and firm on palpation and did not readily blanch upon compression.A panoramic radiograph was taken and revealed no abnormalities. The clinical impression was that of a hemangioma. Excisional biopsy of the lesion was carried out under local anesthesia (2% lidocaine with 1:100,000 epinephrine vasoconstrictor). The palatal bone was noted to be intact during the procedure.

Figure 1. Cavernous hemangioma on soft/hard palate junction.

Figure 2. Low-power view shows presence of large vascular spaces in lamina propria between overlying epithelium and subjacent mucous minor salivary glands. (Hematoxylin-eosin stain; original magnification x 20)

Microscopic examination of the specimen submitted revealed numerous large cavernous spaces lined by endothelial cells and intraluminal red blood cells (Figures 2,3).A diagnosis of cavernous hemangioma was rendered. The surgical site healed without any complications, and there was no recurrence on six-month follow up (Figure 4).
Discussion

Hemangiomas are somewhat common, benign tumors of the oral cavity that are found in 5.5 of every 1000 American adults. The labial mucosa is the most common site for oral mucosal hemangioma (63%), followed by the buccal mucosa and the lateral border of the tongue, with a prevalence of 14% each, respectively. Palatal hemangiomas are uncommon, with fewer than 3% of the cases occurring in this site. Most of the reported cases of palatal hemangioma are of the capillary type. Cavernous hemangiomas of the palate are seen but are rare. The etiopathogenesis of hemangiomas is unclear, although recently, tissue-specific markers were found to be uniquely coexpressed by hemangiomas and placental microvessels. These findings imply a unique relationship between hemangioma and the placenta and suggest new hypotheses concerning the origin of these tumors.13,14 A number of growth factors, including vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), transforming growth factor beta (TGF- ), and interleukin 6 (IL-6) have been demonstrated as regulators of angiogenesis.15 These factors are found in higher concentrations and play a role in proliferative hemangiomas.16 More conclusive research is needed to access the exact role of these growth factors in the pathogenesis of these lesions. Oral hemangiomas clinically appear as circumscribed, painless, blue-red colored swellings, which may blanch upon compression.17 There is usually no bruit or thrill. Histologically, hemangiomas have been classified as capillary and cavernous types

Figure 3. High-power view of large vascular spaces shows endothelial lining and scanty smooth muscle wall. (Hematoxylin-eosin stain; original magnification x 200)

Figure 4. Surgical site six months post-operation.

NYSDJ NOVEMBER 2006 41

depending upon the size of the vascular spaces. These vascular spaces are lined by endothelial cells and lack muscular support. Numerous treatment modalities have been used in the management of hemangiomas of the oral cavity. However, the management of oral hemangiomas usually depends on the size, location and behavior of the lesion and the age of the patient.18 Most hemangiomas are managed conservatively and require no intervention. Conservative management consists of periodic visits and photographic documentation with routine follow up. Only 10% to 20% require intervention because of size, anatomic location and patient-oriented issues.19 High doses of steroids have become a mainstay in the treatment of proliferating hemangiomas, with 30% of patients showing a dramatic response when they are used.20,21 Interferon has also been used in the treatment of hemangiomas and has been documented in many reports to be an effective treatment modality22,23 However, there is some concern about the toxicity of interferon , especially in children. Surgery offers the best chance of cure, but, often, because of the extent of these benign lesions, significant sacrifice of tissue is necessary. As a result, multiple adjunctive procedures have been introduced to eradicate the disease,leaving less of a functional impairment. These adjunctive procedures have also been used to reduce both the blood loss and the morbidity of surgical procedures. Kane and colleagues have developed an excellent management algorithm for treatment of hemangiomas. At initial presentation, a

