sign in sign up
<<
Home , Bruxism, Masseter muscle, Parasomnia, Polysomnography, Sleep disorder, Sleep onset

Physical Evaluation

Polysomnographic analysis of

Marilene de Oliveira Trindade, PhD, MS n Antonio Gomez Rodriguez, MD, MS

The American Academy of (AASM) defines sleep bruxism were analyzed clinically and underwent PSG. The descriptive analysis as a stereotyped characterized by clenching and correlated apnea, , and limb movements in the 12 patients who grinding of the teeth during sleep. Bruxism is found in 14%-20% of exhibited of sleep bruxism. Of these patients, 4 were children, 8% of adults <60 years old, and 3% of adults >60 years old. confirmed through PSG to have bruxism. The mandibular movements of bruxism can be confused with rhythmic In a comparison between the 4 patients with confirmed bruxism (PSGB mandibular movements associated with other sleep disorders, such as group) and the 8 patients confirmed not to have bruxism (NPSGB group), arousals/microarousals, limb movement disorder, and obstructive sleep the respiratory event index was lower in the PSGB group (13.17 and 17.95, apnea/ syndrome. (PSG) is the study of sleep respectively). The mean leg movement index was higher in the PSGB group disorders based on the recording of physiological events throughout than the NPSGB group in total sleep time (21.36 and 8.42, respectively) an entire night of sleep. This system involves , and in time (34.54 and 10.30, respectively). , and of the submental/suprahyoid, Received: June 12, 2012 tibialis anterior, , masseter, and temporal muscles, through which Accepted: December 6, 2012 signs of sleep bruxism can be identified. The aim of the present study was to identify bruxism during a night of sleep in a laboratory. Thirty patients Key words: bruxism, polysomnography

ccording to Silber, sleep is a complex are needed.4,5 There is no consensus regard- involves electroencephalography (EEG), and highly organized physiological ing a specific etiology for bruxism, thus electrooculography (EOG), and electro- state.1 In humans, the sleep-wakeful- multifactor etiology is the term that is most myography (EMG) tests to determine the A 6,7 ness cycle corresponds to 3 major phases: commonly employed. electrical activity in the brain, eyes, and wakefulness, slow-wave sleep with no rapid In the clinical evaluation for the diag- muscles, respectively. Audiovisual monitor- eye movement (NREM), and sleep with nosis of sleep bruxism, a combination ing is also involved. The EMG measures rapid eye movement (REM). REM sleep of at least 2 of the criteria suggested by the electrical activity of the submental/ accounts for approximately 20% to 25% Lavigne & Manzini in Table 1 should suprahyoid regions, thoracic-abdominal of sleep. Stages 1 and 2 NREM account be considered.8 The incidence of sleep movements, oximetry, rate, nasal for over half of overall sleep time, whereas bruxism is 1.9-fold higher among smokers flow pressure, as well as the tibialis anterior, stage 3 NREM, which appears mainly in and individuals who use , , mentalis, masseter, and temporal muscles. the first half of the sleep period, accounts drugs, or other substances that affect the With this system, signs of sleep disorders for 15%.1,2 .9-14 can been identified concomitantly, and epi- Repetitive movements with contact of Individuals with sleep bruxism may sodes of sleep bruxism can be recognized.19 the teeth beyond the normal functions of have other concomitant sleep disorders, and swallowing represents a para- such as obstructive /hypopnea functional behavior known as bruxism or (OSAH), restless leg syndrome, REM sleep movement. Motor activity in behavior disorder, , and other Table 1. Criteria used for the clinical sleep bruxism was included in the AASM parasomnia and disorders.9,15,16 diagnosis of sleep bruxism.8 2005 International Classification of Sleep Sleep bruxism may be accompanied by 2 Disorders: Diagnostic and Coding Manual. secondary risk factors, such as , • History of teeth grinding noises reported Bruxism can be a conscious or unconscious tooth marks on the sides of the , by partner or family member habit, diurnal and/or nocturnal—all of bilateral masseter hypertrophy, occlusal which are seen as separate disorders with trauma, iatrogenic problems, chronic pain • Presence of worn facets on the surface 3 of teeth not compatible with age or different etiologies. The facial muscle in the mandibular musculature or region function contractions of sleep bruxism are associ- of the , and lim- ated with the sound of teeth grinding, ited mandibular movement.5,17,18 • in temporal region which varies in frequency throughout the Polysomnography (PSG) is used for the • Fatigued mandibular musculature at night. Sleep bruxism is found in 14%-20% diagnosis and study of different sleep disor- night or while awake of children, 8% of adults under age 60, ders based on the recording of physiologi- • Lockjaw, or difficulty opening the mouth and 3% of adults over 60. More in-depth cal events throughout an entire night of in the morning investigations, addressing the fact that sleep using electrodes and sensors in a labo- • Dental hypersensitivity sleep bruxism occurs concomitantly with ratory setting. One clinical routine is the teeth clenching during waking hours in the determination of the frequency of rhyth- • Hypertrophy of the masseter muscles presence of oral motor control alterations, mic mandibular movements. This system

