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The anorexia nervosa syndrome
oral medicine Editor: JAMES W. LITTLE, D.M.D., M.S.D. School of Dentistry University ef Minnesota 515 S.E. Delaware St. Minneapolis, Minn. 55455
The anorexia nervosa syndrome William F. Brady, B.A., D.M.D., UNIVERSITY
OF SOUTHERN
F.A.G.D.,*
CALIFORNIA
SCHOOL
El Cajon, Calif. OF DENTISTRY
This article reviews the medical and dental literature on the anorexia nervosa syndrome and presents the oral and systemic manifestations of this serious disease process. A case is reported which demonstrates the generalized destruction of tooth structure, primarily as a result of the direct effect of gastric acid on this patients dentttion during a Iyear period of self-induced vomiting. The systemic, psychological, and social aspects of this syndrome are classically illustrated in this case history.
norexia nervosawas first describedby Sir William A Gull’ in 1868. It was once considereda relatively uncommon but serious disorder. In the last 10 years, however, its incidence has increased considerably. Early diagnosis and treatment of this problem is extremely important if one is to ensurea favorable prognosis. Close cooperationbetweenthe physician and the dentist is in the best interest of the patient and will result in an improved prognosis, not only from a medical but also from a dental point of view. While the dental complications in this syndrome, unlike the systemic effects, may not result in the deathof the patient, they neverthelessmay result in the destruction of the patient’s dentition. The cause-and-effectrelationship betweenthe regurgitationof gastric acid and the loss of enamel and dentin was first reportedin the literature by Hellstrom in 1977. In a previous article, in 1974, Hellstrom had stated that the association of anorexia nervosawith induced vomiting and loss of enamel and dentin had never been reported in the literature. The systemic manifestationsof the anorexianervosa syndrome are usually presentbefore the appearanceof the oral and dental disturbances.An alert dental practitioner may discover these disturbances during the routine review of the patient’s physical examination *Assistant
Professor,
Department
M)30-4220/80/120509+08$00.80/0
of Diagnostic
0
Sciences
1980 The C. V. Mosby Co
and medical history. Since the dentist recalls patients more frequently than the physician, he/she is in an excellent position to recognize the early signs and symptoms of this disease.Prompt referral to and consultation with the patient’s physician will greatly improve the prognosis of this condition. A review of the medical literature reveals an alarming increasein this condition. For example, in 1968the Index Medicus listed 41 publications under anorexia nervosa. Ten years later (1978) there were 136 publications listed. Oral and dental manifestations were absent from these publications. If left unattendedor inadequatelytreated, the patient may succumb to inanition, complicating infection, or suicide.”In view of the seriousnessof this disease,it is easy to seehow the medical profession could consider the oral and dental findings less significant. A survey of the dental literature revealed only six publications under anorexianervosa.Only one of these ,articles appearedin the American literature, and this article made no mention of any possible dental or oral manifestations. By definition, anorexia nervosa is a chronic psychosomatic illness manifesting itself primarily as an eating disorder. The use of the term anorexia with this diseaseis actually a misnomer, since there is no real appetite loss. The reverse usually occurs, the patient 505
510
Brady
claims to have appetite loss, but alternates food avoidancewith overeating and follows this with induced vomiting. The exact cause of anorexia nervosa is unknown. This illness can be viewed from two aspects.The most probable would be psychologic, especially from conflicts engenderedby the experienceof puberty and adolescence.Thorna and Meyer and Feldman5defined the patient’s attitude toward food as a psychotic process. In spite of an emaciatedappearance,the patient perceivesherself as fat, lacks the capacity for emotional experiences,and builds up a senseof security by refraining from food. Periodsof both physical and intellectual hyperactivity are common. The secondprobableetiologic factor in anorexianervosa is neuroendocrinein origin. A disturbancein the “feeding center” in the hypothalamushas beenpostulated on the basisof experimentalstudiesin animalsbut has not been clearly establishedin human beings.3 This syndromedevelops from puberty through the 40’s, the mostcommontime of onsetbeingbetweenthe agesof 14 and 17 years.It occursin femalesat leastten times more often than in males.5,6 An even higher female predilection was reportedin a study by TheanderG7In his group of patients there was a 20 to 1 predominanceof females over males. Thoma,sin 1967, also reported an increasingfrequencyof anorexianervosa in females.Thesepatientsoften becomeobsessed with the idea of being thin, and this resultsin a constant searchfor diets and ways to reducetheir size. Often an ambitious,intelligent, model child, with a fear of adult responsibilitieswhen growing up attempts to escape from this difficult situation by food denial. The patient often has an inner compulsionagainsteating, and every intake of food causesanxiety. The presentincreasing incidence of anorexia nervosa m ight be explainedby the presentemphasison and!socialacceptabilityof having a slender figure in our/society, especially among young women. The systemicmanifestationsof anorexianervosainclude the following: A previously normal 1. SpeciJic psychopathology. personmay show changesin temperament,consisting of impatience,irritability, and depression. There also may have been a precedinghistory of food fads or difficulty in making friends. 2. Self-induced starvation. This is the most characteristic symptom of the diseaseand results in severe weight loss and emaciation. This is “achieved” by strict dieting, in combinationwith orgiastric bouts of overeating(bulimia) followed by self-inducedvomiting or excessiveexercising. Severeweaknessand apathy may alternatewith periods of unusual strength and hyperactivity.
Oral surg. December, 1980
The patient may appeargaunt and weigh as little as 70 pounds.gThe limbs are very thin, the abdomenis flat, and bony prominencessuch as the clavicles and pelvic bonesstand out sharply. 3. Dehydration
and electrolyte balance disturbance.