history and physical examination are performed. An MRI is obtained to determine the extent of the lesion, for extensive spread may not be evident on clinical examination. In the presence of bruits, or pulsatility, an angiography is a useful adjunct study. A determination of the degree of proliferative activity of the lesion must precede a therapeutic assesment. For proliferating lesions, periodic observations or systemic steroid administration represent viable treatment options. For hemangiomas that are not proliferating and are actually exhibiting signs of involution, simple observation is the best management. If the involution is incomplete and arrested, then the lesion can be managed by sclerotherapy, laser therapy or cryotherapy. But these treatment options are rarely used and are usually not the primary modality of management. REFERENCES
1. Metry D. Update on hemangiomas of infancy. Curr Opin Pediatr 2004;16:373-7. 2. Gampper TJ, Morgan RF. Vascular anomalies: hemangiomas. Plast Reconstr Surg. 2002; 110:572-85. 3. Bouquot JE, Gundlach KK. Oral exophytic lesions in 23,616 white Americans over 35 years of age. Oral Surg Oral Med Oral Pathol 1986;62:284-91. 4. Gnepp DR: Diagnostic Surgical Pathology of the Head and Neck. Philadelphia, PA:WB Saunders. 2000. 5. Bajaj MS, Nainiwal SK, Pushker N, Balasubramanya R. Multifocal cavernous hemangioma: a rare presentation. Orbit 2003;22:155-9. 6. Sato M, Tanaka N, Sato T, Amagasa T. Oral and maxillofacial tumours in children: a review. Br J Oral Maxillofac Surg. 1997;35:92-5. 7. Lale AM, Jani P, Coleman N, Ellis PD. A palatal haemangioma in a child. J Laryngol Otol 1998;112:677-8. 8. Ratageri VH, Rajshankar S. Palatal hemangioma with cleft zero. Indian Pediatr 2002;39:693-4. 9. Neville BW. Oral and Maxillofacial Pathology, 2nd Edition. New York, NY: Elsevier. 2002. 10. Minervini F, Rankow RM. Cavernous hemangioma of the soft palate. NYS J Med 1957;57:3686-8. 11. Kiratli H, Bozkurt B, Mocan C. Peripapillary staphyloma associated with orofacial capillary hemangioma. Ophthalmic Genet. 2001;22:249-53. 12. Acikgoz A, Sakallioglu U, Ozdamar S, Uysal A. Rare benign tumours of oral cavitycapillary haemangioma of palatal mucosa: a case report. Int J Paediatr Dent. 2000;10:161-5. 13. North PE, Waner M, Mizeracki A, Mrak RE, Nicholas R, Kincannon J, et al. A unique microvascular phenotype shared by juvenile hemangiomas and human placenta. Arch Dermatol 2001;137:559-70. 14. Folkman J, Klagsbrun M. Angiogenic factors. Science 1987; 235: 442-7. 15. Chang J, Most D, Bresnick S, Mehrara B, Steinbrech DS, Reinisch J, Longaker MT, Turk AE. Proliferative hemangiomas: analysis of cytokine gene expression and angiogenesis. Plast Reconstr Surg. 1999;103:1-9. 16. Regezi JA, Sciubba JJ, Jordan RCK. Oral Pathology: Clinical Pathologic Correlations. 4th Ed. Philadelphia: W.B. Saunders. 2000. 17. Kane WJ, Morris S, Jackson IT, Woods JE. Significant hemangiomas and vascular malformations of the head and neck: clinical management and treatment outcomes. Ann Plast Surg. 1995;35:133-43. 18. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg 1982; 69: 412-22. 19. Fost NC, Esterly NB. Successful treatment of juvenile hemangiomas with prednisone. J Pediatr 1968;72:351-7. 20. Sasaki GH, Pang CY, Wittliff JL. Pathogenesis and treatment of infant skin strawberry hemangiomas: clinical and in vitro studies of hormonal effects. Plast Reconstr Surg 1984;73: 359-70. 21. Greinwald JH Jr, Burke DK, Bonthius DJ, et al. An update on the treatment of hemangiomas in children with interferon alfa-2a. Arch Otolaryngol Head Neck Surg 1999;125:21-7. 22. Blei F, Isakoff M, Deb G. The response of parotid hemangiomas to the use of systemic interferon alfa-2a or corticosteroids. Arch Otolaryngol Head Neck Surg 1997;123:841-4.

