- Email: [email protected]
Bruxism in allergic children
Bruxism
in
allerqie . children,
Meyer B. Marks, M.D. Miami
Beach,
F/a.
A study of hruxism (tooth grinding) )vas cvnducted at the Universi~ @Miami School of’ Medicine, at Jackson Memorial Hospital, Miami. Florida, and at rhe Sleep Disorders Center, Mount Sinai Medical Center, Miami Beach, Florida. A thret$old incidence c?f this pernicious oral habit in allergic c,hildren was di.wlosed t1.v compared to nonallergic children. Dental literature stresses psychogenic firctors, oc(~lusal maladjustments, systemic conditions, and occupational pursuits Jcthich do not pertain to most children. Allergy is rarely considered. Nocturnal hruxism may be initiated reflexly by increused negative pressures in the tympanic cavities from intermittent allergic edema qf the mucosa qf the Eustachian tubes. Embrvologic. unatomic. and neurologic relationships between the mu.scles qf the eardrum. Eustachian tubes, and ,jtrws have a primordial, common ancestrv. Chronic middle ear disturbances mq promote reflex action to the juvvs bJ stimulating the trigeminal nuclei in the brain. Sleep studies at Mount Sinai Medical Center on ullergic. bruxing children have produced some interesting but incomplete results. We are attempting to develop sophisticated devices ,f& monitoring abnormal tubal ,funcriorr whic,h ma! Oc the (‘rux of the hruxism problem.
B
ruxism, or tooth grinding, is an oral habit that is indulged in by many adults and children, except in infancy before the appearance of the first dentition. A noticeable degree of nocturnal bruxism is apparent in children seen in the practice of pediatric allergy.” ’ This fact can be substantiated not only from the history but also by the frequent observation in children, of small ulcerations or ridging on the buccal mucosa opposite the molar teeth on one or both sides of the oral cavity (Fig. I). In addition, the Presented before the seventy-ninth May, 1979, Washington, D.C.
48
annual
session
of the American
GOO2.9416/80/010048+12$01.20/0
Association
0
of Orthodontists.
1980 The C
V
Mosby
Co
Volume II Number 1
Bruxism
in ullergic
children
49
Fig. 1. A, This a-year-old
asthmatic boy with perennial allergic rhinitis has an ulceration on the left buccal mucosa from bruxism (arrow). His tooth grinding can be heard throughout the house. He usually sleeps on his left side. Often such ulcerations are bilateral. B, This 22-year-old youth, who has bronchial asthma and chronic nasal allergy, shows bilateral “ridging” on the buccal mucosafrom bruxism (arrow). He has been a tooth-grinder since early childhood. From infancy to the age of 5 years, he was subject to frequent ear infections. C, This 44-year-old man with bilateral buccal “ridging” is a pronounced tooth grinder (arrow). He remembers having had many attacks of otitis media as a young child, and he has had perennial allergic rhinitis since infancy.
facets of the molar, canine, and even the incisor teeth often show marked wearing of the occlusal surfaces (Fig. 2).
This pernicious sleep disorder seems to be fairly prevalent, in that various investigators report an incidence of 5 to more than 20 percent.3 In a study conducted in the pediatric and pediatric allergy clinics at Jackson Memorial Hospital in Miami, Florida (Fig. 3)) the incidence of tooth grinding in nonallergic children was 20 percent. The latter constituted a control group from the same geographic area. In a similar group of allergic children, matched by age, sex, and color, it was found that 60 percent bruxed. Thus, there was a threefold incidence of bruxism in allergic children as compared with those who were apparently nonallergic. l Etiology
The literature on the etiology of this common oral habit is confined chiefly to dental textbooks and periodicals. An all-encompassing, critical review of bruxism by Glaros and
Fig. 2. A, Upper
incisor and canine teeth in same boy as in Fig. ?, A. Note the marked erosion of these teeth as compared to the lower ones, B, This Syear-old patient with bronchial asthma and allergic rhinitis is still subject to frequent attacks of secretory otitis media. His nocturnal bruxism is exceedingly audible. Note the marked, worn-down facets of all hts lower teeth. C, This lo-year-old child, afflicted with severe chronic asthma and nasal allergy, had been subject to frequent attacks of secretory otitis media up to the age of 6 years. He grinds his teeth Incessantly at nrght. Note ulcerations on the buccal mucosa (arrow). The facets of the canine, premolar. and molar teeth show the ground appearance of severe
nocturnal
bruxism.
Rao4 intimated that the disorder has been largely unexplored in the psychological realm because of an impasse between dental concepts of bruxism and those of psychophysiologic factors. Their review endeavored to show how physical. psychological, and neurophysiologic entities are involved in bruxism. Ramfjord and Ash,j stated that there are three mechanisms that interact to trigger bruxism: emotional tensions, pain or discomfort, and occlusal maladjustments. They emphasized that a state of hypertonicity of the muscles of mastication ensues from central nervous system influences and occlusal disharmony. NadleP emphasized the causes of bruxism as (1) local, (2) systemic, (3) psychological, and (4) occupational. Meklas7 believed that psychogenic and local irritation factors outweighed other causes of bruxism. Local factors in children who grind their teeth include traumatic occlusion, dentigerous cysts, and faulty eruption of deciduous or permanent teeth. It has been suggested that bruxism may become a habit as a result of an unconscious attempt by the patient to establish contact with a greater number of teeth. Malocclusion, which is prominent in allergic children,8 interferes with the proper occlusion of teeth, with possible bruxism. In
Volume 11 Number 1
Bruxism
in allergic
children
51
BRUXISM IN ALLERGIC CHILDREN
Fig. 3. There gic children.
is a threefold
Fig. 4. Tympanometry patency of Eustachian
incidence
of nocturnal
apparatus which tubes, and acoustic
monitors reflexes.
