Bulimia Nervosa: Dental Perspectives
This young woman has lost almost all enamel from the palatal surfaces of her anterior teeth (yellow dentin is exposed). A thin white rim of remaining enamel is seen at gum line and amalgam fillings stand "high and dry" as the teeth erode around them from repeated contact with vomit.
Bouquot JE, Seime RJ. Pract Perio Aesth Dent 1997;
Bulimia nervosa and bulimic behavior are among the most common of the eating disorders, affecting as many as 13% of female college students. Most health professionals are well aware of the strongly compulsive binging, self-induced vomiting and laxative abuse associated with this disease, and yet only a small proportion of affected patients are ever diagnosed, and then only after many years of abuse. As the dental changes seen in most bulimics are recognizable and usually undeniable, the dentist should be attuned to oral and maxillofacial changes of this disorder in order to assist in early diagnosis. Without successful treatment, one in 300 bulimic cases will have a fatal outcome. Even with treatment, one third of affected individuals suffer early relapse and half do not consider themselves cured at 5 years after psychological therapy. This paper discusses the psychological and oral features of this serious and common eating disorder, with special discussion of the differential diagnosis and treatment of the oral manifestations.
The dentist's role in the diagnosis of systemic health problems is well established and there are quite a few disorders for which oral and maxillofacial alterations may be the first manifestations leading to a proper diagnosis. Bulimia nervosa is such a disease, but it has the additional uniqueness of being a disorder with a predominantly psychological foundation. As with many other psychological dysfunctions, physical changes are often slight or completely lacking, even to the eye of a conscientious examining physician. In fact, since the food binging and purging so characteristic of this disease are typically conducted by the patient alone and in secrecy, the dental manifestations of bulimia nervosa may be the only visible proof of this serious, potentially life-threatening disease.
The dental manifestations are recognizable, follow a consistent pattern, and for the most part are undeniable. Of course the major oral change, dental erosion, must be differentiated from other types of erosion and from tooth decalcifying processes unrelated to habitual vomiting, but without appropriate recognition by a knowledgeable dentist or dental hygienist, the consequences of bulimia are likely to go unnoticed by other health professionals until late in the course of the disease. Affected individuals who seek professional care routinely do so only after seven years of uncontrolled eating difficulties, and it has been shown that only a small proportion, fewer than one in ten, ever seek professional care.2-4
Bulimia nervosa and its less severe counterpart, bulimic behavior, have become in recent years a major problem among young women and has been described as an "epidemic" affecting as many as 13% of the women on some college campuses.2-5 The presence during the college years of eating disorders of all kinds should not come as a surprise when one realizes that more than 19% of college students today can be classified as obese or "severely overweight" during this important time of self-image building, and that 76% of 18 year old females who see themselves as fat are striving to lose weight.6
There are some who believe that bulimia is a new entity resulting from our modern cultural obsession with thinness and sexual attractiveness.7 Others claim that there is no substantial proof of a modern bulimia epidemic, only an enhanced interest in the disease.3-5 While the first English-language research paper relating exclusively to bulimia was not published until 1979, earlier reports of tooth changes in anorexia nervosa had been published. As long ago as 1937 a case of severe dental erosion was reported in a 26 year old female described as a "walking skeleton" with many of the symptoms of anorexia nervosa.8,9 The disease is apparently referred to in the Talmud, the collection of Jewish law which is thousands of year old. Regardless of its history, the current prevalence of this disorder is high enough to alarm experts and to cause some to call for inclusion of a bulimia screening in the routine physical examinations performed by primary care physicians.7
It is important to distinguish between bulimia nervosa (defined below) and persons who simply participate in bulimic behaviors. Simple bulimic behaviors such as binging and purging for weight control can be found in 4-13% of female college populations and can even be found in 4% of male college students (Table 1 below).10 True bulimia nervosa, on the other hand, is much less common, especially among males. Both disorders seem to show a racial variability. Bulimia nervosa, for example, is almost unheard of among nonwhite males, and among nonwhite females it is considerably less common than it is among white females (0.7% vs. 2.3%, respectively, in one comparison study).5
Table 1: Prevalence differences between bulimia nervosa and bulimic behavior among college-age adults in one of the few investigations to distinguish between the two disorders.10
|Gender||Bulimia Nervosa||Bulimic Behavior|
Bulimic behavior is, as expected, much more common in the community at large than is true bulimia nervosa, but those seeking professional help are typically the true bulimics.10 Affected persons in the community are much more likely to be obese, or at least overweight, than are bulimic patients in eating disorder clinics.10 In fact, the majority of bulimics who seek professional help are within 10-15% of ideal weight and, if anything, are more likely to be anorectic than overweight.10 The clinic group, furthermore, has a much higher level of "functional impairment" and social maladjustment, they have a more severe eating disorder than the community bulimics, and they are more likely to have additional psychological dysfunctions.