Chronic episodesof frequent vomiting result in severedehydration.Serumpotassiumis the electrolyte most commonlydepleted.Theremay also be a moderatefall in serumsodium.Dry skin may be anothercommonfinding. 4. Amenorrhea. The patient’s urinary output of gonadotrophinsand estrogensis decreased. lo The blood level of estrogensis also found to be low. There is a decreasein the activity of the ovaries, and postmortemexaminationhas demonstrated atrophy of the ovaries.6The menstrualcycle is thus altered,and menstrualperiodsmay be absent for long periods of time. Even after a patient recovers from anorexianervosa,the menstrualperiod may be very slow in returning to normal. 5. Hirsutism. The patient exhibits an abnormal or unusualgrowth of fine downy hair, particularly over the arms, legs and facee3 6. Thermoregulation disorder. The body temperature may be reducedby 1” C. The patient often complainsof intoleranceto cold, with the hands and feet being particularly affected.‘O Oral and dental manifestationsof anorexianervosa include the following: 1. Perimylolysis. This is a severedental manifestation of anorexia nervosa. Hellstrom” defined “perimylolysis as a loss of enameland dentin on the lingual surfacesof the teeth as a result of chemical and mechanicaleffects causedmainly by regurgitationof gastric contentsand activated by the movementsof the tongue.” In severe chronic cases, such as the case reported in this article, all surfacesof the teeth may be affected by this acid erosion. Hellstrom” felt that where buccal erosion was presented,it m ight be due to excessivecomsumptionof fruits andjuices by the patient in order to relieve thirst after vomiting. Parafunctionalhabits, such as bruxism, clenching, and abnormalswallowing habits, m ight also contribute to loss of tooth structure. 2. Dental caries. An excessivecarbohydrateintake and poor oral hygienemay result in an increasein dental caries in thesepatients. Medicationsprescribedby the patient’sphysiciancould contribute to an increasein caries incidence. Examplesof such medicationsare dextrosetablets, Meritene (contains lactose), vitamin C drinks containing sucrose,etc.” 3. Periodontal disease. Periodontal problems are
Volume Number
50 6
common in the anorexia nervosapatient, with gingivitis being the most prevalent. 4. Saliva. The quality, quantity, buffering capacity, and PH of both resting and simulatedsaliva are found to be reduced. Prescribedsedatives,antidepressives,and antispasmoticsmay induce xerostomiain the anorexianervosapatient. Systemic complications,suchasmalnutrition, malabsorption,hormonaldisorders,anemia,andanxiety states,are also associatedwith reducedsecretion of saliva.2 5. Oral mucous membranes. Tissue health is impaired becauseof xerostomia and the resulting reductionin the membrane-lubricatingeffects of the saliva. The possiblelong-term effects of regurgitated gastric acid on esophageal,pharyngeal, and oral tissueshas yet to be reported. I believe that in severechronic casesof this syndrome, wherethe patient might survivefor many years, therecould possiblybe malignantchanges in the involved tissuesdueto the chronicirritating effects of years of vomiting. Two excellent studies were conducted by Hellstrom”, l2 in 1974 and 1977. In both studiesthe patients were divided into two groups,vomiting and nonvomiting. In contrastto the 1974 study, the 1977study revealeda high incidenceof dentalcariesin the vomiting group as well as in the nonvomiting group. This may be explained by the fact that the study had a greaternumberof patientswith excessivecarbohydrate ingestionwho were vomiting for longerperiodsof time than the previous study. The 1974 study showedthat wherefrequentvomiting occurredover long periodsthe clinical appearance was dominatedby erosionwith low incidence of plaque, gingivitis, and caries. Hellstrom** I1 attributed this to the alteration of bacterial plaque by the acid nature of the gastric juice. Thus, bacterial plaque growth was reduced and perimylolysis was increased.Thosepatientswho vomited infrequently or not at all showedno perimylolysis and increasedcaries. Also contrary to the findings in the earlier study, dental plaque was presentto the same extent in both groups. Therefore,vomiting apparently does not affect the quantity and quality of dental plaque. Buccal erosionwas presentin almost all cases of the vomiting group but rare in the nonvomiting patients. The 1974 study did not revealbuccal erosionin the vomiting group. This was probablyagaindue to the short history of vomiting in the first study. DIFFERENTIAL DIAGNOSIS
Included in the differential diagnosisare conditions that involve vomiting, such as pregnancy,pyloric stenosis, strictureor spasmof the esophagus,and gastro-
Anorexia
nervosa syndrome
511
intestinal tract peristalsisdisturbance.I2 Conditionsresulting in short-termepisodesof vomiting would not have severe destructive effects on the dentition. Anorexia nervosashould not be confusedwith what seemsto be a constantstriving to be thin. Many modern diets and dietary schemesmay result in malnutrition and emaciationand, therefore,may be confusedwith anorexianervosa.Dental abrasionand erosion, singly or in combination,may result in a considerableloss of tooth structure.Abrasion may be brought aboutby the use of tobacco, betel nuts, dentifrice, hard toothbrushes,and parafunctionalhabits, such as bruxism, abnormalswallowing, and clenching. Erosion may be idiopathic or a result of excessiveconsumption of fruits, such as lemons. THERAPY Psychiatric treatment
It is extremelyimportantthat the dentistwork closely with the patient’spersonalphysicianand psychiatristin the managementof the personwith anorexianervosa.A favorableprognosisis dependentupon the successof psychiatrictherapy. Dietary changes and nutritional supplements
If the physicianincreasesthe amountof carbohydrate in the patient’sdiet, therewill alsobe an increasein the deleteriouseffects of carbohydrateson the patient’s damaged dentition. The dentist should discuss the cariogenic nature of carbohydrateswith the patient’s physician, and perhaps a different dietary approach could be used. For example, increasingthe patient’s protein intake will benefit his general health while being less damagingto the dentition. In 1975 RuggGunn and associates14 showedthat cheeseraisesthe pH and the calcium concentrationof dental plaque, thus resulting in an anticarieseffect. Sedatives, antidepressives and anttspasmotics
These medicationsare used in the treatmentof the patient’s anxiety and depressionstates,along with the vomiting habit. Prophylaxis, fluorides, and oral hygiene
In early and less severecasesof anorexianervosa, the dentist should try to impressupon the patient that severedestructiveeffectson the hard and soft tissuesof the mouth will occur if this problem is not eliminated. Most patients, young personsin particular, are quite disturbedwhen it is suggestedthat they will eventually loose all their teeth. Theseearly casesof anorexianervosa should be given frequent prophylaxis and oral hygienereinforcement.In severecasesfrequentcareful prophylaxisand fluoride treatmentsare helpful because
512 Brudy
Oral Surg. December, 1980
Fig. 1. Abnormal growth of fine downy hair as seen in hirsutism.