bruxism
middle
in allergic
ear
children
pressures,
as compared
compliance
to nonaller-
of eardrums,
children the habit is frequently associated with the transition from the deciduous to the permanent dentition. Systemic factors are etiologically significant but are difficult to evaluate. Intestinal parasitic infestations may play a role. Frequently their eradication will reduce or even eliminate bruxism. Gastrointestinal disturbances from food allergy, enzymic imbalances in digestion causing chronic abdominal distress, and persistent, recurrent urologic dysfunction may be responsible for nocturnal bruxism. Miller,g as well as Brauer and colleagues,” discussed nutritional and vitamin deficiencies as possible elements for inducing tooth grinding. Endocrine disorders, particularly those relating to hyperthyroidism, may lead to bruxism. Many hyperkinetic children are bruxists. Nadler” believed that histamine released during stress may act as an exciting agent in the initiation of bruxism. He
52 Marh
Fig. 5. Ear probe transmits a sound noninvasive.
used in conjunction of known intensity
with the tympanometer. to the eardrum. It causes
It fits tightly into the pattent’s ear and no pain or discomfort and is entirely
observed that nocturnal clenching and gnashing of the teeth often allay symptoms of allergic itching and tickling of the palate and ears and aid in terminating episodes of sneezing and coughing. There is a significant statistical association between bruxists and their blood relatives.” The role that genetic influences play in tooth grinding cannot be ignored. It is not unusual in the practice of pediatric allergy to elicit a history of bruxism in several members of the same family. Psychogenic factors as the primary cause of bruxism seem to dominate the dental literature.4. “L ” Most investigators report that emotional tension may be expressed through a number of nervous habits, one of which is bruxism. Research studies have shown a positive relationship between tooth grinding and repressed aggression, unconscious expressions of oral gratification, and both conscious and unconscious anxiety. lsSI6 Meklas7 hypothesized that grinding the teeth may date back to prehistoric times when teeth were used as weapons. During stress or frustration, some persons regress, he reasoned, and express anger or hostility by grinding or gnashing their teeth. In our fastmoving, television-oriented, materialistic, and anxiety-ridden society, the child or adult is restricted by cultural demands to acceptable social behavioral patterns. Suppression of overt acts of hostility and aggression may result in an unconscious outlet in the form of nocturnal bruxism. HartI had earlier pointed out that the primitive gnashing of teeth carried on by our ancestors during the day when angry became repressed as we became “civilized” and has reasserted itself in sleep and dreams as an atavistic release mechanism. BartmeierlH suggested that children who have recently reached the point of vocal expression and who are restrained from self-assertion and the release of aggressive feelings often begin grinding their teeth. Reding and associates’” equated nocturnal bruxism
Volume 77 Number 1
Bruxism
in allergic
cchildren
53
BRUXISM IN ALLERGIC CHMREN El MALE UFEMALE
o-
o-
o-
o-
0, Fig. 6. Bar graph depicting were nocturnal hard-core
TOTAL
forty-six allergic tooth grinders.
children
BRUXIST NO-BRUXIST between
the ages
of 4 and 14 years.
Thirty
children
with periods of rapid eye movements (REM) indicative of dreaming. A later study by Reding and colleagues ,20 using a greater number of patients, disclosed that bruxism occurred in all stages of sleep, predominantly Stage 2. Broughton” hypothesized that sleep disorders, such as enuresis, sonnambulism, and nightmares, generally occur during a lightening of sleep. He believed that sleep disorders occur during the transitions from Stages 3 and 4 to Stages 1 and 2. During the transitional period, normal as well as bruxist subjects experience movement, autonomic discharge, and other signs of arousal. Tooth grinding can therefore be triggered by internal or external physical or emotional sleepdisturbing stimuli. Childhood bruxism may be related to other oral habits, such as chronic biting and chewing of toys and pencils, thumb- and finger-sucking, tongue thrusting, and mouth breathing. It has been reported that oral habits such as these are more common and prolonged into adolescence in allergic children.22 Occupational CUUS~S rarely can be considered in children, as employment for monetary gain does not usually apply. Athletes, whether amateur or professional, often indulge in bruxism because of their great desire to excel. Part-time occupations by students requiring precise measurements may lead to bruxism. 23 Compulsive overachievers who voluntarily work hard to succeed may eventually become involuntary or subconscious nocturnal bruxists.
BRUXISM IN ALLERGIC CHILDREN !ClJNT’DI 21 3il
E? MALE 0 FEMALE
TOTAL,’ SIG.ABil. Fig. 7. Twenty-one metric
Method
problems.
of the thirty bruxists Of sixteen nonbruxing
SIG.ABN.
demonstrated allergic chtldren,
NON-BRUXISTI SIG.ABN.
significant abnormal impedance only two had similar problems.
or tympano-
and materials
Electroacoustic impedance bridge studies to date have shown a high incidence of increased negative pressures in the middle ear cavities, with concomitant auditory tubal dysfunction in allergic bruxists. The apparatus, when used for tympanometry, is noninvasive and causes no pain or discomfort to the patient (Fig. 4). The examiner is allowed to place a tightly fitting ear probe into one of the child’s ears, occluding the external auditory canal (Fig. 5). In this manner, ear measurements, including middle ear pressures (negative and positive), compliance of the eardrum, patency of the Eustachian tube, and acoustic reflexes, are monitored. Investigations at the Division of Audiology, University of Miami School of Medicine, of forty-six allergic children between the ages of 4 and 14 years (sixteen females and thirty males) disclosed that thirty children were nocturnal tooth grinders (Fig. 6). All forty-six children manifested symptoms of either perennial allergic rhinitis, asthma, or combinations of both disorders. Occasionally, overt middle ear disease was present, but generally symptoms of otitis media in the children attending the Pediatric Allergy Clinic were uncommon, with the exception of hearing difficulties. Of the thirty who were bruxists, ten were girls and twenty were boys. Twenty-one children (Fig. 7) demonstrated significant abnormal impedance problems. including increased negative pressures above minus 100
Volume 77 Number 1
Bruxism
in allergic
children
55
BRUXISM IN ALLERGIC CHILDREN (CONT’D)
El MALE 0 fEMAlE
5t
3119
BRUXIST/NON-BRIJXIST/ PEilSISi. PERSIST: PERSIST. PROBLEMSPROBLEMSPROBLEMS Fig.