Bulimia is a disorder of teenage and young adult females, with the onset of compulsive behavior typically in the adolescent years. More than 85% of affected patients are women and the mean age at diagnosis is approximately 19 years, but cases have been diagnosed in persons as young as 12 years of age and older than 35 years of age.2 Bulimic patients identified through dental clinics are younger by several years than those identified through eating disorder clinics, a hopeful indication of dentistry's ability to identifying cases early in the course of the disease.11 Early diagnosis is important because the treatment of early cases is more successful and because most cases are not diagnosed until 6-8 years after the onset of the eating disorder.10 Unfortunately, it is not unusual for a patient to present to an eating disorder clinic after 13 or more years of laxative abuse and secret binging and vomiting.10
An impressive proportion of bulimic nervosa patients report significant physical and sexual abuse during their early years, and three of every four affected women have serious anxiety disorders, usually preceding the onset of the bulimia itself.10,12 Depression is also a major secondary feature of bulimia nervosa patients and almost half develop alcohol or another drug dependency.12 There is a inordinate tendency for additional dysfunctions to be of the strongly compulsive variety.12
Bulimia nervosa was originally classified as a subtype of anorexia nervosa and is still said to occur in more than 20% of patients suffering from the latter disorder.13 Major differences exist, however, between the psychological and clinical features of bulimia nervosa and anorexia nervosa, and these have led many authorities to consider the two to be separate and distinct diseases which frequently occur together, i.e. have common co-morbidity.12 Individuals affected by either disease have a strong preoccupation with food consumption and weight control, but pure bulimia nervosa traditionally lacks the starvation and wasting associated with anorexia nervosa.
Bulimia nervosa is characterized by uncontrolled ingestion of large (huge?!) quantities of food, followed by either involuntary or, more usually, self-induced vomiting (Table 2 below).5,13 The affected person feels a considerable loss of control during eating and feels that it is impossible to stop eating.2 The average patient induces vomiting at least once a day, more often during times of emotional stress ( range: 1-18 times weekly; average: 12 times weekly).14,15 This activity is usually done late in the evening when it is not uncommon to vomit four to six times. Prior to vomiting, and sometimes without vomiting at all, a patient may consume during a single session as much as 10,000-20,000 food calories (average: 3,000-6,000 calories). Typically the food is sweet or starchy and is often swallowed with little or no chewing. Abdominal pains are not an infrequent result of these abnormal behaviors.
Table 2: Diagnostic criteria for bulimia nervosa as defined by the American Psychiatric Association.14
The binge/purge phenomenon is episodic and dependent on social settings and the ease with which it might be done without observation by others. Fasting for 24 hours at least once a week is also practiced by almost a third of all bulimic patients.5 Self-administered diuretics and thyroid hormone are additional means used by patients to reduce weight by increasing metabolic activity, sometimes with the production of serious disease states such as thyrotoxicosis.1
The voraciousness of the binging in this disorder (bulimia is a Latin term derived from the Greek term for "ox hunger") does not always lead to obesity. On the contrary, we have mentioned that the self-induced vomiting is often combined with abuse of laxatives and diuretics to keep a bulimic patient's weight normal or near normal for those patients seeking professional help.7 This weight control often combines with a conscientious attention to make-up and dress to result in a very attractive physical appearance, at least for those seeking the assistance of eating disorder clinics. The dentist must not be threatening. As with true anorectics and those with other psychiatric disorders, bulimia nervosa patients have a problem with self-image. They suffer from almost a terror of being rejected and a constant need for approval from others.2 They are secretive, ashamed, guilt-ridden and self-deprecating about their abnormal eating, and they are often depressed. These psychological problems require the concerned dentist to be very nonthreatening and nonconfrontational in his or her approach to the patient. This is especially true because so many bulimic patients are aware of the fact that their dentist can see abnormalities in their mouths which might make them suspicious of chronic vomiting. Denial is such a large part of the picture of bulimia that it should be expected at the initial discussion.