42 NYSDJ NOVEMBER 2006

THE LUMEN TECHNIQUE

Retrieval of Broken Gold Screws in Dental Implants
Scott A. Fauvell, D.D.S.; Gaetano Gialanella, D.D.S.; Kevin J. Penna, D.D.S.
Abstract A technique for removing a broken abutment screw from internally threaded endosseous implants and salvaging the endosseous implant is presented. The technique involves the use of inexpensive instruments found in dental offices.
Figure 1. Eminent Italian dentist, Bartolomeo Ruspini, who practiced in London. Family portrait was made when Ruspini was about 40 years old. Figure 1. Retention screw fractured below head of implant.

AT THE NASSAU UNIVERSITY MEDICAL CENTER, fracturing of gold implant retention screws occurred on two separate occasions.The fractures occurred directly beneath the screw heads while tightening custom abutments during the bisque bake try-in visit (Figure 1). A number of techniques were attempted before using what we termed theLumen Technique. On both occasions, this technique was successful in retrieving the remaining portion of the screw and, therefore, avoiding condemnation of the implant to a traditional post, core and crown. The most common reason for screw fractures is undetected loosening. This may be due to bruxism, unfavorable superstructure, overloading or malfunction.1,2,3 Screw fractures may also occur as a result of prosthetic failure, which is inevitable when patients do not follow the established recall schedule. Upon detection of a loose screw, the underlying cause should be determined before any action is taken. Simply retightening the retention screw may alter its metallic properties through cyclic fatigue, also resulting in fracture. When the first screw fracture occurred, we tried three previously established methods for retrieval. First, we attempted wedging an explorer or spreader between the implant and retention screw to counterturn the screw. Ultrasonic was then attempted, also without success. We then turned to what we deemed a risky option, creating a hex in the remaining portion using a small round carbide bur, hoping to retrieve it with a unigrip driver. This too was unsuccessful. Reluctant to condemn the implant to traditional fixed prosthodontics, we began searching for our own solution. We came across disposable applicator tips for the aerosol indicator marking spray, Occlude (Pascal Co. Inc., Bellevue, WA), in our dental lab. By seating the applicator tip with apical pressure in the implant fixture, we wedged it between the implant and the screw surface.We then counterturned and successfully retrieved the retention screw (Figure 2). Its small

Figure 2. Retrieved fractured retention screw delivered on applicator tip.

lumen and rigidity provided the necessary means to deliver the portion of the screw that remained in the implant. The second time this screw fracture occurred, we went straight to the Lumen Technique and the fractured screw was again delivered immediately. Even considering the varying implant widths and different implant companies, most retention screws are approximately the same width. However, if you encounter a wider retention screw, spinning an 11 blade within the applicator tip will open its lumen to accommodate the size difference. When comparing the multiple methods available for retrieving fractured abutment screws, we feel that our technique has a few advantages. The applicator tips are accessible, as many general practitioners use Occlude spray. It is safe, as it preserves the internal machined surface of the implant.When comparing it with other commercial screw retrieval kits, it proves to be very inexpensive. While we have only been able to test this method on a limited number of cases, we feel that it is a useful technique to add to a dentists repertoire when addressing a fractured screw. REFERENCES
1. Nergiz I, Schmage P, Shahin R. Removal of a fractured implant abutment screw: a clinical report. J Prosthet Dent 2004;91(6): 513-7. 2. Williamson RT, Robinson FG. Retrieval technique for fractured implant screws. J Prosthet Dent 2001;86(5):549-50. 3. Weiss EI, Kozak D, Gross MD. Effect of repeated closures on opening torque values in seven abutment-implant systems. J Prosthet Dent 2000;84:194-9.
NYSDJ NOVEMBER 2006 43