56 January/February 2014 General www.agd.org Prior to initiating the exam, calibration with bruxism than individuals without this Sleep Unit of the Vigo General University of the muscles is performed based on disorder.28 The increase in motor activity Hospital in Spain. Of the 30 patients the maximal voluntary clenching of the in individuals with bruxism is understand- evaluated through PSG, a questionnaire teeth for 15 seconds. A 10% increase in able, as microarousals are associated with specifically addressing bruxism, and the amplitude in relation to maximal voluntary intrinsic differences in cortical autonomic reports of bedroom partners, 12 exhib- clenching, whether or not accompanied recruitment and motor activation of the ited signs and symptoms of bruxism; 4 by body movement, is considered to char- muscles of the body and .29 had the diagnosis confirmed by PSG. acterize a bruxism episode during sleep.20 The pathophysiology of bruxism is not All participants signed a statement of Conditions associated with aging and pain yet fully understood. Oral somatosen- informed consent agreeing to participate are important factors influencing sleep sory stimuli in the presence of occlusal in the study, in compliance with the organization, and the prevalence of some abnormalities may trigger the synthesis of norms established by the Vigo General sleep disorders (such as sleep apnea) is catecholamines, thereby enhancing sym- University Hospital. higher in an older population. Older sub- pathetic tonus (a partial constriction of Besides the conventional PSG instru- jects (>60 years) present fewer sleep brux- blood vessels instigated by the sympathetic ments, electrodes were also placed on ism episodes per hour of sleep than younger nervous system), thus increasing muscle the right and left masseter muscles. sleep bruxers.21 Age may also influence the reflex. Muscle symptoms in the face and Calibration of the PSG apparatus was occurrence of rhythmic masticatory muscle head reported by individuals with bruxism performed based on the contraction of activity in the elderly population. should be distinguished from those indica- the masseter muscles corresponding to Bruxism has been associated with poor tive of other sleep disorders. Orofacial 10% greater amplitude in relation to sleep quality in patients with chronic pain symptoms associated with temporoman- maximal voluntary teeth clenching for 15 or OSAH. The association between oro- dibular disorder, such as limited mouth seconds. The mean number and duration facial pain symptoms and sleep bruxism opening, joint noises, and facial muscle of total facial contraction movements is probaby not independent of the interac- pain, may also be associated with sleep were calculated for the respective episodes tion between pain and poor sleep. Sleep bruxism. Recent studies have strength- in different NREM and REM phases apnea, like insomnia, has been associated ened the association between bruxism during a night of sleep in the PSGB with increased pain sensivity (decreased and apnea, but others have not found a group (n = 4). The index of total facial pain threshold).22,23 significant number of respiratory disor- contraction movements in both duration Sleep bruxism predominantly occurs ders or oxygen desaturation cases among and number was then calculated. The in NREM Stage 2 (60%-80% of cases), individuals with bruxism.29 In some PSG index and mean number of contractions although it is important to note that some studies, teeth clenching and RMM were of the mentalis muscle and the masseters authors have suggested that grinding in found in 40%-60% of adult patients with were obtained by measuring the total the REM phase has a greater destructive OSAH.22 However, these studies sought number of events when these muscles potential for teeth.20,24,25 To facilitate the to demonstrate a temporal association contracted either in an isolated fashion diagnosis of sleep bruxism, variables such between apnea events and electromyo- or simultaneously in the 4 participants of as total sleep time, latency, graphic episodes of RMM in patients the group. The percentages of the modes distribution of sleep stages, periodic limb with OSAH, suggesting that post-apnea of contractions were calculated. movements, OSAH, and frequency of respiratory activation may be responsible The number and duration of the times arousals and microarousals are investi- for the respiratory activation that precedes that the masseter muscles contracted gated.24 Roehrs et al demonstrated that RMM. Instead, masseter muscle activity were recorded, and the same was done for is defined as an unconscious is believed to occur at the end of apnea the mentalis muscle. These recordings transition from 3 to 15 seconds of cerebral events in the form of a nonspecific oral were made to obtain the total index of impulses of EEG activity, either alone motor activation causing apnea-induced bruxism events during all sleep phases in or accompanied by tachycardia and an arousal.16 Further studies are needed to 1 night of sleep for the PSGB patients. increase in EMG.25 These events, together determine whether the concomitant occur- Data from the PSG analysis were also with teeth grinding, distinguish individu- rence of sleep bruxism in patients with used to determine the mean total number als with bruxism from those without this OSAH is more associated with the degree and index of the following events in both condition.26 Studies have revealed that the of sleep fragmentation rather than an NREM and REM: apnea, leg movement occurrence of sleep bruxism is influenced increase in post-apnea arousals. (LM), and arousals. The same procedure by multiple factors, such as psychological/ The aim of the present study was to was carried out for the NPSGB group. personality traits, genetics, neurochemical identify bruxism during a night in a sleep The total number of activity, and oropharyngeal function.20,27 laboratory and determine possible correla- events (apnea, LM, and arousals) in the Rhythmic mandibular movements tions with other sleep disorders. NREM and REM phases and the index (RMM) constitute the most frequent data of the PSGB group were compared motor activity observed during sleep and Materials and methods to those of the NPSGB group. In the are classified as bruxism in the presence of The calibration of maximal voluntary descriptive analysis, bruxism events were teeth grinding. The frequency of RMM teeth clenching was performed on 30 correlated with apnea, LM, and arousal during sleep is 3-fold greater in individuals patients who sought treatment at the events in both groups.