This disorder can produce a variety of metabolic and electrolytic imbalances, especially when combined with anorexia nervosa or aggravated by the abuse of laxatives, diuretics, thyroid hormone replacement medications and cathartics. Amenorrhea and dehydration are a common and early phenomenon of bulimic patients with anorectic tendencies.2,6 The skin and mucous membranes frequently become dry. Some patients have developed abnormal EEGs. Less frequent signs and symptoms include metabolic alkalosis, Raynaud's phenomenon, arthralgia, dry eyes (xerophthalmia), low levels of serum protein, zinc depletion, low levels of tryptophan and serotonin, low levels of serum calcium and chloride, high levels of alkaline phosphatase, and high levels of serum amylase and cortisol.19-23 These produce a variety of symptoms with varying severity, but it should be emphasized that in clinical practice, even high frequency purgers may show no electrolyte abnormalities or systemic symptoms. In other words, the absence of abnormalities does not preclude a person being diagnosed as bulimic.
Bulimia nervosa can have a fatal outcome. Fortunately, the disease seems to be much less lethal than anorexia nervosa. This may change as longer follow-up studies are published, but for now the reports indicate that approximately 6% of anorectics will die of the complications of their psychological disorder, while only 0.3% of bulimics will die of their disease.30 The deaths associated with bulimia have resulted from either suicide or complications of severe weight loss.30 To put things in perspective, it should be mentioned that more people in bulimia follow-up studies have died of accidents than of their disease.
The serum electrolyte abnormalities seen in serious bulimia nervosa patients may eventually provide good markers of severe binging and vomiting behaviors, but only if the clinician is suspicious enough to request the appropriate laboratory evaluation. Acute tryptophan depletion, hyperphosphatemia, and hyperamylasemia are among the most recognizable markers of this type.20-23
Elevated levels of serum amylase have been suggested not only as a good diagnostic tool for confirming the diagnosis of bulimia, but also as a monitoring test for post-treatment cases.24 This phenomenon has been found in more than one fourth of bulimic patients, possibly related to protein-calorie malnutrition, or binging with large amounts of carbohydrate-containing foods, or the effect of stomach acid on the salivary glands.24 Elevated serum amylase is normally associated with such serious conditions a pancreatitis, parotitis, alcoholism, tumors, renal insufficiency and macroamylasemia.24
It is no secret that dental erosion is the premier sign of habitual vomiting, but it is important to differentiate between bulimia erosion and other types of erosion (18% of adults have one form or another when teeth are thoroughly examined.1) and between dental erosion and other forms of tooth loss or decalcification.
Abrasion is one such problem, commonly encountered in the dental office and sometimes confused with erosion. Abrasion, however, is the mechanical wearing away of hard tooth structures by external agents, while erosion is the nonbacterial chemical dissolution of hard tooth surfaces.25 The pattern of wear in abrasion is dependent upon the exact cause of the abrasion, with bruxism and heavy, horizontal toothbrushing being the most common culprits, while erosion does not correlate with functional wear patterns. The causative habit of abrasion is almost always able to be ascertained, while the cause of erosion is often not discovered, although in a research setting with extensive evaluation, etiology is typically ascertained, including:26
With more sophisticated 24-hour pH testing in an esophageal laboratory, the proportion of erosion patients with gastroesophageal reflux disease may be as high as 83%.1The appearance is also different between abraded and eroded lesions. Affected tooth surfaces in abrasion typically have a flat, sharp, angular appearance (Figure 1), while erosive lesions have a smooth, spoon-shaped or cupped-out appearance (Figure 2). Pulpal exposure and tooth sensitivity are rarely encountered in the slow process of abrasion, while pulp sensitivity is a common problem in erosion cases, although actual pulpal exposure is rare. Finally, metal and plastic restorations in abrasion cases are worn by the abrading process (Figure 3), while metal or plastic restorations are unaffected by the erosive process and remain as elevated plateaus, sometimes referred to as "amalgam islands" (Figure 4).