8. Repeated tympanometric allergic children had persistent bruxists.
studies for 1 year ear problems. Sixteen
disclosed that of the nineteen
nineteen patients
of the original forty-six were decided nocturnal
and middle ear effusions. Of these, six were girls and fifteen were boys. Of sixteen allergic nonbruxing children (Fig. 7) included in this report, only two had the same significant abnormal problems. Repeated audiometric studies for 1 year (Fig. 8) disclosed that nineteen of the original forty-six allergic patients continued to have persistent ear problems. Of the nineteen fifteen were boys and four were girls. Sixteen patients of this group (twelve boys and four girls) were decided nocturnal bruxists. Three children, all boys, gave no history of nocturnal bruxism, although they had abnormal tympanograms. Of the remaining twenty-seven allergic children, evidence of middle ear and auditory tubal dysfunction was encountered less frequently (Fig. 9). In this group, there were fourteen bruxists and thirteen nonbruxists. In the bruxist patients, there were seven boys and seven girls. In the nonbruxist children, there were eight boys and five girls. Discussion Nocturnal bruxism may be considered a universal sleep disorder of the greatest magnitude. It affects children and adults of all ages, with the possible exception of infants prior to eruption of the first dentition. It could be responsible for much dental pathosis and may be a major etiologic factor in temporomandibular joint dysfunction of adult life.
BRUXISM IN ALLERGIC CHllDREN ‘CONT’O]
14i27
13127
Oi TOTAL BRUXIST - NON-BRUXIST NOPERSIST. NOPERSIST. NOPERSIST PROBLEMS PROBLEMS PROBLEMS Fig. 9. The remaining twenty-seven allergic children and auditory tubal dysfunction. There were fourteen
of the forty-six showed bruxists and thirteen
less evidence of middle ear nonbruxists in this group.
Repetitive nocturnal bruxism may possibly be initiated reflexly by increased negative or disturbed pressures in the tympanic cavities from intermittent allergic edema of the mucosa of the Eustachian tubes (Fig. 10). Arlenz4 suggested the term otomandibular syndrome for certain disorders of the temporomandibular joint associated with spasm of muscles of mastication. He believed that otologic symptoms related to temporomandibular joint dysfunction were innately neuromuscular and anatomically involved with both the mandible and the ear. Embryologically, the middle ear and the auditory tube developed from the first pharyngeal pouch. Two of the ossicles of the tympanic cavity, the malleus and the incus, are believed to have been derived from the proximal ends of each mandibular (Meckel’s) cartilage and arch, respectively. Shortly thereafter, the entire mandible became ossified from the remaining fibrous membrane of Meckel’s cartilage.” The trigeminal nerve innervates the muscles of mastication which comprise the temporalis, masseter, both pterygoids, the mylohyoid, and the anterior belly of the digastric muscle. Two other muscles are also innervated by the trigeminal nerve. These are (1) the tensor tympani, an ancient reptilian jaw muscle which, by evolutionary migration, reached the middle ear, carrying the nerve with it, and (2) the tensor velipalatini, a muscle so unique that it is the only one of the soft palate innervated by the trigeminal nerve and the only muscle of that group that functions to open the Eustachian tube.*’ However, Rood and Doyle27 stated that, according to their recent studies on human fetal and adult Eustachian tubes, three muscles arise from a single paratubal mass embryologically. They are
Volume 77 Number 1
Fig. 10. Intermittent factor in the etiology
Bruxism in allergic
allergic edema of the Eustachian of nocturnal bruxism.
tubes
during
sleep
may
children
be considered
57
a major
(1) the tensor tympani, (2) the tensor velipalatini, and (3) the dilator tubae. All are innervated by the trigeminal nerve and, as stated earlier, evolved from the reptilian mandible over 200 million years ago. Rood and Doyle indicated that it is the muscle fibers of the dilator tubae that open the Eustachian tube, and not the tensor velipalatini. Allergic spasm, then, of either the tensor velipalatini muscle or the dilator tubae muscle may cause abnormal functioning of the Eustachian tube. The relationship between the mandible and middle ear disorders indicates that, early in the developing embryo, neural patterns are established in the brainstem in the region of the sensory and motor nuclei of the trigeminal nerve. A significant embryologic, anatomic, and neural connection exists between the lower jaws, auditory tubes, and tympanic cavities. Edema of the epithelial lining of the tubal orifices or tympanic cavities creating abnormal negative pressure gradients may institute nocturnal bruxism reflexly through the central nervous system. Satoh and Haradaz8 induced bruxism artificially by administering sonic, photic, and tactile stimuli eliciting tooth grinding comparable to that which occurs spontaneously. These observations support our view that the middle ear and the malfunctioning allergic edematous Eustachian tube may reflexly initiate bruxism. Ordinarily, the auditory tubes are kept open during waking hours by swallowing, chewing, yawning, sneezing, and the like, thus equilibrating the atmospheric pressure on both sides of the eardrum. During sleep, most of these functions cease, with the exception of swallowing saliva. It is believed that allergic children who are nocturnal bruxists have dryness of the oral cavity from mouth breathing and, consequently, have a lessened quantity of saliva. The need for swallowing is thus diminished, enhancing the tendency to indulge in tooth grinding at night. At the Sleep Disorders Center at Mount Sinai Medical Center in Miami Beach, we
have recently commenced studies on children and adult allerplc j)rux~st~~.i’lic pr.t:llntinarc data indicate subtle but definite changes in the pressures of the t) mpanum and tlustachian tube function enough to signal the trigeminal nuclei in the brain to set off a iootbprinding pattern shown on our monitoring devices. Although at the present time wc arc unable to show when the actual opening of’ the Eustachian tube occurs and bruxism ceases. we arc attempting to develop some sophisticated instruments to delineate \waliowiq mechanisms which may then synergistically induce Eustachian tubal opening along with c~ssa-. tion of tooth grinding. That allergy may play a definite role in nocturnal bruxism is evidenced during exacerbations of perennial allergic rhinitis, asthma attacks. upper respiratory tract infections. and excessive exposure to pollens, molds, dust, and animal danders which induce more tooth grinding. Some parents can correlate an increase in bruxism with ingeatlon of certain foods of a highly allergenic potential. It must not be construed that allergic disorders of the respiratory tract in children. particularly those affecting middle ears and Eustachian tubes, are the only initiating causes of this widespread oral habit. Certainly, the 4ology (?f noc~turtwi br~xisrn must be mu/fijizctoriul; and only through painstaking research efforts will the riddle be solved. According to Holborow,‘” the critical period of Eustachian tubal inefficiency is relatively short, usually from birth to about 7 years of age. He stated that the incidence of secretory otitis media largely found between the ages of 4 and 7 is due to tubal malfunction. Perhaps most bruxism in allergic children begins in this ape group and extends into adulthood. When modern allergy management is commenced early, emphasizing strict environmental and dietary control measures along with immunotherapy when necessary. most parents note that nocturnal bruxism diminishes considerably or ceases completely. In adults, bruxism may persist in spite of successful allergy management. This is because the sleep disorder becomes ingrained, particularly in stressful situations. Conclusion Without deprecating other prominently mentioned causes of bruxism, such as psychological influences, occlusal defects, and genetic factors, allergic sensitization must be considered seriously. Intermittent allergic edema of the Eustachian tube causes changes to occur in the tympanic cavity, reflexly initiating bruxism as a means of obtaining a patent Eustachian tube. Bruxism in allergic persons may have its origin in infancy and early childhood. Acknowledgment is made to Leonard Caputo. M.D., now in Mobile. Alabama. who collaborated in acquiring data for the tympanometric studies; Joan Gluck, M.D., Miami, Florida, who recorded the numbers of bruxists among nonallergic as well as allergic children; Elysee Halem. M.D., who assisted in the sleep studies of allergic bruxist children; and Martin Cohn, M.D.. Director of the Sleep Disorders Center, Mount Sinai Medical Center, Miami Beach. Florida. who performed sleep studies on both allergic children and adults. REFERENCES 1. Marks, M. B., and Gluck, J. C.: Bruxism Allergy and Immunology of the Association
in allergic children, presented at the Postgraduate of Convalescent Homes and Hospitals for Asthmatic
Course in Children.