www.agd.org General Dentistry January/February 2014 57 Physical Evaluation Polysomnographic analysis of bruxism

Table 3. Mean number and indices of arousal, apnea, and leg movement (LM) according to phases of sleep in PSGB group.

Patient 1 Patient 2 Patient 3 Patient 4 Mean Arousal number NREM 51.00 90.00 34.00 6.00 45.25 REM 24.00 35.00 23.00 10.00 23.00 Total 75.00 125.00 57.00 16.00 68.25

Table 2. Mean isolated and combined mentalis and Arousal index masseter contractions in PSGB group. NREM 10.17 21.06 6.83 1.17 9.81 REM 35.12 27.45 29.36 10.53 25.62 Index Patient 1 Patient 2 Patient 3 Patient 4 Mean Total 12.98 23.19 9.94 2.64 12.19 Mentalis Apnea number NREM 16.09 19.78 6.83 23.22 16.48 NREM 109.00 72.00 12.00 14.00 51.75 REM 30.73 7.84 24.26 8.42 17.81 REM 43.00 64.00 6.00 19.00 33.00 TST 17.66 17.36 9.24 20.93 16.30 Total 152.00 136.00 18.00 33.00 84.75 Masseter Apnea index NREM 0.87 0.19 0.00 0.98 0.51 NREM 19.07 13.44 2.41 2.73 9.41 REM 2.93 0.00 0.00 2.11 1.26 REM 62.93 50.20 7.66 20.00 35.20 TST 1.09 0.15 0.00 1.15 0.60 Total 23.75 20.35 3.14 5.44 13.17 Masseter + Mentalis LM number NREM 11.20 6.91 2.61 3.9 6.15 NREM 63.00 106.00 124.00 101.00 98.50 REM 16.10 7.84 24.26 8.42 14.15 REM 12.00 50.00 25.00 47.00 33.50 TST 11.72 7.03 5.58 4.62 7.24 Total 75.00 156.00 149.00 148.00 132.00 Total movements 195.00 164.00 85.00 162.00 151.50 LM index Mentalis (%) 57.95 70.73 62.35 78.40 67.36 NREM 11.02 19.78 24.92 19.71 18.86 Masseter (%) 3.59 0.61 0.00 4.32 2.13 REM 17.56 39.22 31.91 49.47 34.54 Mentalis + Masseter (%) 38.46 28.66 37.65 17.28 30.51 Total 11.72 23.34 25.99 24.40 21.36