The typical appearance of dental erosion also makes it easy to distinguish it from dental caries, with its soft, irregular, discolored surfaces densely populated with bacteria (Figure 5). Caries affects primarily interproximal surfaces and occlusal pits and fissures, while erosion affects facial and lingual surfaces primarily, and the flat areas of the occlusal surfaces (Figure 6). Focal areas of mottled white decalcification, such as demarcated opacities of enamel (focal decalcification; Figure 7) are occasionally seen in the base of eroded lesions, but they are much more likely to be found in incipient caries, environmental or hereditary amelogenesis imperfecta (Figures 8 & 9), or fluorosis (Figure 10). Occasional developmental enamel hypoplasias with smooth surfaces may mimic dental erosion, especially the concave areas sometimes seen in mild Turner's tooth, produced by contact of the developing crown with the acidic fluids of an overlying abscessed primary tooth (Figure 11).
If the dentist is to properly diagnose bulimic erosion, he or she must not only be able to distinguish erosion from these other causes of enamel loss and decalcification, but must also distinguish habitual vomiting effects from other types of erosion.26-31 As with abraded teeth, different patterns of erosion are encountered and these patterns are of substantial diagnostic importance. Erosion of the facial surfaces of the maxillary anterior teeth, for example, can usually be attributable to a dietary source of acid, such as citric fruits (lemon sucking habit) or habitually placed candies, especially citric flavored candies (Figure 12). Soft drinks and fruit juices can also produce enamel erosion, even juices as mild as apple juice and grape juice. Wine is also capable of eroding enamel; uniform loss of enamel is, in fact, an occupational hazard of the wine tasting profession. When these liquids are swished around habitually in the mouth their effect is more severe and more widespread, usually affecting the majority of tooth surfaces, especially those of the maxillary anterior teeth (Figure 6).
Occupational exposure to aerosolized acid in a workplace, such as a lead battery factory, may produce erosion of tooth surfaces exposed to the atmosphere. Usually the incisal edges and the facial surfaces (sometimes the palatal surfaces) of the anterior maxillary teeth are involved.1 A similar loss of tooth structure has been reported to result from exposure to improperly maintained water in gas-chlorinated swimming pools.1
Erosion of the occlusal and palatal surfaces of the maxillary molars, without involvement of the anterior teeth, is most often secondary to regurgitation of stomach acid from hiatal hernia, from gastroesophageal reflux, or from nausea related to disease or medication.1,29 In such cases the acid remains in the pharynx and posterior mouth, and the amount of erosion is directly correlated with the frequency and duration of the problem.30 Regurgitation patients are usually much older than are the habitual vomiters of bulimia, although resent studies have indicated that this may also be a problem in children.30 The mandibular molars are usually spared in this process because the tongue naturally curves to accumulate the vomitus in a trough, thereby preventing it from touching the posterior mandibular teeth.
The persistent or recurring vomiting of bulimia and bulimic behavior produces a similar and very characteristic pattern of erosion, sometimes referred to as perimylolysis or perimolysis.6 Smooth enamel loss is first seen on the palatal surfaces of the maxillary central and lateral incisors, the surfaces most directly in the path of the induced vomitus. In decreasing order of frequency the following additional surfaces are affected:11,26-31
This pattern differs from other patterns of erosion and is usually rather easily distinguished from the other patterns (Figures 4, 13, 14). As the palatal surfaces of the maxillary incisors erode, the incisal edges become more and more thin and translucent, eventually producing a knife-edge which is easily crazed and chipped (Figure 15). Occlusal surfaces often take on something of a flat, faceted or cupped-out (saucerized) appearance, resulting from abrasion of softened enamel during grinding and bruxing activities (Figure 16).
The amount of enamel loss is not well correlated with the number of vomiting episodes daily or weekly, perhaps because most of the stomach's acid is expelled with the first episode, but there is good correlation with the duration of habitual vomiting. Dental erosion in a bulimic patient usually becomes obvious within three years, but not all patients develop erosion.26-31 As previously mentioned, the patient with extensive enamel erosion will complain of increased sensitivity of the teeth to heat, cold, and acidic foods.
Other orofacial features. Not all of the oral and maxillofacial changes of bulimia are tooth related. Chronic sore throat with erythematous mucosa, especially of the uvula and posterior soft palate, are frequent changes related to recurring\vomiting. Occasional patients have traumatic petechiae or submucosal hemorrhages of the palatal mucosa. Scratch marks on the soft palate may be seen to result from fingernails injuring the mucosa when the patient sticks her finger deep in the throat to induce vomiting. This chronic habit can, likewise, lead to the development of characteristic scars and callouses on the back of the finger used to induce vomiting. Burning tongue is an occasional feature.