April 1, 1976, San Francisco, Calif. 2. O’Connell.
E. J., Arbeiter,
H. I.. and &arts,
C. I..: Unpublished
observations
by pediatric
allergists
Volume 17 Number
Brtrxism
1
in allergic
children
59
3. Shafer, W. G., Hine, M. K., and Levy, B. M.: A textbook of oral pathology, Philadelphia, 1974, W. B. Saunders Company. 4. Glares, A. G., and Rao, S. M.: Bruxism: A critical review, Psychol. Bull. 84: 767-781, 1977. 5. Ramfjord, S. P., and Ash, M. M., Jr.: Occlusion, ed 2, Philadelphia, 1971, W. B. Saunders Company. 6. Nadler, S. C.: Bruxism, a classification: Critical review, J. Am. Dent. Assoc. 54: 615-622, 1957. 7. Meklas, J. F.: Bruxism-Diagnosis and treatment, J. Acad. Gen. Dent. 19: 31-36, 1971. 8. Marks, M. B.: Allergy in relation to orofacial dental deformities in children: A review, J. Allergy 36: 293-302, 1965. 9. Miller, S. C.: Textbook of periodontia (oral medicine), ed 2, Philadelphia, 1943, The Blakiston Company. 10. Brauer, J. C., Higley, L. B., Massler, M., and Schour, I.: Dentistry for children, ed. 2, Philadelphia, 1947, The Blakiston Company. 11. Nadler, S. C.: Personal communication. 12. Bunting, R. W., and Hill, T. J.: Textbook of oral pathology for students and practitioners of dentistry, ed. 2, Philadelphia, 1940, Lea & Febiger. 13. Boyens, P. J.: Value of autosuggestion in the therapy of “bruxism” and other biting habits, J. Am. Dent. Assoc. 27: 1773, 1940. 14. Campbell, D. Cl.: Psychosomatic mechanisms in oral disease, AM. J. ORTHOD. ORAL SURG. 31: 440-446, 1945. 15. Shapiro, S., and Shanon, J.: Bruxism as an emotional reactive disturbance, Ariz. Dent. J. 12: 13-18, 1966. 16. Vemallis, F. F.: Teeth-grinding: Some relationships to anxiety, hostility and hyperactivity, J. Clin. Psychol. 11: 389-391, 1955. 17. Hart, H. H.: Practical psychiatric problems in dentistry, J. Dent. Med. 3: 83, 1948. 18. Bartmeier, L. H.: Psychiatric study of a man suffering from a convulsive disorder, Bull. Menninger Clin. 7: 62, 1943. 19. Reding, G. R., Rubright, W. C., Rechtschaffen, A., and Daniels, R. S.: Sleep pattern of tooth grinding: Its relationship to dreaming, Science 145: 725-726, 1964. 20. Reding, G. R., Zepelin, H., Robinson, J. E., Zimmerman, S. O., and Smith, V. H.: Nocturnal teethgrinding: All-night psychophysiologic studies, J. Dent, Res. 47: 786-797, 1968. 21. Broughton, R. J.: Sleep disorders: Disorders of arousal? Science 159: 1070.1078, 1968. 22. Marks, M. B.: Oral habits in allergic children, J. Asthma Res. 4: 39-46, 1966. 23. Bedecker, C. F.: Occlusal neurosis, its causes and treatment, J. Dent. Sot. N. Y. 8: 6, 1941. 24. Arlen, H.: The otomandibular syndrome: A new concept, Ear Nose Throat J. 56: 26-30, 1977. 25. Development of the ear. In Gass, C. M. (editor): Gray’s Anatomy of the human body, Philadelphia, 1973, Lea & Febiger. 26. Paparella, M. M., and Shrumrick, D. A.: Otolaryngology, Vo12. Ear, Philadelphia, 1973, W. B. Saunders Company. 27. Rood, S. B., and Doyle, W. J.: Morphology of tensor veli palatini. tensor tympani, and dilator tubae muscles, Ann. Otol. Rhinol. Laryngol. 87: 202-210, 1978. 28. Satoh, T., and Harada, Y.: Electrophysiological study on tooth-grinding during sleep, Electroencephalogr. Clin. Neurophysiol. 35: 267-275, 1973. 29. Holborow, C.: Eustachian tubal function, changes in anatomy and function with age and the relationship of these changes to aural pathology, Arch. Otohuyngol. 92: 624-626. 1970. 333 Arthur
Godfrey
Rd. (33140)
in
allerqie . children,
Meyer B. Marks, M.D. Miami
Beach,
F/a.