Results in REM). The mean LM index (events/ affected by an increase in arousals and A mean total of 151.5 movements were period) was 21.36 for TST (34.54 in microarousals.16 Analyses involving more counted, including movements in the REM) (Table 3). than 1 night of sleep are needed regard- mentalis muscle, the masseter muscles, In the comparison of the PSGB and ing the clarification of whether or not and the mentalis and massester (MM) NPSGB groups, the TST respiratory LM is associated with a greater number muscles simultaneously. The mean dura- event index was lower in the PSGB group of arousals in the REM phase. According tion of the movements was similar in the (13.17 and 17.95, respectively). The mean to Lavigne et al, bruxism is a secondary 3 groups. The total masseter, mentalis, LM index was higher in the PSGB group motor activity of endogenous microarous- and MM movement index (events/period) (21.36 TST and 34.54 REM) in compari- als represented by the cardiac-autonomous in relation to total sleep time (TST) was son to the NPSGB group (8.42 TST and EEG cycle and motor fluctuations.23 Thus, 24.14 (33.22 in REM). The movement 10.30 REM) (Table 4). an increase in activity of the brain and index was greater in the mentalis (16.30) autonomous nervous system precedes teeth than the masseters (0.60) and the MM Discussion grinding in humans. Bader reports that a (7.24) (Table 2). The mean arousal index The data for the LM index in this study large number of bruxism episodes occur in (events/period) was 12.19 for TST (25.62 for both groups are in agreement with conjunction with other bodily movements in REM). The TST respiratory event findings reported by Kato & Blanchet, and these movements are interlinked with index (events/period), which is an indica- who found that individuals with bruxism the occurrence of arousals.29 Lavigne et al tion for apnea, was 13.17 for TST (35.20 also exhibit restless leg syndrome and are postulated that the occurrence of bruxism