Benign enlargement of the parotid and submaxillary glands (sialadenosis, parotidomegaly, nutrtional "mumps") has also been reported in bulimic patients and may be the first evidence of disease, especially in those with anorectic overtones (Figure 17).19,24,32 Xerostomia is also common in the malnutritioned bulimic patient, sometimes being quite extreme and quite painful.19
In patients who vomit regularily, a low level of dental plaque accumulation has been found, and in general the oral hygiene and periodontal status of bulimic patients is good.6 Caries rates have been generally low, although there seems to be in some patients a predisposition to cervical caries and the rapidly destructive "leathery" dentinal lesion which undermines large areas of enamel.7
The treatment for bulimia nervosa is primarily psychiatric or psychological counseling, but only 50% of bulimia nervosa patients consider themselves fully recovered 5-10 years after treatment.33 Approximately one-third of treated patients will suffer a relapse within four years after treatment.33,34 This rather poor cure rate and high relapse rate has led some authorities to recommend continuous or "maintenance" therapy after the initial treatment.34
There is a question of whether or not today's treatments are truly beneficial. In the short run, studies show that treatment is obviously better than no treatment for this eating disorder. Of the treatments available now, cognitive behavior therapy and interpersonal psychotherapy seem to have the best short-term success with bulimia nervosa.33,34 However, in a recent study, five or more years after diagnosis the proportion of recovered persons is about the same whether or not they received professional therapy.33 Those patients with bulimia superimposed on anorexia nervosa may be cured of their bulimia but not of their anorexia. Likewise, persons with coexisting personality disorders of other kinds have a lower recovery rate after treatment than those without such disorders. This is especially true for those with the so--called "multi-impulsevist syndrome," a syndrome defined as including at least three of the following behaviors:33
It must always be kept in mind when evaluating therapies, that those patients actually making it to a psychologist's or psychiatrist's office are among the most severely ill of those with bulimic habits. While the proportion of therapy failures is discouraging, new techniques are constantly evolving and it is expected that success rates will improve over time.
Early diagnosis and treatment of the bulimic condition itself is the key to preventing severe dental sequelae of protracted, frequent vomiting.35 The maintenance of routine preventive and oral hygiene procedures should be encouraged, including the application of topical fluoride during routine dental visits. Restorative procedures can be performed on severely eroded teeth and tooth surfaces, this is aided by the fact that cervical enamel is usually spared by the erosive process. The application of fluoride, resin composites, and pit-and-fissure sealants may assist in control of hypersensitive dentin. No treatment is available for those patients with salivary gland enlargement other than the elimination of the eating disorder.19
If the vomiting persists, restorative procedures short of full crown coverage with subgingival margins will not stop the erosion, and attention should be paid to methods designed to protect tooth surfaces from the continued acid exposure. During vomiting, protection of the teeth with magnesium hydroxide (alkali) filled plastic splints may be useful, and the use of bicarbonate rinses shortly after vomiting has been recommended.18 Topical daily sodium fluoride applications, or as a 0.05% neutral pH sodium fluoride mouthwash combined with bicarbonate after each vomiting incident, may be helpful, as may the brushing of the teeth with a fluoridated toothpaste immediately prior to vomiting. Toothbrushing after vomiting should be discouraged, as the softened enamel is susceptible to abrasion during that time.18 After vomiting, a fluoridated mouthrinse, or even clean water rinse, may be helpful. Acid foods and drinks should be avoided, if at all possible. Increased salivary flow may be improved through the use of sugar-free gums, lemon drops, or salivary-stimulating medications.
Bulimia nervosa and bulimic behavior can be early diagnosed through appropriate and informed evaluation of dental and oral changes. A variety of psychological and dental therapies, tried and untried, are available for identified patients willing to work with a dentist and psychologist or psychiatrist. Early diagnosis is important for the prognosis of the psychological counseling and for the prevention of further destruction of remaining tooth structures.
1. Schroeder PL, Filler SJ, Ramirez B, et al. Dental erosion and acid reflux disease. Ann Intern Med 1995; 122:809-815.
2. Fairburn CG. Area review: bulimia nervosa. Ann Behav Med 1987; 9:3-7.
3. Whitaker A, Davies M, Shaffer D, et al. The struggle to be thin: a survey of anorexic and bulimic symptoms in a non-referred adolescent population. Psychol Med 1989; 19:143-163.