of the loss of enamel.The use of 0.05 percentsodium fluoride rinses will also reduce sensitivity of exposed dentin and increasecariesresistance.”Holloway, Mellanby, and StewartI4 found a 30 percent reduction in erosion after topical application of sodium fluoride (2 parts/10 percentF). Dental restorative treatment
This shouldbe mainly preventiveand palliative until the patient’s physician reports that progresshas been made in the patient’s treatment.This would mean that vomiting is no longer a problem. The dentist will be aware of such obvious changesin the patient as increase in weight, improved personal appearance,reduced anxiety, and improved mental attitude. The patient will exhibit increasedinterestin his or her general and oral health, the latter being exemplified by improved oral hygiene. Synthetic restoration materials, such as plastics, silicates, composites,and amalgams, should be used in early or less severecases.However, in caseswhere loss of tooth structure is not extensive but the caries rate is high, silicate, becauseof its fluoride content, would be preferableto composite.In severecases the restoration of lost tooth structure is best accomplishedby full and partial cast restorations. CASE REPORT On April 29, 1976, a 20-year-old Caucasian woman presented complaining of sensitivity of the upper and lower anterior teeth. She was experiencing pain on chewing and from hot and cold liquids. Clinical and radiographic examination revealed a loss of enamel from the lingual surfaces of all upper and lower anterior teeth, resulting in exposed dentin. The posterior teeth showed decalcification at the buccal and lingual gingival areas as well as loss of occlusal enamel. There was no evidence of caries or periapical pathosis. Oral
Figs. 2 and 3. Extensive loss of enamel and dentin on the lingual surfaces of the upper and lower anterior teeth.
hygiene level was good, and only minimal gingival inflammation was present. Physical examination revealed that the patient appeared underweight and emaciated. Her clavicles and pelvic bones were very prominent, and she showed very little breast development. An excessive growth of hair was noted about the face. The vital signs were as follows: height, 5 feet 4 inches; weight, 90 pounds; pulse, 60; respiration, 20; blood pressure, 102/80; and temperature, 98.3” F. The past medical history was essentially normal, except for menstrual irregularity. A review of the dental record revealed that the patient had undergone dental examinations at yearly intervals. She had received systemic fluorides up to age 12, along with professional oral hygiene instruction. Three impacted third molars were removed in 1973. These extractions were routine, with minimal postoperative problems. At this time the patient might be described as being very attractive, 17 years old, athletic, intelligent (honor student), 5 feet 4 inches tall, and weighing 135 pounds. Her general health was excellent and,
outsideof beingslightly hyperactiveand in needof a great deal of attention, her psychological profile was essentially normal.
Volume 50 Number 6
Anorexiu nerwsa syndrome 513
Fig. 4. Loss of enamel and dentin on the facial and incisal surfaces of the maxillary and mandibular anterior teeth. These changes have resulted in a decreased vertical dimension and a loss of anterior guidance. In January, 1974, the last of her impacted third molars was removed. Unlike the previous three impactions, this one proved to be extremely difficult and, as a result, her postoperative problems were quite severe. They included pain, swelling, trismus, and infection. The infection was controlled with antibiotics and the pain with A.P.C. and codeine. Considerable nausea and vomiting occurred, and the patient lost 11 pounds in 2 weeks. The patient was next seen approximately 8 months later for a routine examination. Small white areas were noted at the buccal gingival aspect of the lower first and second molars. These areas had not been present previously and appeared to be decalcifications. She was asked if she had increased her consumption of sugar, particularly acid beverages and fruits. Her reply was negative. She asked if 1 noticed how thin she was. She attributed the loss of 15 pounds to a special diet. It seems that prior to the last third molar removal the patient was becoming quite concerned about her weight. The loss of weight during the postoperative period following that difficult extraction because of her inability to keep food down led her to consider, and consequently adopt, induced vomiting as a weight-control method. The patient denied induced vomiting, even when caught in the act by her parents, and refused medical help when it was offered. In May, 1976, after a review of her and medical and dental history and consultation with her parents, the following recommendations were made: (1) immediate medical attention; (2) the importance of being completely honest with her physician when discussing her problem; (3) dental treatment at this time would be limited to frequent prophylaxis and fluoride treatments; (4) oral hygiene procedures would be reviewed and fluoride rinses would be prescribed. The patient agreed to see her physician who, after reviewing her case, recommended consultation with an endocrinologist. After complete examination, including a physical examination, laboratory tests, and a review of the patient’s medical history, a diagnosis of anorexia nervosa was made.
Figs. 5 and 6. Loss of enamel and dentin from the upper and lower anterior teeth 5 years later.
514
Brady
Oral Surg. December, 1980
Figs. 7 and 8. Normal posterior teeth, 1972.
Figs. 9 and 10. Loss of enamel and dentin from the occlusal and interproximal surfaces 5 years later.