A study of hruxism (tooth grinding) )vas cvnducted at the Universi~ @Miami School of’ Medicine, at Jackson Memorial Hospital, Miami. Florida, and at rhe Sleep Disorders Center, Mount Sinai Medical Center, Miami Beach, Florida. A thret$old incidence c?f this pernicious oral habit in allergic c,hildren was di.wlosed t1.v compared to nonallergic children. Dental literature stresses psychogenic firctors, oc(~lusal maladjustments, systemic conditions, and occupational pursuits Jcthich do not pertain to most children. Allergy is rarely considered. Nocturnal hruxism may be initiated reflexly by increused negative pressures in the tympanic cavities from intermittent allergic edema qf the mucosa qf the Eustachian tubes. Embrvologic. unatomic. and neurologic relationships between the mu.scles qf the eardrum. Eustachian tubes, and ,jtrws have a primordial, common ancestrv. Chronic middle ear disturbances mq promote reflex action to the juvvs bJ stimulating the trigeminal nuclei in the brain. Sleep studies at Mount Sinai Medical Center on ullergic. bruxing children have produced some interesting but incomplete results. We are attempting to develop sophisticated devices ,f& monitoring abnormal tubal ,funcriorr whic,h ma! Oc the (‘rux of the hruxism problem.
B
ruxism, or tooth grinding, is an oral habit that is indulged in by many adults and children, except in infancy before the appearance of the first dentition. A noticeable degree of nocturnal bruxism is apparent in children seen in the practice of pediatric allergy.” ’ This fact can be substantiated not only from the history but also by the frequent observation in children, of small ulcerations or ridging on the buccal mucosa opposite the molar teeth on one or both sides of the oral cavity (Fig. I). In addition, the Presented before the seventy-ninth May, 1979, Washington, D.C.
48
annual
session
of the American
GOO2.9416/80/010048+12$01.20/0
Association
0
of Orthodontists.
1980 The C
V
Mosby
Co
Volume II Number 1
Bruxism
in ullergic
children
49
Fig. 1. A, This a-year-old
asthmatic boy with perennial allergic rhinitis has an ulceration on the left buccal mucosa from bruxism (arrow). His tooth grinding can be heard throughout the house. He usually sleeps on his left side. Often such ulcerations are bilateral. B, This 22-year-old youth, who has bronchial asthma and chronic nasal allergy, shows bilateral “ridging” on the buccal mucosafrom bruxism (arrow). He has been a tooth-grinder since early childhood. From infancy to the age of 5 years, he was subject to frequent ear infections. C, This 44-year-old man with bilateral buccal “ridging” is a pronounced tooth grinder (arrow). He remembers having had many attacks of otitis media as a young child, and he has had perennial allergic rhinitis since infancy.
facets of the molar, canine, and even the incisor teeth often show marked wearing of the occlusal surfaces (Fig. 2).
This pernicious sleep disorder seems to be fairly prevalent, in that various investigators report an incidence of 5 to more than 20 percent.3 In a study conducted in the pediatric and pediatric allergy clinics at Jackson Memorial Hospital in Miami, Florida (Fig. 3)) the incidence of tooth grinding in nonallergic children was 20 percent. The latter constituted a control group from the same geographic area. In a similar group of allergic children, matched by age, sex, and color, it was found that 60 percent bruxed. Thus, there was a threefold incidence of bruxism in allergic children as compared with those who were apparently nonallergic. l Etiology
The literature on the etiology of this common oral habit is confined chiefly to dental textbooks and periodicals. An all-encompassing, critical review of bruxism by Glaros and
Fig. 2. A, Upper
incisor and canine teeth in same boy as in Fig. ?, A. Note the marked erosion of these teeth as compared to the lower ones, B, This Syear-old patient with bronchial asthma and allergic rhinitis is still subject to frequent attacks of secretory otitis media. His nocturnal bruxism is exceedingly audible. Note the marked, worn-down facets of all hts lower teeth. C, This lo-year-old child, afflicted with severe chronic asthma and nasal allergy, had been subject to frequent attacks of secretory otitis media up to the age of 6 years. He grinds his teeth Incessantly at nrght. Note ulcerations on the buccal mucosa (arrow). The facets of the canine, premolar. and molar teeth show the ground appearance of severe
nocturnal
bruxism.
Rao4 intimated that the disorder has been largely unexplored in the psychological realm because of an impasse between dental concepts of bruxism and those of psychophysiologic factors. Their review endeavored to show how physical. psychological, and neurophysiologic entities are involved in bruxism. Ramfjord and Ash,j stated that there are three mechanisms that interact to trigger bruxism: emotional tensions, pain or discomfort, and occlusal maladjustments. They emphasized that a state of hypertonicity of the muscles of mastication ensues from central nervous system influences and occlusal disharmony. NadleP emphasized the causes of bruxism as (1) local, (2) systemic, (3) psychological, and (4) occupational. Meklas7 believed that psychogenic and local irritation factors outweighed other causes of bruxism. Local factors in children who grind their teeth include traumatic occlusion, dentigerous cysts, and faulty eruption of deciduous or permanent teeth. It has been suggested that bruxism may become a habit as a result of an unconscious attempt by the patient to establish contact with a greater number of teeth. Malocclusion, which is prominent in allergic children,8 interferes with the proper occlusion of teeth, with possible bruxism. In
Volume 11 Number 1
Bruxism
in allergic
children
51
BRUXISM IN ALLERGIC CHILDREN
Fig. 3. There gic children.
is a threefold
Fig. 4. Tympanometry patency of Eustachian
incidence
of nocturnal
apparatus which tubes, and acoustic
monitors reflexes.