4. Fairburn CG, Beglin SJ. Studies of the epidemiology of bulimia nervosa. Am J Psychiatry 1990; 147:401-408.
5. Pemberton AR, Vernon SW, Lee ES. Prevalence and correlates of bulimia nervosa and bulimic behaviors in a racially diverse sample of undergraduate students in two universities in Southeast Texas. Am J Epidemiol 1996; 144:450-455.
6. Hurst PS, Lacey JH, Crisp AH. Teeth, vomiting and diet: a study of the dental characteristics of seventeen anorexia nervosa patients. Postgrad Med J 1977; 53:298-305.
7.Welds K. Anorexia and bulimia more prevalent in American society, especially among young women. Internat J Fertility Menopausal Stud 1995; 40:6:290.
8. Russell G. Bulimia nervosa: an ominous variant of anorexia nervosa. Psychol Med 1979; 9:429-448.
9. Bargen JA, Austin LT. Decalcification of teeth as a result of obstipation with long continued vomiting: report of a case. J Amer Dent Assoc 1937; 24:1271-1273.
10. Fairburn CG, Welch SL, Norman PA, et al. Bias and bulimia nervosa: how typical are clinic cases? Am J Psychiatry 1996; 153:386-391.
11. Robb ND, Smith BGN, Geidrys-Leeper E. The distribution of erosion in the dentitions of patients with eating disorders. Br Dent J 1995; 178:171-175.
12. Bulik CM, Sullivan PF, Carter FA, Joyce PR. Lifetime anxiety disorders in women with bulimia nervosa. Compreh Psychiatry 1996; 37:368-374.
13. Roberts MW, Li S-H. Oral findings in anorexia nervosa and bulimia nervosa: a study of 47 cases. J Am Dent Assoc 1987; 115:407-410.
14. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 4th edition. Washington, DC; American Psychiatric Association, 1994.
15. Casper RC, et al. Bulimia, its incidence and clinical importance in patients with anorexia nervosa. Arch Gen Psychiatry 1980; 37:1030-1035.
16. Mitchell JE, Pyle RL, Eckert ED. Frequency and duration of binge-eating episodes in patients with bulimia. Am J Psychiatry 1981; 138:835-836.
17. Crow S, Mitchell J, Kendall D. Levothyroxine abuse and bulimia nervosa. Psychosomatics 1997; 38:151-153.
18. Simmons MS, Grayden SK, Mitchell JE. The need for psychiatric-dental liaison in the treatment of bulimia. Am J Psychiatry 1986; 143:783-784.
19. Hasler JF. Parotid enlargement: a presenting sign inn anorexia nervosa. Oral Surg Oral Med Oral Pathol 1982; 53:567-573.
20. Bonne OB, Gur E, Berry EM. Hyperphosphatemia -- an objective marker for bulimia nervosa. Comprehen Psychiat 1995; 36:236-240.
21. Weltzin TE, Fernstrom MH,, Fernstrom JD, et al. Acute tryptophan depletion and increased food-intake and irritability in bulimia nervosa. Amer J Psychiatry 1995; 152:1668-1671.
22. Crow SJ, Salisbury JJ, Crosby R, Mitchell JE. Serum electrolytes as markers of vomiting in bulimia nervosa. Psychosomat Med 1995; 57:72.
23. Metzger ED, Levine JM, Wolfe BE, et al. Relationship between salivary gland size and hyperamylasemia in bulimia nervosa. Psychosomat Med 1995; 57:85.
24. Gwirtsman HE, Yager J, Gillard BK, Lerner L. Serum amylase and its isoenzymes in normal weight bulimia. Internat J Eating Disorders 1986; 355-361.
25. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral & maxillofacial pathology. Philadelphia; W.B. Saunders. 1995: 48-51.
26. Harrison JL, et al. Dental effects and management of bulimia nervosa. Gen Dent 1985; 33:65-68.
27. Altshuler BD, Dechow PC, Dechow PC, Waller DA, et al. An investigation of the oral pathologies occurring in bulimia nervosa. Intenat J Eating Disorders 1990; 9:191-199.