The endocrinologist strongly recommended psychiatric therapy as the best possible solution to this problem. The patient declined these recommendations, for undetermined reasons. The patient was not seen again until Feb. 19, 1979. She complained of sensitivity and pain in her teeth when eating and drinking. She stated that her teeth appeared shorter and felt rough in many areas. At this time the medical history was updated, vital signs were recorded, and a clinical examination of hard and soft tissues was made. Full-mouth radiographs, mounted diagnostic study casts, and oral photographs were also taken. Resting and simulated salivary samples were taken. The results of these diagnostic procedures were as follows: The systemic manifestations of this syndrome, found in 1976, had greatly increased in severity. For example, her weight was now approximately 8.5pounds and her appearance was one of emaciation. Hirsutism had increased, as can be seen in Fig. 1. The oral manifestations were far more severe than in 1974 and 1976. Perimylolysis had increased to the extent that it now involved all tooth surfaces (Figs. 2, 3, 4, 13, and 14). The pulp chambers were visible clinically on the lingual surfaces of the lower anterior teeth and on the palatal surfaces of the upper anterior teeth. A comparison of the 1972 radiographs with those taken in 1979 clearly illustrates the extensive loss of enamel and dentin (Figs. 5 to 12). The margins of
the amalgam restorations were now above the level of the tooth structure (Figs. 13 and 14). Gingivitis (Fig. 4) was still only a minor problem and there was no dental caries present at this time. The pH of both resting and simulated saliva was found to be reduced, along with the saliva’s buffering capacity. The patient had suffered a decrease in vertical dimension because of the loss of occlusal and incisal tooth structure (Figs. 4, 13, and 14). A very traumatic group function type of occlusion with prematurities and a lateral slide had now replaced the mutually protected anterior guidance relationship. Parafunctional habits, such as bruxism and clenching, also developed, perhaps as a result of the patient’s severe psychological problems. The patient was seen on March 10, 1979, for consultation. At this time the findings were presented along with the proposed treatment. Since the patient had previously rejected professional help with her problem, it was decided that “a lay the cards on the table” approach might help her realize the seriousness of the situation. It was emphasized that the over-all prognosis of her case at this point was very poor. She was progressively destroying not only her dentition but herself as well. Without psychiatric help, the end result would be complete loss of her natural dentition and ultimately her life as well. It was proposed that dental treatment be done in two phases. The first phase would include prophylaxis, fluoride
Volume 50 Number 6
Anorexia nervma syulrome
Figs. 11 and 12. Normal upper and lower anterior teeth, 1972.
Figs. 13 and 14. Loss of enamel and dentin from the occlusal, buccal, and lingual surfaces of the posterior teeth.
5 15
516 Brady treatments, oral hygiene reinforcement, occlusal adjustment, and night guard construction. During this phase the patient would be receiving psychotherapy. When her psychiatrist thought that satisfactory progress was being made, the second phase of her dental therapy would be initiated. Evidence of progressin the treatmentof anorexia nervosa would include the following: elimination of the induced vomiting habit, weight gain, improvement of personality profile, return of menstrual regularity, etc. The dental treatment at this point would involve a full-mouth reconstruction to restore lost tooth structure and vertical dimension and establish proper esthetics and a stable occlusion. It became obvious at this point that the patient had not
previously realized how seriousher situation really was. The extent of both the medical and dental treatmentneeded,along with its cost, seemed to shock her and she agreed to see a psychiatrist. She is currently undergoing therapy.
SUMMARY Anorexia nervosa, once considered a rare illness, is now increasing at a disturbing rate. Changes in culturally determined attitudes in recent years have removed much of the social class bias for this syndrome. It can no longer be considered a problem of any particular group based on age, sex, or social class. In anorexia nervosa, as in any other disease process, it is important to make a diagnosis as early as possible in order to ensure a favorable prognosis. The dentist is in a unique position, since he sees patients more frequently than the physician, which gives him an opportunity to detect the presence of this syndrome in its early stages. The clinical manifestations of the disease, both systemic and oral, have been described and illustrated. Familiarity with the nature of this serious disease process will better serve the needs of patients.
Oral Surg. December, 1980 REFERENCES
1. Gull, W. W.: Anorexia Nervosa (Apepsia Hysterica, Anorexia Hysterica), Trans. Clin. Sot. Lond. 7: 22, 1874. 2. Hellstrom, I.: Oral Complications in Anorexia Nervosa, Stand.
J. Dent. Res. 85: 71-86, 1977. 3.
Krupp, M. A., and Chatton, M. J.: Current Medical Diagnosis Treatment, ed. 16, Los Altos, Calif.,
1977, Lange Medical
Publications, p. 764. 4. Thoma, H.: Anorexia Nervosa, Bern-Stuttgart, 5. 6. 7. 8. 9.
10.
11. 12
13.
14.
1961, KuberKlett. Meyer, J. E., and Feldmann, H.: Anorexia Nervosa Symposium in Gottinger, Stuttgart, 1965. Masland, R. P., Jr.: Medical Problems of the Adolescent, Dent. Clin. North Am. 13: 303-311, 1969. Theander, S.: Anorexia Nervosa, Acta Psychiatr. Stand., Suppl. __ 214, 1970. Thoma, K.: Anorexia Nervosa, New York, 1967, International Universities Press. Lyght, C. E. (Editor): The Merck Manual of Diagnosis and Therapy, ed. 11, Rahway, N. J., 1966, Merck, Sharp & Dohme Research Laboratories, pp. 1120-l 122. Beeson, P. B., and McDermott, W.: Textbook of Medicine, ed. 14, Philadelphia, 1975, W. B. Saunders Company, pp. 13861387. Hellsborn, I.: Anorexia Nervosa-Odontologic Problems, Sven. Tandlak. Tidskr. 67: 253-269, 1974. Baden, E.: Environmental Pathology of the Teeth, In Gorlin, R. J., and Goldman, K. M. (editors): Thoma’s Oral Pathology, ed. 6, St. Louis, 1970, Tbe C. V. Mosby Company, chap. 4. Rugg-Gunn, A. J., Edgar, W. M., Geddes, D. A. M., and Jenkins, G. N.: The Effect of Different Meal Patterns Upon PlaquepH in Human Subjects, Br. Dent. J. 139: 351-356, 1975. Holloway, P. J., Mellanby, M., and Stewart, R. J. C.: Fruit Drinks and Tooth Erosion, Br. Dent. J. 104: 305-309, 1958.