58 January/February 2014 General Dentistry www.agd.org also proposed that OSAH was caused by Diagnostic and Coding Manual. 2005. Available at: Table 4. Mean number and indices hypoxia and breathing difficulty, result- http://www.esst.org/adds/ICSD.pdf. Accessed October of arousal, apnea, and leg move- 15, 2013. ing in multiple oral phenomena, including 3. Kato T, Dal-Fabbro C, Lavigne GJ. Current knowledge 9 ment (LM) according to phases of teeth clenching. Ohayan et al suggested on awake and sleep bruxism: overview. Alpha Ome- sleep in NPSGB vs PSGB groups. further investigations were needed in gan. 2003;96(2):24-32. order to determine whether teeth grinding 4. Lavigne GJ, Manzini C, Kato T. Sleep bruxism. In: is actually linked more to OSAH than Kryger MH, Roth T, Dement WC, eds. Principles and NPSGB PSGB Practice of . 4th ed. Philadelphia: Else- post-apnea arousal.9 Apnea number vier Saunders; 2005:946. The swallowing of saliva is reduced 5. Lavigne GJ, Khoury S, Abe S, Yamaguchi T, Raphael K. NREM 82.125 51.750 10-fold during sleep, and the activation Bruxism physiology and pathology: an overview for REM 25.125 33.000 of this reflex is associated with arous- clinicians. J Oral Rehabil. 2008;35(7):476-494. 6. Nobilo, KA. Tecnica de nobilo para o tratamento do Total 107.250 84.750 als. According to Miyawaki et al, there bruxismo; caso clinico. Ver Odontol. 2000;5(1):26-29. is a greater need during the swallowing Apnea index 7. Okeson, JP. Tratamento das Desordens Temporoman- of saliva for the preservation of airway dibulares Oclusao. 4th ed. Sao Paulo: Artes Medicas; NREM 16.490 9.410 patency and esophageal lubrication, and 2000:449. 8. Lavigne GJ, Manzini C. Bruxism. In: Kryger MH, Roth T, REM 28.400 35.200 sleep bruxism may occur as part of these 20 Dement WC, eds. Principles and Practice of Sleep Med- Total 17.950 13.170 physiological events. Both Lavigne et al icine. 3rd ed. Philadelphia: WB Saunders; 2000: and Bader reported an association between 773-785. LM number sleep bruxism and poor sleep quality in 9. Ohayon MM, Li KK, Guilleminault C. Risk factors for NREM 42.875 98.500 elderly individuals with OSAH.11,29 In sleep bruxism in the general population. Chest. 2001;119(1):53-61. REM 9.875 33.500 the present study, however, no association 10. Ahlberg J, Savolainen A, Rantala M, Lindholm H, Ko- was found between apnea and brux- Total 52.750 132.000 nonen, M. Reported bruxism and biopsychosocial ism. Therefore, further investigations symptoms: a longitudinal study. Community Dent Oral LM index are needed, involving larger samples of Epidemiol. 2004;32(4):307-311. NREM 8.150 18.860 patients and a longer study duration. 11. Lavigne GJ, Lobbezoo F, Rompre PH, Nielsen TA, Mont- plaisir J. Cigarette smoking as a risk factor or an exac- REM 10.300 34.540 erbating factor for and sleep Conclusion bruxism. Sleep. 1997;20(4):290-293. Total 8.420 21.360 Patients with bruxism diagnosed based 12. Hojo A, Haketa T, Baba K, Igarashi Y. Association be- Arousal on a clinical examination and positive tween the amount of alcohol intake and masseter muscle activity levels recorded during sleep in healthy Number 47.880 68.250 PSG findings had poorer sleep quality in young women. Int J Prosthodont. 2007;20(3): Index 7.590 12.190 relation to individuals for whom bruxism 251-255. was not confirmed by PSG, as evidenced 13. Manfredini D, Land N, Fantoni F, Segu M, Bosco M. in the greater number of arousals, longer Anxiety symptoms in clinically diagnosed bruxers. intrasleep wakefulness, lesser sleep effi- J Oral Rhabil. 2005;32(8):584-588. 14. Suwa S, Takahara M, Shirakawa S, et al. Sleep bruxism episodes is more associated with the peri- ciency, and a greater number of sleep and its relationship to sleep habits and lifestyle of ele- odic fluctuations found in arousals than phase changes. No association was found mentary school children in Japan. Sleep Biol Rhythms. the influence of sudden changes in the between episodes of bruxism and the 2009;7(2):93-102. autonomous nervous system during sleep.5 number of apnea events, but there appears 15. Kato T. Sleep bruxism and its relation to -hypopnea syndrome. Sleep Biol Rhythms. According to Bader, sleep onset latency, to be an association with LM. This finding 2004;2:1-15. TST, and duration of sleep stages in suggests the need for further studies in 16. Kato T, Blanchet PJ. Orofacial movement disorders in individuals with bruxism generally do order to clarify this possible association. sleep. In: Lavigne GJ, Cistulli PA, Smith MT, eds. Sleep not differ from individuals without this Medicine for Dentists. A Practical Overview. Hanover condition.29 Individuals with bruxism do Author information Park, IL: Quintessence; 2009. 17. Baba K, Haketa T, Sasaki Y, Ohyama T, Clark GT. Associ- tend to return to a light sleep, and there Dr. Trindade is a teacher, Odontology ation between masseter muscle activity levels record- is an increase in the amount of time spent Integrated Clinical, Department of ed during sleep and signs and symptoms of in this light sleep in comparison to deep Prosthesis and Buccofacial Surgery, temporomandibular disorders in healthy young adults. sleep, thereby increasing the fragmenta- Health Science Center, Federal University J Orofac Pain. 2005;19(3):226-231. 18. Tosun T, Karabuda C, Cuhadaroglu C. Evaluation of tion of sleep, and consequently a greater of Pernambuco, Brazil. Dr. Rodriguez sleep bruxism by polysomnographic analysis in pa- number of arousals, increased intrasleep is a neurophysiologist, Department tients with dental implants. Int J Oral Maxillofac Im- wakefulness, a greater number of tran- of Neurophysiology, Hospital de A plants. 2003;18(2):286-292. sient changes in phases of sleep due to Coruna, Spain. 19. Malow BA, Aldrich MS. Polyssomnography. In: Chokro- the increased responsiveness of oromotor verty S, Hening W, Walters A, eds. Sleep and Move- ment Disorders. Philadelphia: Butterworth/Heinemann; activity to microarousals, and reduced References 2003. sleep efficiency.23,26,29 Ohayon et al 1. Silber MH. Staging sleep. Sleep Med Clin. 2009;4: 20. Miyawaki S, Lavigne GJ, Pierre M, Guitard F, Montplai- reported an association between bruxism 343-352. sir JY, Kato T. Association between sleep bruxism, swal- 2. American Academy of Sleep Medicine. The Internation- lowing-related laryngeal movement, and sleep and OSAH resulting in nonrestorative al Classification of Sleep Disorders, Revised: sleep and daytime sleepiness.9 The authors positions. Sleep. 2003;26(4):461-465.