JACOB HEMET
DENTIST TO ROYALTY AND ENTREPRENEUR EXTRAORDINAIRE
Malvin E. Ring, D.D.S., M.L.S.
Abstract One of the most prominent dentists in late-18th century London was Jacob Hemet, member of a long family of dentists. He was appointed royal dentist to Queen Charlotte, wife of George the Third, and to Georges favorite daughter, Amelia, and the Prince of Wales. He advertised widely, both in this country and in several European countries, including his native France. However, what makes him noteworthy is the fact that he was the very first person to patent a dentifrice and the first to use marketing techniques similar to those used by the foremost toothpaste manufacturers of today.

IN THE LATE 18TH CENTURY, England began to rival France as a center of advances in dentistry.Although the first book on dentistry in English was published in York in 1685 by Charles Allen, it was not on a par with what was produced a century later. By the latter part of the 18th century, an attempt was made to more or less follow scientific principles, as far as they were then understood. Thomas Berdmore, court dentist to George III, made a significant contribution with the publication in 1768 of his comprehensive text, A Treatise on the Disorders and Deformities of the Teeth and Gums.1
44 NYSDJ NOVEMBER 2006

At about the same time, one of the most advanced and influential dentists, Bartolomeo Ruspini, Italian-trained and practicing in London, brought out his Treatise on the Teeth.2 Ruspini had a substantial influence on the younger dentists who followed him. One of his preceptoral students was R. C. Skinner, who immigrated to the United States and authored the first book on dentistry in America. Ruspini himself came to America a number of times, practicing in New York City, but each time returned to England (Figure 1). An important figure in English dentistry during the last quarter of the 18th century was Jacob Hemet, but very little has been written about him.Where Berdmore was dentist to King George the Third, Hemet was appointed dentist to his Queen as well as to the Prince of Wales and the Princess Amelia, King Georges favorite daughter (Figure 2).Although he advertised that he practiced dentistry in all its branches, he was obviously much more interested in being an entrepreneur, manufacturer and salesman of dentifrice. This in itself would not make him different from the many others who were practicing dentistry in England in the 1780s and 1790s. What set him apart was the fact that he was the first to patent his dentifrices and to travel throughout Europe and even to America to publicizeand sellhis product.
Dire Circumstances

What makes Dr. Hemets story even more interesting is the fact that he cultivated the nobility and concentrated on serving only the

Figure 1. Eminent Italian dentist, Bartolomeo Ruspini, who practiced in London. Family portrait was made when Ruspini was about 40 years old.

Figure 2. Portrait of King George the Third, painted around 1760.

wealthiest; he repeatedly addressed his advertisements to the gentry. This was at a time when economic conditions in England were so bad that the disparity between rich and poor was enormous. The beginning of industrialization allowed for the cultivation of great wealth; however, the wealth could only be obtained by relatively few at the expense of a majority that became poor. In King George IIIs reign, over three million acres were appropriated, and this shattered the simple economic structure of English village life. Small farms were swallowed up by bigger farms to improve productivity. But a series of poor harvests crippled the poor, and the continuous wars, with France and the American colonies, put a tremendous strain on living conditions. Rickets and scurvy were rampant, and among the remedies for loosened teeth were scurvy grass or gittings to put in the chilrens ale. The poor could avail themselves only of that dentistry that was practiced by blacksmiths, hairdressers, corn-doctors and innumerable charlatans.3 The contrast between the life led by the poorer classes and that led by the rich was immense...a few families owned huge tracts of the countryside, some of them amounting to hundreds of thousands of acres...Such estates supported their proprietors in great luxury, and provided them with the very best that [England] had to offer.4 London, however, was different. It was crammed with the poor, most of whom had been dispossessed from their land when they could no longer meet their mortgage payments. This came about because the Industrial Revolution and the widespread use of machines reduced the need for human labor. Included in this huge

number of struggling poor were a relatively few, whose wealth was equal to that of all the rest combined. It was to this small minority of the upper class that Hemet made his appeals5 (Figure 3).
A Family of Dentists