Reprint
requests to:
Dr. William F. Brady Department of Diagnostic Sciences University of Southern California School of Dentistry
West 34th St. Los Angeles, Calif. 90007
925
The anorexia nervosa syndrome William F. Brady, B.A., D.M.D., UNIVERSITY
OF SOUTHERN
F.A.G.D.,*
CALIFORNIA
SCHOOL
El Cajon, Calif. OF DENTISTRY
This article reviews the medical and dental literature on the anorexia nervosa syndrome and presents the oral and systemic manifestations of this serious disease process. A case is reported which demonstrates the generalized destruction of tooth structure, primarily as a result of the direct effect of gastric acid on this patients dentttion during a Iyear period of self-induced vomiting. The systemic, psychological, and social aspects of this syndrome are classically illustrated in this case history.
norexia nervosawas first describedby Sir William A Gull’ in 1868. It was once considereda relatively uncommon but serious disorder. In the last 10 years, however, its incidence has increased considerably. Early diagnosis and treatment of this problem is extremely important if one is to ensurea favorable prognosis. Close cooperationbetweenthe physician and the dentist is in the best interest of the patient and will result in an improved prognosis, not only from a medical but also from a dental point of view. While the dental complications in this syndrome, unlike the systemic effects, may not result in the deathof the patient, they neverthelessmay result in the destruction of the patient’s dentition. The cause-and-effectrelationship betweenthe regurgitationof gastric acid and the loss of enamel and dentin was first reportedin the literature by Hellstrom in 1977. In a previous article, in 1974, Hellstrom had stated that the association of anorexia nervosawith induced vomiting and loss of enamel and dentin had never been reported in the literature. The systemic manifestationsof the anorexianervosa syndrome are usually presentbefore the appearanceof the oral and dental disturbances.An alert dental practitioner may discover these disturbances during the routine review of the patient’s physical examination *Assistant
Professor,
Department
M)30-4220/80/120509+08$00.80/0
of Diagnostic
0
Sciences
1980 The C. V. Mosby Co
and medical history. Since the dentist recalls patients more frequently than the physician, he/she is in an excellent position to recognize the early signs and symptoms of this disease.Prompt referral to and consultation with the patient’s physician will greatly improve the prognosis of this condition. A review of the medical literature reveals an alarming increasein this condition. For example, in 1968the Index Medicus listed 41 publications under anorexia nervosa. Ten years later (1978) there were 136 publications listed. Oral and dental manifestations were absent from these publications. If left unattendedor inadequatelytreated, the patient may succumb to inanition, complicating infection, or suicide.”In view of the seriousnessof this disease,it is easy to seehow the medical profession could consider the oral and dental findings less significant. A survey of the dental literature revealed only six publications under anorexianervosa.Only one of these ,articles appearedin the American literature, and this article made no mention of any possible dental or oral manifestations. By definition, anorexia nervosa is a chronic psychosomatic illness manifesting itself primarily as an eating disorder. The use of the term anorexia with this diseaseis actually a misnomer, since there is no real appetite loss. The reverse usually occurs, the patient 505
510
Brady
claims to have appetite loss, but alternates food avoidancewith overeating and follows this with induced vomiting. The exact cause of anorexia nervosa is unknown. This illness can be viewed from two aspects.The most probable would be psychologic, especially from conflicts engenderedby the experienceof puberty and adolescence.Thorna and Meyer and Feldman5defined the patient’s attitude toward food as a psychotic process. In spite of an emaciatedappearance,the patient perceivesherself as fat, lacks the capacity for emotional experiences,and builds up a senseof security by refraining from food. Periodsof both physical and intellectual hyperactivity are common. The secondprobableetiologic factor in anorexianervosa is neuroendocrinein origin. A disturbancein the “feeding center” in the hypothalamushas beenpostulated on the basisof experimentalstudiesin animalsbut has not been clearly establishedin human beings.3 This syndromedevelops from puberty through the 40’s, the mostcommontime of onsetbeingbetweenthe agesof 14 and 17 years.It occursin femalesat leastten times more often than in males.5,6 An even higher female predilection was reportedin a study by TheanderG7In his group of patients there was a 20 to 1 predominanceof females over males. Thoma,sin 1967, also reported an increasingfrequencyof anorexianervosa in females.Thesepatientsoften becomeobsessed with the idea of being thin, and this resultsin a constant searchfor diets and ways to reducetheir size. Often an ambitious,intelligent, model child, with a fear of adult responsibilitieswhen growing up attempts to escape from this difficult situation by food denial. The patient often has an inner compulsionagainsteating, and every intake of food causesanxiety. The presentincreasing incidence of anorexia nervosa m ight be explainedby the presentemphasison and!socialacceptabilityof having a slender figure in our/society, especially among young women. The systemicmanifestationsof anorexianervosainclude the following: A previously normal 1. SpeciJic psychopathology. personmay show changesin temperament,consisting of impatience,irritability, and depression. There also may have been a precedinghistory of food fads or difficulty in making friends. 2. Self-induced starvation. This is the most characteristic symptom of the diseaseand results in severe weight loss and emaciation. This is “achieved” by strict dieting, in combinationwith orgiastric bouts of overeating(bulimia) followed by self-inducedvomiting or excessiveexercising. Severeweaknessand apathy may alternatewith periods of unusual strength and hyperactivity.
Oral surg. December, 1980
The patient may appeargaunt and weigh as little as 70 pounds.gThe limbs are very thin, the abdomenis flat, and bony prominencessuch as the clavicles and pelvic bonesstand out sharply. 3. Dehydration
and electrolyte balance disturbance.