www.agd.org General Dentistry January/February 2014 59 Published with permission by the Academy of General Dentistry. © Copyright 2013 by the Academy of General Dentistry. All rights reserved. For printed and electronic reprints of this article for distribution, please contact [email protected].

21. Khoury S, Rouleau GA, Rompre PH, Mayer P, Montplai- sir JY, Lavigne GJ. A significant increase in breathing amplitude precedes sleep bruxism. Chest. 2008; 134(2):332-337. 22. Sjoholm TT, Lowe AA, Miyamoto K, Fleetham JA, Ryan CF. Sleep bruxism in patients with sleep-disordered breathing. Arch Orol Biol. 2000;45(10):889-896. 23. Lavigne GJ, Guitar F, Rompre PH, Montplaisir JY. Vari- ability in sleep bruxism activity over time. J Sleep Res. 2001;10(3):237-244. 24. Dal Fabro C, Seabra MV,Tufik S. A linear study of a man with sleep bruxism in 30 consecutive nights – correlation reports. J Sleep Res. 1997;26:547. 25. Roehrs T, Zorick FJ, Roth T, Transient and short-term insomnias. Kryger MH, Roth T, Dement WC, eds. In: Principles and Practice of Sleep Medicine. 3rd ed. Phil- adelphia: W.B. Saunders; 2000:624-632. 26. Kato T, Blanchet PJ, Montplaisir JY, et al. Sleep bruxism and other disorders with orofacial activity during sleep. In: Chokroverty S, Hening W, Walters A, eds. Sleep and Movement Disorders. Philadelphia: Butter- worth/Heinemann; 2003. 27. Gastaldo E, Quatrale R, Graziani A, et al. The excitabili- ty of the trigeminal motor system in sleep bruxism: a transcranial magnetic stimulation and brainstem reflex study. J Orofac Pain. 2006;20:145-155. 28. Okeson JP. Management of Temporomandibular Disor- ders and . 5th ed. St Louis: Mosby; 2003. 29. Bader G. Sleep: A Comprehensive Handbook. Lee-Chiong TL, ed. New York: Wiley-Liss; 2006.

60 January/February 2014 General Dentistry www.agd.org