The Huguenots were Protestants who were severely persecuted, and often murdered, by the reigning Catholic monarchs of 17th-century France. Many of them fled to England, and Jacob Hemets ancestors, who apparently had some experience and clinical training in dentistry, were among them. Moreover, some Huguenots who had been skilled artisans in France, such as goldsmiths, watchmakers and jewelers, decided that their manual dexterity qualified them to be prosthodontists of a sort; and ligaturing some ivory teeth to the teeth on either side of a gap didnt demand any real clinical knowledge. The first of the Hemet family to arrive in England was Peter Hemet Sr. (1670-1747). He had been born in Caen, France, and he arrived in London in 1687. He was licensed to practice as a surgeon in 1702 and was soon appointed Operator for the Teeth to Queen Anne. He was obviously a very successful dentist, because when he died, in 1747, he left the enormous fortune of 20,000. He had two sons, one of whom was Peter Hemet Jr. (1696-1754), who inherited his fathers dental practice as well as his royal appointment, and was also named dentist to the Prince of Wales and King George II. The other son, Francis Hemet, of whom little is known, was the father of Jacob Hemet, the subject of this paper, whose year of birth is given as either 1727 or 1729.6
NYSDJ NOVEMBER 2006 45

Figure 3. Typical street scene in an affluent part of London in late 1700s, at about the time Dr. Hemet was practicing there.

Accumulation of such wealth through dentistry is not hard to understand when we consider the fees charged by those who catered to the upper classes. The flamboyant dentist Martin van Butchell, anxious to attract only the very wealthy, publicized that his fees were among the very highest in London. He charged 5 for a single artificial tooth, 42 for a full lower denture and 63 for a full upper. And he insisted that all fees were to be paid in advance7 (Figure 4). It was apparently obvious from Jacob Hemets zeal for marketing that he had a greater predilection for business than patient care, since Londons Town and Country Magazine in 1777 had this to say about him:

He was designed for a mercantile life, but not being very fond of plodding at the counting-house desk, and having a lucky name for drawing of teeth, upon the demise of some of his relations who bore it, and had gained reputation as dentists, he turned operator, as it were, in spite of his teeth. He dropt the pen, and took up the pelican, which soon screwed him into chariot. In an advertisement he ran in August 1790, Hemet claimed that he had been in active practice for more than 40 years. This would mean that he most likely began practice in the late 1740s, his first office being on Great Portland Street.When his appointment as dentist to Queen Charlotte was announced in June 1776, his office was on Little Tichfield Street, near Oxford Market. When he was about 61 years old, he took on an apothecarysurgeon, Thomas Scarman, as a partner, but soon thereafter retired from the active pursuit of dentistry and moved to Hastings, in Sussex. Unfortunately, his retirement was very short, for he died of a stroke on August 22, 1790, at the age of either 61 or 63, and was buried in St. Clement Danes.8
Life as an Entrepreneur

Advertising by dentists was commonplace from dentistrys earliest days in Europe and in America. The earliest advertisements in this country were by two brothers-in-law in New York City. One, James Reading, styled himself a tooth drawer, but whose true trade is not known. The other was James Mills, who stated he was a wig maker as well as a tooth drawer. Their ads appeared as early as January 1735.9 Jacob Hemet,much like the modern purveyor of consumer goods, advertised widely in areas where he never practiced,and placed his ads