bruxism
middle
in allergic
ear
children
pressures,
as compared
compliance
to nonaller-
of eardrums,
children the habit is frequently associated with the transition from the deciduous to the permanent dentition. Systemic factors are etiologically significant but are difficult to evaluate. Intestinal parasitic infestations may play a role. Frequently their eradication will reduce or even eliminate bruxism. Gastrointestinal disturbances from food allergy, enzymic imbalances in digestion causing chronic abdominal distress, and persistent, recurrent urologic dysfunction may be responsible for nocturnal bruxism. Miller,g as well as Brauer and colleagues,” discussed nutritional and vitamin deficiencies as possible elements for inducing tooth grinding. Endocrine disorders, particularly those relating to hyperthyroidism, may lead to bruxism. Many hyperkinetic children are bruxists. Nadler” believed that histamine released during stress may act as an exciting agent in the initiation of bruxism. He
52 Marh
Fig. 5. Ear probe transmits a sound noninvasive.
used in conjunction of known intensity
with the tympanometer. to the eardrum. It causes
It fits tightly into the pattent’s ear and no pain or discomfort and is entirely
observed that nocturnal clenching and gnashing of the teeth often allay symptoms of allergic itching and tickling of the palate and ears and aid in terminating episodes of sneezing and coughing. There is a significant statistical association between bruxists and their blood relatives.” The role that genetic influences play in tooth grinding cannot be ignored. It is not unusual in the practice of pediatric allergy to elicit a history of bruxism in several members of the same family. Psychogenic factors as the primary cause of bruxism seem to dominate the dental literature.4. “L ” Most investigators report that emotional tension may be expressed through a number of nervous habits, one of which is bruxism. Research studies have shown a positive relationship between tooth grinding and repressed aggression, unconscious expressions of oral gratification, and both conscious and unconscious anxiety. lsSI6 Meklas7 hypothesized that grinding the teeth may date back to prehistoric times when teeth were used as weapons. During stress or frustration, some persons regress, he reasoned, and express anger or hostility by grinding or gnashing their teeth. In our fastmoving, television-oriented, materialistic, and anxiety-ridden society, the child or adult is restricted by cultural demands to acceptable social behavioral patterns. Suppression of overt acts of hostility and aggression may result in an unconscious outlet in the form of nocturnal bruxism. HartI had earlier pointed out that the primitive gnashing of teeth carried on by our ancestors during the day when angry became repressed as we became “civilized” and has reasserted itself in sleep and dreams as an atavistic release mechanism. BartmeierlH suggested that children who have recently reached the point of vocal expression and who are restrained from self-assertion and the release of aggressive feelings often begin grinding their teeth. Reding and associates’” equated nocturnal bruxism
Volume 77 Number 1
Bruxism
in allergic
cchildren
53
BRUXISM IN ALLERGIC CHMREN El MALE UFEMALE
o-
o-
o-
o-
0, Fig. 6. Bar graph depicting were nocturnal hard-core
TOTAL
forty-six allergic tooth grinders.
children
BRUXIST NO-BRUXIST between
the ages
of 4 and 14 years.
Thirty
children
with periods of rapid eye movements (REM) indicative of dreaming. A later study by Reding and colleagues ,20 using a greater number of patients, disclosed that bruxism occurred in all stages of sleep, predominantly Stage 2. Broughton” hypothesized that sleep disorders, such as enuresis, sonnambulism, and nightmares, generally occur during a lightening of sleep. He believed that sleep disorders occur during the transitions from Stages 3 and 4 to Stages 1 and 2. During the transitional period, normal as well as bruxist subjects experience movement, autonomic discharge, and other signs of arousal. Tooth grinding can therefore be triggered by internal or external physical or emotional sleepdisturbing stimuli. Childhood bruxism may be related to other oral habits, such as chronic biting and chewing of toys and pencils, thumb- and finger-sucking, tongue thrusting, and mouth breathing. It has been reported that oral habits such as these are more common and prolonged into adolescence in allergic children.22 Occupational CUUS~S rarely can be considered in children, as employment for monetary gain does not usually apply. Athletes, whether amateur or professional, often indulge in bruxism because of their great desire to excel. Part-time occupations by students requiring precise measurements may lead to bruxism. 23 Compulsive overachievers who voluntarily work hard to succeed may eventually become involuntary or subconscious nocturnal bruxists.
BRUXISM IN ALLERGIC CHILDREN !ClJNT’DI 21 3il
E? MALE 0 FEMALE
TOTAL,’ SIG.ABil. Fig. 7. Twenty-one metric
Method
problems.
of the thirty bruxists Of sixteen nonbruxing
SIG.ABN.
demonstrated allergic chtldren,
NON-BRUXISTI SIG.ABN.
significant abnormal impedance only two had similar problems.
or tympano-
and materials
Electroacoustic impedance bridge studies to date have shown a high incidence of increased negative pressures in the middle ear cavities, with concomitant auditory tubal dysfunction in allergic bruxists. The apparatus, when used for tympanometry, is noninvasive and causes no pain or discomfort to the patient (Fig. 4). The examiner is allowed to place a tightly fitting ear probe into one of the child’s ears, occluding the external auditory canal (Fig. 5). In this manner, ear measurements, including middle ear pressures (negative and positive), compliance of the eardrum, patency of the Eustachian tube, and acoustic reflexes, are monitored. Investigations at the Division of Audiology, University of Miami School of Medicine, of forty-six allergic children between the ages of 4 and 14 years (sixteen females and thirty males) disclosed that thirty children were nocturnal tooth grinders (Fig. 6). All forty-six children manifested symptoms of either perennial allergic rhinitis, asthma, or combinations of both disorders. Occasionally, overt middle ear disease was present, but generally symptoms of otitis media in the children attending the Pediatric Allergy Clinic were uncommon, with the exception of hearing difficulties. Of the thirty who were bruxists, ten were girls and twenty were boys. Twenty-one children (Fig. 7) demonstrated significant abnormal impedance problems. including increased negative pressures above minus 100
Volume 77 Number 1
Bruxism
in allergic
children
55
BRUXISM IN ALLERGIC CHILDREN (CONT’D)
El MALE 0 fEMAlE
5t
3119
BRUXIST/NON-BRIJXIST/ PEilSISi. PERSIST: PERSIST. PROBLEMSPROBLEMSPROBLEMS Fig.