Chronic episodesof frequent vomiting result in severedehydration.Serumpotassiumis the electrolyte most commonlydepleted.Theremay also be a moderatefall in serumsodium.Dry skin may be anothercommonfinding. 4. Amenorrhea. The patient’s urinary output of gonadotrophinsand estrogensis decreased. lo The blood level of estrogensis also found to be low. There is a decreasein the activity of the ovaries, and postmortemexaminationhas demonstrated atrophy of the ovaries.6The menstrualcycle is thus altered,and menstrualperiodsmay be absent for long periods of time. Even after a patient recovers from anorexianervosa,the menstrualperiod may be very slow in returning to normal. 5. Hirsutism. The patient exhibits an abnormal or unusualgrowth of fine downy hair, particularly over the arms, legs and facee3 6. Thermoregulation disorder. The body temperature may be reducedby 1” C. The patient often complainsof intoleranceto cold, with the hands and feet being particularly affected.‘O Oral and dental manifestationsof anorexianervosa include the following: 1. Perimylolysis. This is a severedental manifestation of anorexia nervosa. Hellstrom” defined “perimylolysis as a loss of enameland dentin on the lingual surfacesof the teeth as a result of chemical and mechanicaleffects causedmainly by regurgitationof gastric contentsand activated by the movementsof the tongue.” In severe chronic cases, such as the case reported in this article, all surfacesof the teeth may be affected by this acid erosion. Hellstrom” felt that where buccal erosion was presented,it m ight be due to excessivecomsumptionof fruits andjuices by the patient in order to relieve thirst after vomiting. Parafunctionalhabits, such as bruxism, clenching, and abnormalswallowing habits, m ight also contribute to loss of tooth structure. 2. Dental caries. An excessivecarbohydrateintake and poor oral hygienemay result in an increasein dental caries in thesepatients. Medicationsprescribedby the patient’sphysiciancould contribute to an increasein caries incidence. Examplesof such medicationsare dextrosetablets, Meritene (contains lactose), vitamin C drinks containing sucrose,etc.” 3. Periodontal disease. Periodontal problems are
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common in the anorexia nervosapatient, with gingivitis being the most prevalent. 4. Saliva. The quality, quantity, buffering capacity, and PH of both resting and simulatedsaliva are found to be reduced. Prescribedsedatives,antidepressives,and antispasmoticsmay induce xerostomiain the anorexianervosapatient. Systemic complications,suchasmalnutrition, malabsorption,hormonaldisorders,anemia,andanxiety states,are also associatedwith reducedsecretion of saliva.2 5. Oral mucous membranes. Tissue health is impaired becauseof xerostomia and the resulting reductionin the membrane-lubricatingeffects of the saliva. The possiblelong-term effects of regurgitated gastric acid on esophageal,pharyngeal, and oral tissueshas yet to be reported. I believe that in severechronic casesof this syndrome, wherethe patient might survivefor many years, therecould possiblybe malignantchanges in the involved tissuesdueto the chronicirritating effects of years of vomiting. Two excellent studies were conducted by Hellstrom”, l2 in 1974 and 1977. In both studiesthe patients were divided into two groups,vomiting and nonvomiting. In contrastto the 1974 study, the 1977study revealeda high incidenceof dentalcariesin the vomiting group as well as in the nonvomiting group. This may be explained by the fact that the study had a greaternumberof patientswith excessivecarbohydrate ingestionwho were vomiting for longerperiodsof time than the previous study. The 1974 study showedthat wherefrequentvomiting occurredover long periodsthe clinical appearance was dominatedby erosionwith low incidence of plaque, gingivitis, and caries. Hellstrom** I1 attributed this to the alteration of bacterial plaque by the acid nature of the gastric juice. Thus, bacterial plaque growth was reduced and perimylolysis was increased.Thosepatientswho vomited infrequently or not at all showedno perimylolysis and increasedcaries. Also contrary to the findings in the earlier study, dental plaque was presentto the same extent in both groups. Therefore,vomiting apparently does not affect the quantity and quality of dental plaque. Buccal erosionwas presentin almost all cases of the vomiting group but rare in the nonvomiting patients. The 1974 study did not revealbuccal erosionin the vomiting group. This was probablyagaindue to the short history of vomiting in the first study. DIFFERENTIAL DIAGNOSIS
Included in the differential diagnosisare conditions that involve vomiting, such as pregnancy,pyloric stenosis, strictureor spasmof the esophagus,and gastro-
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intestinal tract peristalsisdisturbance.I2 Conditionsresulting in short-termepisodesof vomiting would not have severe destructive effects on the dentition. Anorexia nervosashould not be confusedwith what seemsto be a constantstriving to be thin. Many modern diets and dietary schemesmay result in malnutrition and emaciationand, therefore,may be confusedwith anorexianervosa.Dental abrasionand erosion, singly or in combination,may result in a considerableloss of tooth structure.Abrasion may be brought aboutby the use of tobacco, betel nuts, dentifrice, hard toothbrushes,and parafunctionalhabits, such as bruxism, abnormalswallowing, and clenching. Erosion may be idiopathic or a result of excessiveconsumption of fruits, such as lemons. THERAPY Psychiatric treatment
It is extremelyimportantthat the dentistwork closely with the patient’spersonalphysicianand psychiatristin the managementof the personwith anorexianervosa.A favorableprognosisis dependentupon the successof psychiatrictherapy. Dietary changes and nutritional supplements
If the physicianincreasesthe amountof carbohydrate in the patient’sdiet, therewill alsobe an increasein the deleteriouseffects of carbohydrateson the patient’s damaged dentition. The dentist should discuss the cariogenic nature of carbohydrateswith the patient’s physician, and perhaps a different dietary approach could be used. For example, increasingthe patient’s protein intake will benefit his general health while being less damagingto the dentition. In 1975 RuggGunn and associates14 showedthat cheeseraisesthe pH and the calcium concentrationof dental plaque, thus resulting in an anticarieseffect. Sedatives, antidepressives and anttspasmotics
These medicationsare used in the treatmentof the patient’s anxiety and depressionstates,along with the vomiting habit. Prophylaxis, fluorides, and oral hygiene
In early and less severecasesof anorexianervosa, the dentist should try to impressupon the patient that severedestructiveeffectson the hard and soft tissuesof the mouth will occur if this problem is not eliminated. Most patients, young personsin particular, are quite disturbedwhen it is suggestedthat they will eventually loose all their teeth. Theseearly casesof anorexianervosa should be given frequent prophylaxis and oral hygienereinforcement.In severecasesfrequentcareful prophylaxisand fluoride treatmentsare helpful because
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Oral Surg. December, 1980
Fig. 1. Abnormal growth of fine downy hair as seen in hirsutism.