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in numerous media. In 1768, his advertisement appeared in the London Chronicle. In 1769, it was displayed in a New York newspaper, and in 1770, in the Philadelphia Pennsylvania Journal. In some cities, primarily in Massachusetts, he apparently practiced for short periods, as noted in his ads in Boston newspapers of 1772 and 1773.10 In contrast to advertisements by his contemporaries, which stressed the fact that they filled teeth, extracted them if necessary, and constructed full or partial dentures, Hemets ads were devoted exclusively to singing the praises of his dentifrices. These dentifrices, he claimed, were the answer to all the problems pertaining to the teeth and the gingiva. The promotion of mouthwashes and dentifrices was found in ads of other dentists of the time. The eminent Italian-turnedBritish dentist, Bartolomeo Ruspini, in an advertisement in Ariss Birmingham Gazette of January 22, 1787, stated that his dentifrice was sold in tin containers, which carried on their lids his coat of arms, and further, that each purchaser would receive a copy of his booklet Treatise on the Teeth.11 But Hemet was unusual in that he was the first to patent his creations. On January 22, 1773, he received Patent Number 1031 for his two cleansers: Essence of Pearl and Pearl Dentifrice. This small extract from his patent application gives some idea of the materials he used for his concoctions: To form the essence of pearl the following substances are used: amber, alcohol, benzoin, native mineral alkali, the odorous particles of the flowers of oranges and roses extracted by watery infusion, an essential and vegetable salt, vitrifiable earth and orrice root, the fruit of the aromatic aracus. These different ingredients are digested, and that which comes over on distillation is the essence of pearl. The pearl dentifrice is made by thoroughly incorporating together the insoluble particles which remain after making the essence, adding to them the aromatic substances mentioned above. In 1998, the Tate Gallery in London held an exhibition of the drawings of the renowned British artist J.M.W. Turner,Turner and the Scientists. One of the drawings is that of a dentists office and laboratory, and pictured is a still, most likely the kind that Dr. Hemet used to distill his Essence of Pearl dentifrice.12 A quote from one of Hemets advertisements of 1790 perfectly captures his claims: But as some Persons may not yet be acquainted with their peculiar Properties, he begs Leave to mention that the Essence of Pearl and Pearl dentifrice are greatly superior both in Elegance and Efficacy to any Thing hitherto made use of, that they will effectually preserve the Teeth in a perfect sound State even to old Age, will render them white and beautiful, without in the least impairing the Enamel, fasten such as are loose, keep such as are already decayed from becoming worse, prevent the Toothache, perfectly cure the Scurvy in the Gums, and make them grow fast and close to the Teeth, they likewise render the Breath delicately sweet, and remedy almost all those Disorders, that are the Consequence of scorbutic Gums and bad Teeth. In a later portion of the ad he recommends his dentifrices to those who have the Care of Children, assuring them that they were perfectly safe for even the tenderest teeth, yet will prevent a premature decay of the first teeth and will prevent those swelled Faces

Figure 4. London dentist who catered to upper classes treating fashionably and luxuriously dressed patient.

and violent Pains which Children are so much subject to in the shedding of them. Then he promised that use of his material would insure that the second teeth erupt in perfect fashion and last for the remainder of the persons life. Great claims, indeed!13 His dentifrices were sold by perfumers and apothecaries in many of the major cities of Europe, as well as in England. Jacob Hemet, as a producer and distributor of dentifrice, was far ahead of his time. One can consider him the ancestor of the modern toothpaste companies, who also rely on mass advertising, blanketing nations with the claims of their products. REFERENCES
1. Berdmore T. A Treatise on the Disorders and Deformities of the Teeth and Gums. London, privately printed, 1768. 2. Ruspini B. A Treatise on the Teeth, Their Structure and Various Diseases. 8th Edition. London: Rivington et al. 1797. 3. Harvey W. Some Dental and Social Conditions of 1690-1852 connected with St. Brides Church, Fleet Street, London. Medical History 1968;12(1). 4. Hart R.English Life in the Nineteenth Century.New York:G.P.Putnams Sons.1971;page 18. 5. Green D R. From Artisans to Paupers: Economic Change and Poverty in London 17901870. Aldershot, England: Scholar Press. 1995. 6. Dobson J. The Royal Dentists. Annals of the Royal College of Surgeons of England. 1970;46:192. 7. Menzies Campbell J.From a Trade to a Profession.Edinburgh,privately printed.1958:167. 8. Hargreaves AS. White as Whales Bones: Dental Services in Early Modern England. Leeds: Northern Universities Press. 1998. 9. Asbell MB. Dentistry: A Historical Perspective. Bryn Mawr, PA: Dorrance & Co. 1988:87. 10. Weinberger BW.An Introduction to the History of Dentistry in America.C.V.Mosby.1948:32. 11. Menzies Campbell J. Dentistry Then and Now. Edinburgh, privately printed. 1981:63. 12. Bishop M, Gelbier S, King J.Science and technology in Turners Georgian dentists rooms. British Dental Journal 2005;198:299-305. 13. Advertisement, The London Packet or New Lloyds Evening Post No. 456, September 23, 1772, page 4, column 4.
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VIEWPOINT