8. Repeated tympanometric allergic children had persistent bruxists.
studies for 1 year ear problems. Sixteen
disclosed that of the nineteen
nineteen patients
of the original forty-six were decided nocturnal
and middle ear effusions. Of these, six were girls and fifteen were boys. Of sixteen allergic nonbruxing children (Fig. 7) included in this report, only two had the same significant abnormal problems. Repeated audiometric studies for 1 year (Fig. 8) disclosed that nineteen of the original forty-six allergic patients continued to have persistent ear problems. Of the nineteen fifteen were boys and four were girls. Sixteen patients of this group (twelve boys and four girls) were decided nocturnal bruxists. Three children, all boys, gave no history of nocturnal bruxism, although they had abnormal tympanograms. Of the remaining twenty-seven allergic children, evidence of middle ear and auditory tubal dysfunction was encountered less frequently (Fig. 9). In this group, there were fourteen bruxists and thirteen nonbruxists. In the bruxist patients, there were seven boys and seven girls. In the nonbruxist children, there were eight boys and five girls. Discussion Nocturnal bruxism may be considered a universal sleep disorder of the greatest magnitude. It affects children and adults of all ages, with the possible exception of infants prior to eruption of the first dentition. It could be responsible for much dental pathosis and may be a major etiologic factor in temporomandibular joint dysfunction of adult life.
BRUXISM IN ALLERGIC CHllDREN ‘CONT’O]
14i27
13127
Oi TOTAL BRUXIST - NON-BRUXIST NOPERSIST. NOPERSIST. NOPERSIST PROBLEMS PROBLEMS PROBLEMS Fig. 9. The remaining twenty-seven allergic children and auditory tubal dysfunction. There were fourteen
of the forty-six showed bruxists and thirteen
less evidence of middle ear nonbruxists in this group.
Repetitive nocturnal bruxism may possibly be initiated reflexly by increased negative or disturbed pressures in the tympanic cavities from intermittent allergic edema of the mucosa of the Eustachian tubes (Fig. 10). Arlenz4 suggested the term otomandibular syndrome for certain disorders of the temporomandibular joint associated with spasm of muscles of mastication. He believed that otologic symptoms related to temporomandibular joint dysfunction were innately neuromuscular and anatomically involved with both the mandible and the ear. Embryologically, the middle ear and the auditory tube developed from the first pharyngeal pouch. Two of the ossicles of the tympanic cavity, the malleus and the incus, are believed to have been derived from the proximal ends of each mandibular (Meckel’s) cartilage and arch, respectively. Shortly thereafter, the entire mandible became ossified from the remaining fibrous membrane of Meckel’s cartilage.” The trigeminal nerve innervates the muscles of mastication which comprise the temporalis, masseter, both pterygoids, the mylohyoid, and the anterior belly of the digastric muscle. Two other muscles are also innervated by the trigeminal nerve. These are (1) the tensor tympani, an ancient reptilian jaw muscle which, by evolutionary migration, reached the middle ear, carrying the nerve with it, and (2) the tensor velipalatini, a muscle so unique that it is the only one of the soft palate innervated by the trigeminal nerve and the only muscle of that group that functions to open the Eustachian tube.*’ However, Rood and Doyle27 stated that, according to their recent studies on human fetal and adult Eustachian tubes, three muscles arise from a single paratubal mass embryologically. They are
Volume 77 Number 1
Fig. 10. Intermittent factor in the etiology
Bruxism in allergic
allergic edema of the Eustachian of nocturnal bruxism.
tubes
during
sleep
may
children
be considered
57
a major
(1) the tensor tympani, (2) the tensor velipalatini, and (3) the dilator tubae. All are innervated by the trigeminal nerve and, as stated earlier, evolved from the reptilian mandible over 200 million years ago. Rood and Doyle indicated that it is the muscle fibers of the dilator tubae that open the Eustachian tube, and not the tensor velipalatini. Allergic spasm, then, of either the tensor velipalatini muscle or the dilator tubae muscle may cause abnormal functioning of the Eustachian tube. The relationship between the mandible and middle ear disorders indicates that, early in the developing embryo, neural patterns are established in the brainstem in the region of the sensory and motor nuclei of the trigeminal nerve. A significant embryologic, anatomic, and neural connection exists between the lower jaws, auditory tubes, and tympanic cavities. Edema of the epithelial lining of the tubal orifices or tympanic cavities creating abnormal negative pressure gradients may institute nocturnal bruxism reflexly through the central nervous system. Satoh and Haradaz8 induced bruxism artificially by administering sonic, photic, and tactile stimuli eliciting tooth grinding comparable to that which occurs spontaneously. These observations support our view that the middle ear and the malfunctioning allergic edematous Eustachian tube may reflexly initiate bruxism. Ordinarily, the auditory tubes are kept open during waking hours by swallowing, chewing, yawning, sneezing, and the like, thus equilibrating the atmospheric pressure on both sides of the eardrum. During sleep, most of these functions cease, with the exception of swallowing saliva. It is believed that allergic children who are nocturnal bruxists have dryness of the oral cavity from mouth breathing and, consequently, have a lessened quantity of saliva. The need for swallowing is thus diminished, enhancing the tendency to indulge in tooth grinding at night. At the Sleep Disorders Center at Mount Sinai Medical Center in Miami Beach, we
have recently commenced studies on children and adult allerplc j)rux~st~~.i’lic pr.t:llntinarc data indicate subtle but definite changes in the pressures of the t) mpanum and tlustachian tube function enough to signal the trigeminal nuclei in the brain to set off a iootbprinding pattern shown on our monitoring devices. Although at the present time wc arc unable to show when the actual opening of’ the Eustachian tube occurs and bruxism ceases. we arc attempting to develop some sophisticated instruments to delineate \waliowiq mechanisms which may then synergistically induce Eustachian tubal opening along with c~ssa-. tion of tooth grinding. That allergy may play a definite role in nocturnal bruxism is evidenced during exacerbations of perennial allergic rhinitis, asthma attacks. upper respiratory tract infections. and excessive exposure to pollens, molds, dust, and animal danders which induce more tooth grinding. Some parents can correlate an increase in bruxism with ingeatlon of certain foods of a highly allergenic potential. It must not be construed that allergic disorders of the respiratory tract in children. particularly those affecting middle ears and Eustachian tubes, are the only initiating causes of this widespread oral habit. Certainly, the 4ology (?f noc~turtwi br~xisrn must be mu/fijizctoriul; and only through painstaking research efforts will the riddle be solved. According to Holborow,‘” the critical period of Eustachian tubal inefficiency is relatively short, usually from birth to about 7 years of age. He stated that the incidence of secretory otitis media largely found between the ages of 4 and 7 is due to tubal malfunction. Perhaps most bruxism in allergic children begins in this ape group and extends into adulthood. When modern allergy management is commenced early, emphasizing strict environmental and dietary control measures along with immunotherapy when necessary. most parents note that nocturnal bruxism diminishes considerably or ceases completely. In adults, bruxism may persist in spite of successful allergy management. This is because the sleep disorder becomes ingrained, particularly in stressful situations. Conclusion Without deprecating other prominently mentioned causes of bruxism, such as psychological influences, occlusal defects, and genetic factors, allergic sensitization must be considered seriously. Intermittent allergic edema of the Eustachian tube causes changes to occur in the tympanic cavity, reflexly initiating bruxism as a means of obtaining a patent Eustachian tube. Bruxism in allergic persons may have its origin in infancy and early childhood. Acknowledgment is made to Leonard Caputo. M.D., now in Mobile. Alabama. who collaborated in acquiring data for the tympanometric studies; Joan Gluck, M.D., Miami, Florida, who recorded the numbers of bruxists among nonallergic as well as allergic children; Elysee Halem. M.D., who assisted in the sleep studies of allergic bruxist children; and Martin Cohn, M.D.. Director of the Sleep Disorders Center, Mount Sinai Medical Center, Miami Beach. Florida. who performed sleep studies on both allergic children and adults. REFERENCES 1. Marks, M. B., and Gluck, J. C.: Bruxism Allergy and Immunology of the Association
in allergic children, presented at the Postgraduate of Convalescent Homes and Hospitals for Asthmatic
Course in Children.