of the loss of enamel.The use of 0.05 percentsodium fluoride rinses will also reduce sensitivity of exposed dentin and increasecariesresistance.”Holloway, Mellanby, and StewartI4 found a 30 percent reduction in erosion after topical application of sodium fluoride (2 parts/10 percentF). Dental restorative treatment
This shouldbe mainly preventiveand palliative until the patient’s physician reports that progresshas been made in the patient’s treatment.This would mean that vomiting is no longer a problem. The dentist will be aware of such obvious changesin the patient as increase in weight, improved personal appearance,reduced anxiety, and improved mental attitude. The patient will exhibit increasedinterestin his or her general and oral health, the latter being exemplified by improved oral hygiene. Synthetic restoration materials, such as plastics, silicates, composites,and amalgams, should be used in early or less severecases.However, in caseswhere loss of tooth structure is not extensive but the caries rate is high, silicate, becauseof its fluoride content, would be preferableto composite.In severecases the restoration of lost tooth structure is best accomplishedby full and partial cast restorations. CASE REPORT On April 29, 1976, a 20-year-old Caucasian woman presented complaining of sensitivity of the upper and lower anterior teeth. She was experiencing pain on chewing and from hot and cold liquids. Clinical and radiographic examination revealed a loss of enamel from the lingual surfaces of all upper and lower anterior teeth, resulting in exposed dentin. The posterior teeth showed decalcification at the buccal and lingual gingival areas as well as loss of occlusal enamel. There was no evidence of caries or periapical pathosis. Oral
Figs. 2 and 3. Extensive loss of enamel and dentin on the lingual surfaces of the upper and lower anterior teeth.
hygiene level was good, and only minimal gingival inflammation was present. Physical examination revealed that the patient appeared underweight and emaciated. Her clavicles and pelvic bones were very prominent, and she showed very little breast development. An excessive growth of hair was noted about the face. The vital signs were as follows: height, 5 feet 4 inches; weight, 90 pounds; pulse, 60; respiration, 20; blood pressure, 102/80; and temperature, 98.3” F. The past medical history was essentially normal, except for menstrual irregularity. A review of the dental record revealed that the patient had undergone dental examinations at yearly intervals. She had received systemic fluorides up to age 12, along with professional oral hygiene instruction. Three impacted third molars were removed in 1973. These extractions were routine, with minimal postoperative problems. At this time the patient might be described as being very attractive, 17 years old, athletic, intelligent (honor student), 5 feet 4 inches tall, and weighing 135 pounds. Her general health was excellent and,
outsideof beingslightly hyperactiveand in needof a great deal of attention, her psychological profile was essentially normal.
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Fig. 4. Loss of enamel and dentin on the facial and incisal surfaces of the maxillary and mandibular anterior teeth. These changes have resulted in a decreased vertical dimension and a loss of anterior guidance. In January, 1974, the last of her impacted third molars was removed. Unlike the previous three impactions, this one proved to be extremely difficult and, as a result, her postoperative problems were quite severe. They included pain, swelling, trismus, and infection. The infection was controlled with antibiotics and the pain with A.P.C. and codeine. Considerable nausea and vomiting occurred, and the patient lost 11 pounds in 2 weeks. The patient was next seen approximately 8 months later for a routine examination. Small white areas were noted at the buccal gingival aspect of the lower first and second molars. These areas had not been present previously and appeared to be decalcifications. She was asked if she had increased her consumption of sugar, particularly acid beverages and fruits. Her reply was negative. She asked if 1 noticed how thin she was. She attributed the loss of 15 pounds to a special diet. It seems that prior to the last third molar removal the patient was becoming quite concerned about her weight. The loss of weight during the postoperative period following that difficult extraction because of her inability to keep food down led her to consider, and consequently adopt, induced vomiting as a weight-control method. The patient denied induced vomiting, even when caught in the act by her parents, and refused medical help when it was offered. In May, 1976, after a review of her and medical and dental history and consultation with her parents, the following recommendations were made: (1) immediate medical attention; (2) the importance of being completely honest with her physician when discussing her problem; (3) dental treatment at this time would be limited to frequent prophylaxis and fluoride treatments; (4) oral hygiene procedures would be reviewed and fluoride rinses would be prescribed. The patient agreed to see her physician who, after reviewing her case, recommended consultation with an endocrinologist. After complete examination, including a physical examination, laboratory tests, and a review of the patient’s medical history, a diagnosis of anorexia nervosa was made.
Figs. 5 and 6. Loss of enamel and dentin from the upper and lower anterior teeth 5 years later.
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Figs. 7 and 8. Normal posterior teeth, 1972.
Figs. 9 and 10. Loss of enamel and dentin from the occlusal and interproximal surfaces 5 years later.