Dental Urban Myths

Should We Worry?
Jeffrey Galler, D.D.S.

I HAVE ALWAYS believed that the overwhelming majority of dentists are extremely competent and knowledgeable.Until recently. Last month, four incidents occurred that shook my confidence in some of my colleagues.And now I wonder if all dentists are as well informed as they should be.
Bone-crushing Misinformation

I could not believe it. The infomercial appeared in a local community newsletter. It was written by a dental colleague who is a good friend and an excellent clinician. I re-read his Is Fosamax Destroying Jaw Bones? article two times just to make sure I was not mistaken. In the article, the dentist raises concerns about Fosamax and other oral bisphosphonates, such as Actonel and Boniva, severely damaging the jaw. He relates the story of a woman in Los Angeles who never suspected that the pills she took to strengthen her bones could severely damage her jawand who required three oral surgeries to remove all the dead bone.
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The author explains that when a person has a tooth removed, there is normally dead and dying bone that is removed by osteoclastic activity so that new bone can be subsequently laid down. Because Fosamax blocks the osteoclasts, the possible end result is that the dead or dying bone cannot be removed by the body. The author cautions that these bisphosphonate drugs should be considered far more cautiously by younger women and that the drugs effects are cumulative. He goes on to report that since 2001 there have been 2,400 cases of serious jaw bone damage due to patients taking Fosamax and other bone-building medications like it. Why is this article a problem? Nowhere in the article does the author explain that bisphosphonate-associated osteonecrosis is an extremely rare condition. Nor does the author report that almost all of these rare osteonecrosis reports have occurred in cancer patients receiving bisphosphonate therapy intravenously.

According to the ADA Council on Scientific Affairs, it is even rarer for osteonecrosis of the jaw to develop in patients taking oral bisphosphonates for osteoporosis or Pagets disease. The CSA quotes a Merck and Co. report that there are fewer than 200 reported cases of osteonecrosis in the more than 20 million patients taking oral bisphosphonates. But none of these facts is reported by the author of Is Fosamax Destroying Jaw Bones? Instead, he counsels readers to question whether they really need to be on bone drugs at all. He advises, Ask your medical doctor, Are you sure I really need to be taking this medication? Are you aware of the effect that Fosamax and other similar drugs can have on the jaw bone? Many patients wont ask these questions of their physicians, but, instead, will simply be frightened and stop taking their prescribed Fosamax. How many hip fractures, bone injuries, shrunken and stooped spines will be caused, inadvertently, by this article?

(Dentists who wish to be well informed should read the bisphosphonate therapy guidelines in the August 2006 issue of the Journal of the American Dental Association.) The dentist concludes his article with the generous advice, If your medical doctor or family dentist needs more information, please feel free to have them contact me at my office.
Inconceivably Poor Judgment