April 1, 1976, San Francisco, Calif. 2. O’Connell.
E. J., Arbeiter,
H. I.. and &arts,
C. I..: Unpublished
observations
by pediatric
allergists
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Brtrxism
1
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children
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3. Shafer, W. G., Hine, M. K., and Levy, B. M.: A textbook of oral pathology, Philadelphia, 1974, W. B. Saunders Company. 4. Glares, A. G., and Rao, S. M.: Bruxism: A critical review, Psychol. Bull. 84: 767-781, 1977. 5. Ramfjord, S. P., and Ash, M. M., Jr.: Occlusion, ed 2, Philadelphia, 1971, W. B. Saunders Company. 6. Nadler, S. C.: Bruxism, a classification: Critical review, J. Am. Dent. Assoc. 54: 615-622, 1957. 7. Meklas, J. F.: Bruxism-Diagnosis and treatment, J. Acad. Gen. Dent. 19: 31-36, 1971. 8. Marks, M. B.: Allergy in relation to orofacial dental deformities in children: A review, J. Allergy 36: 293-302, 1965. 9. Miller, S. C.: Textbook of periodontia (oral medicine), ed 2, Philadelphia, 1943, The Blakiston Company. 10. Brauer, J. C., Higley, L. B., Massler, M., and Schour, I.: Dentistry for children, ed. 2, Philadelphia, 1947, The Blakiston Company. 11. Nadler, S. C.: Personal communication. 12. Bunting, R. W., and Hill, T. J.: Textbook of oral pathology for students and practitioners of dentistry, ed. 2, Philadelphia, 1940, Lea & Febiger. 13. Boyens, P. J.: Value of autosuggestion in the therapy of “bruxism” and other biting habits, J. Am. Dent. Assoc. 27: 1773, 1940. 14. Campbell, D. Cl.: Psychosomatic mechanisms in oral disease, AM. J. ORTHOD. ORAL SURG. 31: 440-446, 1945. 15. Shapiro, S., and Shanon, J.: Bruxism as an emotional reactive disturbance, Ariz. Dent. J. 12: 13-18, 1966. 16. Vemallis, F. F.: Teeth-grinding: Some relationships to anxiety, hostility and hyperactivity, J. Clin. Psychol. 11: 389-391, 1955. 17. Hart, H. H.: Practical psychiatric problems in dentistry, J. Dent. Med. 3: 83, 1948. 18. Bartmeier, L. H.: Psychiatric study of a man suffering from a convulsive disorder, Bull. Menninger Clin. 7: 62, 1943. 19. Reding, G. R., Rubright, W. C., Rechtschaffen, A., and Daniels, R. S.: Sleep pattern of tooth grinding: Its relationship to dreaming, Science 145: 725-726, 1964. 20. Reding, G. R., Zepelin, H., Robinson, J. E., Zimmerman, S. O., and Smith, V. H.: Nocturnal teethgrinding: All-night psychophysiologic studies, J. Dent, Res. 47: 786-797, 1968. 21. Broughton, R. J.: Sleep disorders: Disorders of arousal? Science 159: 1070.1078, 1968. 22. Marks, M. B.: Oral habits in allergic children, J. Asthma Res. 4: 39-46, 1966. 23. Bedecker, C. F.: Occlusal neurosis, its causes and treatment, J. Dent. Sot. N. Y. 8: 6, 1941. 24. Arlen, H.: The otomandibular syndrome: A new concept, Ear Nose Throat J. 56: 26-30, 1977. 25. Development of the ear. In Gass, C. M. (editor): Gray’s Anatomy of the human body, Philadelphia, 1973, Lea & Febiger. 26. Paparella, M. M., and Shrumrick, D. A.: Otolaryngology, Vo12. Ear, Philadelphia, 1973, W. B. Saunders Company. 27. Rood, S. B., and Doyle, W. J.: Morphology of tensor veli palatini. tensor tympani, and dilator tubae muscles, Ann. Otol. Rhinol. Laryngol. 87: 202-210, 1978. 28. Satoh, T., and Harada, Y.: Electrophysiological study on tooth-grinding during sleep, Electroencephalogr. Clin. Neurophysiol. 35: 267-275, 1973. 29. Holborow, C.: Eustachian tubal function, changes in anatomy and function with age and the relationship of these changes to aural pathology, Arch. Otohuyngol. 92: 624-626. 1970. 333 Arthur
Godfrey
Rd. (33140)