The endocrinologist strongly recommended psychiatric therapy as the best possible solution to this problem. The patient declined these recommendations, for undetermined reasons. The patient was not seen again until Feb. 19, 1979. She complained of sensitivity and pain in her teeth when eating and drinking. She stated that her teeth appeared shorter and felt rough in many areas. At this time the medical history was updated, vital signs were recorded, and a clinical examination of hard and soft tissues was made. Full-mouth radiographs, mounted diagnostic study casts, and oral photographs were also taken. Resting and simulated salivary samples were taken. The results of these diagnostic procedures were as follows: The systemic manifestations of this syndrome, found in 1976, had greatly increased in severity. For example, her weight was now approximately 8.5pounds and her appearance was one of emaciation. Hirsutism had increased, as can be seen in Fig. 1. The oral manifestations were far more severe than in 1974 and 1976. Perimylolysis had increased to the extent that it now involved all tooth surfaces (Figs. 2, 3, 4, 13, and 14). The pulp chambers were visible clinically on the lingual surfaces of the lower anterior teeth and on the palatal surfaces of the upper anterior teeth. A comparison of the 1972 radiographs with those taken in 1979 clearly illustrates the extensive loss of enamel and dentin (Figs. 5 to 12). The margins of
the amalgam restorations were now above the level of the tooth structure (Figs. 13 and 14). Gingivitis (Fig. 4) was still only a minor problem and there was no dental caries present at this time. The pH of both resting and simulated saliva was found to be reduced, along with the saliva’s buffering capacity. The patient had suffered a decrease in vertical dimension because of the loss of occlusal and incisal tooth structure (Figs. 4, 13, and 14). A very traumatic group function type of occlusion with prematurities and a lateral slide had now replaced the mutually protected anterior guidance relationship. Parafunctional habits, such as bruxism and clenching, also developed, perhaps as a result of the patient’s severe psychological problems. The patient was seen on March 10, 1979, for consultation. At this time the findings were presented along with the proposed treatment. Since the patient had previously rejected professional help with her problem, it was decided that “a lay the cards on the table” approach might help her realize the seriousness of the situation. It was emphasized that the over-all prognosis of her case at this point was very poor. She was progressively destroying not only her dentition but herself as well. Without psychiatric help, the end result would be complete loss of her natural dentition and ultimately her life as well. It was proposed that dental treatment be done in two phases. The first phase would include prophylaxis, fluoride
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Figs. 11 and 12. Normal upper and lower anterior teeth, 1972.
Figs. 13 and 14. Loss of enamel and dentin from the occlusal, buccal, and lingual surfaces of the posterior teeth.
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516 Brady treatments, oral hygiene reinforcement, occlusal adjustment, and night guard construction. During this phase the patient would be receiving psychotherapy. When her psychiatrist thought that satisfactory progress was being made, the second phase of her dental therapy would be initiated. Evidence of progressin the treatmentof anorexia nervosa would include the following: elimination of the induced vomiting habit, weight gain, improvement of personality profile, return of menstrual regularity, etc. The dental treatment at this point would involve a full-mouth reconstruction to restore lost tooth structure and vertical dimension and establish proper esthetics and a stable occlusion. It became obvious at this point that the patient had not
previously realized how seriousher situation really was. The extent of both the medical and dental treatmentneeded,along with its cost, seemed to shock her and she agreed to see a psychiatrist. She is currently undergoing therapy.
SUMMARY Anorexia nervosa, once considered a rare illness, is now increasing at a disturbing rate. Changes in culturally determined attitudes in recent years have removed much of the social class bias for this syndrome. It can no longer be considered a problem of any particular group based on age, sex, or social class. In anorexia nervosa, as in any other disease process, it is important to make a diagnosis as early as possible in order to ensure a favorable prognosis. The dentist is in a unique position, since he sees patients more frequently than the physician, which gives him an opportunity to detect the presence of this syndrome in its early stages. The clinical manifestations of the disease, both systemic and oral, have been described and illustrated. Familiarity with the nature of this serious disease process will better serve the needs of patients.
Oral Surg. December, 1980 REFERENCES
1. Gull, W. W.: Anorexia Nervosa (Apepsia Hysterica, Anorexia Hysterica), Trans. Clin. Sot. Lond. 7: 22, 1874. 2. Hellstrom, I.: Oral Complications in Anorexia Nervosa, Stand.
J. Dent. Res. 85: 71-86, 1977. 3.
Krupp, M. A., and Chatton, M. J.: Current Medical Diagnosis Treatment, ed. 16, Los Altos, Calif.,
1977, Lange Medical
Publications, p. 764. 4. Thoma, H.: Anorexia Nervosa, Bern-Stuttgart, 5. 6. 7. 8. 9.
10.
11. 12
13.
14.
1961, KuberKlett. Meyer, J. E., and Feldmann, H.: Anorexia Nervosa Symposium in Gottinger, Stuttgart, 1965. Masland, R. P., Jr.: Medical Problems of the Adolescent, Dent. Clin. North Am. 13: 303-311, 1969. Theander, S.: Anorexia Nervosa, Acta Psychiatr. Stand., Suppl. __ 214, 1970. Thoma, K.: Anorexia Nervosa, New York, 1967, International Universities Press. Lyght, C. E. (Editor): The Merck Manual of Diagnosis and Therapy, ed. 11, Rahway, N. J., 1966, Merck, Sharp & Dohme Research Laboratories, pp. 1120-l 122. Beeson, P. B., and McDermott, W.: Textbook of Medicine, ed. 14, Philadelphia, 1975, W. B. Saunders Company, pp. 13861387. Hellsborn, I.: Anorexia Nervosa-Odontologic Problems, Sven. Tandlak. Tidskr. 67: 253-269, 1974. Baden, E.: Environmental Pathology of the Teeth, In Gorlin, R. J., and Goldman, K. M. (editors): Thoma’s Oral Pathology, ed. 6, St. Louis, 1970, Tbe C. V. Mosby Company, chap. 4. Rugg-Gunn, A. J., Edgar, W. M., Geddes, D. A. M., and Jenkins, G. N.: The Effect of Different Meal Patterns Upon PlaquepH in Human Subjects, Br. Dent. J. 139: 351-356, 1975. Holloway, P. J., Mellanby, M., and Stewart, R. J. C.: Fruit Drinks and Tooth Erosion, Br. Dent. J. 104: 305-309, 1958.
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