The new patient, who had just moved into my neighborhood, settled herself into the dental chair. I asked her about her prior dental experiences. My old dentist was absolutely wonderful, she gushed.Do you know what he did for me? When I was pregnant last year and needed a root canal, he told me that I couldnt get an injection. But he was so nice, and he did the root canal really slowly. I went to him four days in a row, and it was incredibly painful and absolutely horrible, but he was very kind and gentle and helped me through the entire ordeal. Afterwards, my dental assistant tried to describe the look on my face. Of course, we all want to minimize any danger to a pregnant patient, especially during the first or last trimester. Perhaps we will try to postpone invasive or elective procedures when possible, or use anesthetics without epinephrine. But is it possible that there is actually a licensed dentist out there who really believes that it is safer or healthier to have performed this root canal therapy without any anesthesia in these circumstances? Is this dentist a sadist or merely sadly misinformed and ignorant?
Getting to the Root of the Problem

After a few moments of conversation, I established that she was not in any discomfort or distress and that the tooth didnt bother her or have any sharp, uncomfortable, rough edges. But dont you understand? sobbed the patient. The voice on the phone sounded very alarmed.The 48 hours are almost up! My mind was racing, trying to understand the significance of 48 hours. The patient went on to explain that she had just met a dentist friend, who informed her that when a temporary filling in a root canal-treated tooth is out for 48 hours, then the tooth automatically needs to have the root canal redone. I was stunned.While I always admire a dentist who can use his verbal skills to induce a patient into accepting needed treatment, this patient was not given to exaggeration. It sounded like her dentistfriend really believed it. Where did this myth originate?
Amalgam Wars

I was at home late on a Saturday night and a very agitated patient was on the phone with me. Do you remember the root canal you did last year, and you told me to do a crown, but I didnt get a chance to do it yet? she began. Well, she continued, the temporary filling is out! Can I come to your office immediately?

She is one of my favorite part-time dental assistants of all time and was telling me about her professors lecture in her Brooklyn College, Nutrition 101 class. The professor warned her captive audience of note-taking students, Remember! Never let your dentist put in one of those mercury fillings. Sivan, my dental assistant, is very bright and inquisitive, and I pride myself on having a well-informed team. I explained that these amalgam fillings are the subject of some controversy in dentistry and that while some dentists no longer place amalgam fillings because of fears of mercury-related toxicity, most professional dental organizations, researchers, dental schools and published articles continue to report no scientific evidence of any amalgam dangers. Nevertheless, I continued, many dental offices, like ours, are placing fewer and fewer amalgam fillings and more and more tooth-colored fillings, because resin restorations are prettier and less destructive of tooth structure.

I concluded that there are still situations, such as a subgingival Class V on an upper left third molar, where an amalgam would be superior to a resin filling and that while we routinely see perfectly functioning large MOD amalgams that I placed 30 years ago, sadly, I have no such expectations of todays direct resins. The story does not end there. The following week, Sivan and her friend were seated in a restaurant. My assistant was explaining to her friend what she had learned about amalgams. A dentist, eavesdropping from the next table, leaned over and interrupted them. He exclaimed, Oh yeah? Your dentist doesnt know anything! He should read the overwhelming and definitive scientific proof about the dangers of amalgam! Now,I try to respect everyones opinion. I dont even fault the eavesdropping dentist for insinuating himself into my dental assistants dinner date. I even respect his right to come to a position regarding amalgam that differs from my view. But, overwhelming scientific evidence about the dangers of amalgam? Please, dont make me laugh.
Is Anything Lacking?

We should never be surprised by, or disappointed in, colleagues who may have opinions different from ours. However, a blanket condemnation of Fosamax? The assertion that pregnant women can never receive a local anesthetic? Automatically retreating a root canal-tooth if the temporary is out for two days? Concluding that there is overwhelming evidence regarding amalgam health risks? In a July 2006 editorial in the Journal of the American Dental Association, the editor, in discussing dental school education, opines,What is lacking is an emphasis on giving students the tools and skills that will enable them to assess and apply new knowledge independently. Should we worry?
Dr. Galler is chairman of the Peer Review and Quality Assurance Committee of the Second District Dental Society. He practices general dentistry in Brooklyn and is a frequent contributor to The New York State Dental Journal
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