28. Grippo JO, Simring M. Dental erosion revisit ed. J Amer Dent Assoc 1995; 126:619-623.
29. Barlett DW, Evans DF, Anggiansah A, Smith BGN. A study of the association between gastro-oesophageal reflux and palatal dental erosion. Brit Dent J 1996; 181:125-131.
30. Nunn J, Shaw L, Smith A. Tooth wear -- dental erosion. Brit Dent J 1996; 180:349-352.
31. Scheutzel P. Etiology of dental erosion -- intrinsic factors. Europ J Oral Sciences 1996; 104:178-190.
32. Levin PA, et al. Benign parotid enlargement in bulimia. Ann Intern Med 1980; 93:827-829.
33. Keel PK, Mitchell JE. Outcome in bulimia nervosa. Am J Psychiat 1997; 154:313-321.
34. Olmsted MP, Kaplan AS. Predictors of relapse in bulimia nervosa. Psychosomat Med 1997; 59:103.
35. Kleier DJ, Aragon SB, Anerbach RE. Dental management of the chronic vomiting patient. J Am Dent Assoc 1984; 108:618-621.
Figure 1: This case of toothbrush abrasion shows the classic sharp, angular and flat appearance of mechanical wear.
Figure 2: Erosion lesions of the facial surfaces of the lateral incisor and cuspid (secondary to frequently "parking" a lemon drop candy in the area) shows the classic saucerization with rounded edges and a smooth, glistening surface.
Figure 3: Adjacent restorations typically show signs of abrasion along with the abrasion of the adjacent enamel. Here one can see toothbrush bristle grooves in enamel and gold.
Figure 4: Erosion of enamel of all palatal surfaces of the maxillary teeth is worse on the incisors. Loss of enamel from the occlusal surfaces has left amalgam islands elevated above the remaining tooth structure. The amalgam edges have rounded out from wear.
Figure 5: Carious lesions have a tough, leathery base which is discolored. The outline is irregular and the lesional edges may be undermined.
Figure 6: Severe erosion of almost all tooth surfaces except interproximal and cervical enamel has resulted from 5 years of a daily habit of swishing colas around the mouth prior to swallowing.
Figure 7: Demarcated opacifications, as seen here on the labial aspects of the maxillary incisors, are irregular in outline and lack the shiny base of an erosive lesion. These are usually environmental is nature.
Figure 8: Irregular, dull white opacifications may also be hereditary defects, as seen here in a case of amelogenesis imperfecta.
Figure 9: Hypoplastic forms of hereditary amelogenesis imperfecta may show focal areas of missing enamel, often discolored somewhat, but these are easily distinguished from environmental alterations by ascertaining from the patient that the teeth have been affected since eruption.
Figure 10: The mottled enamel of fluorosis is initially white, dull and irregularly outlined, but with time some areas take on a brown stain.
Figure 11: Turner's tooth defects may sometimes be smooth, cupped-out areas of the crown, but they are produced during crown development and so are present at the time of eruption. (photo courtesy of Dr. Robert Gorlin, University of Minnesota).
Figure 12: Severe enamel erosion from the chronic sucking of lemon wedges has left a combination of smooth glistening surfaces and saucerized areas. Note the sparing of the interproximal and cervical enamel, and note the semitranslucent, chipped, knife-edged incisal edges.
Figure 13: Habitual vomiting throws stomach acid against the anterior maxillary teeth, eroding the palatal surfaces of the incisors, cuspids and bicuspids. Almost all enamel is missing from the incisor palatal surfaces and the teeth are very sensitive to hot and cold. In this case the molars are relatively less involved than the more anterior teeth.
Figure 14: The pattern of erosion is very important in determining the appropriate differential diagnosis. Several common patterns are shown above.
Figure 15: Even without examining inside the mouth, severe loss of maxillary incisor palatal surface enamel can be inferred by the thinness and the ragged, chipped nature of the incisal edges.
Figure 16.: When erosion is combined with bruxing, severe cupping out of occlusal surfaces can be seen, often with exposure of underlying dentin. Acid has kept the margins of the lesions somewhat rounded, as opposed to the angular nature of the margins of simple abrasion lesions.
Figure 17: Enlargement of parotid glands may be unilateral and is often not very pronounced. The affected gland is firm to palpation and may be tender. In this case, parotid involvement is only evident by a slight bulge beneath the ear.