Relationship between Sleep Bruxism and Obstructive Sleep Apnea in Children and Adolescents

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Preliminary Title of Research: Temporal relation between sleep bruxism and obstructive sleep apnea in children and adolescents.

Significance:

  • The exact etiology of sleep bruxism is yet to be discovered. Many scholars and studies over the years have attempted to unveil the causes sleep bruxism, but none have yet to prevail. Some of the literature suggested that sleep bruxism and obstructive sleep apnea-hypopnea are interrelated. Investigating the temporal association between sleep bruxism and obstructive sleep apnea is one way that can help us to truly understand whether such an association exists. The temporal association between the two conditions have studied on adults, but none to our own knowledge investigated this association on children and adolescents. This study aims at investigating the temporal association between sleep bruxism and obstructive sleep apnea in children and adolescents.

Hypothesis:

  • Null hypothesis H0: A temporal association is found between sleep bruxism and sleep apnea-hypopnea events, and more specifically, if a sleep apnea-hypopnea event terminates before the commencement of a sleep bruxism event.
  • Alternative hypothesis H1: No temporal association is found between sleep bruxism and sleep apnea-hypopnea events.

Aims:

  • To investigate the temporal association between sleep bruxism and obstructive sleep apnea in children and adolescents with obstructive sleep apnea.

Background:

  • The classification and definitions of bruxism has varied throughout the years. In 2013, international consensus was reached by a group of bruxism experts that bruxism “is a repetitive masticatory muscle activity characterized by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible [1]. This definition was well-cited in the literature to almost 40 citations per annum [2]. It was also included in the Guidelines for Assessment Diagnosis, and Management of Orofacial Pain of the American Academy of Orofacial Pain [3], and the third edition of the International Classification of Sleep Disorders [4]. This proves the vast adaptation of this definition in the dental field. But this definition had its shortcoming and was further clarified as sleep bruxism or awake bruxism, depending on its circadian phenotype. [2]. Studies evaluating bruxism in children determined that in a healthy individual bruxism must not be considered as a disease but rather a normal part of development. In others it can be considered a risk factor for certain clinical conditions and may have negative consequences for the health of a patient. In this context, bruxism can be found associated to a plethora of comorbid conditions such headaches, GERD, TMD and orofacial pain, anxiety, dental sleep disorders, ADHD and many more [5]. Herrera el al. found a direct association between sleep architecture, daytime cognitive behavioral functioning and bruxism in a group of children ages 5 to 15-year-old [6]. Many efforts have been made in the recent years to obtain a better understanding into the pathophysiology and clinical connections of bruxism and its associated conditions. Unfortunately, up to now these efforts have come short of completely comprehending it.
  • Obstructive sleep apnea (OSA) is a serious and life-threatening sleep disorder associated by the complete or partial collapse of the upper respiratory airway. OSA has harmful side effects that can include cardiovascular, and metabolic consequences, inability to concentrate in school, poor academic performance, behavioral problems and poor growth and development. As a consequence of an obstructive event the oxygen saturation in the blood can decrease causing a microarousal, a response mechanism that would wake the patient and allow breathing to commence. Although a number of screening tools exist to diagnose sleep bruxism, a nocturnal polysomnography is the gold standard for making a diagnosis [7-11]. According to an epidemiological review by Franklin and Lindberg in 2015, populations based in the US, China, Spain, India, Korea, Japan and Sweden had a prevalence of obstructive sleep apnea defined at an apnea-hypopnea index (AHI) ≥5 was 22% in males and 17% in females [12]. The Prevalence of OSA in children ranged from 0% to 5.7%, with obesity being an independent risk factor [9]. Unlike in adults, AHI is quantified differently in children. Most sleep centers consider an obstructive AHI ≤1/hr to be normal, 1< AHI ≤5 to be mild OSA, 5< AHI ≤10 to be moderate OSA, and an AHI >10/hr as severe OSA in children [13].
  • Bruxism has been found to have a temporal association to the observed microarousals during an obstructive event in adults, presenting in many cases immediately after an event [14]. However, the scarce amount of studies available on this topic have not been able to truly shed light on the pathophysiology or even true presence of this association. Some of the literature suggests that a correlation between OSA and sleep bruxism [15, 16]. This conclusion was based on PSG recording of patients with OSA that the onset of apnea or hypopnea event precedes the event of sleep bruxism [15]. Tan et al (2019) found sleep bruxism coincided in a third of adults suffering from OSA [16]. Other evidences suggest there is no tangible temporal association between OSA and sleep bruxism [17].
  • The information collected by this study aims at further understanding the temporal association between sleep apnea-hypopnea and sleep bruxism events and thus to confirm or deny the association between the two phenomena.

Materials and methods:

Study design and subject characteristics:

  • This study is a prospective chart review. The study population will be recruited from the University of Kentucky Sleep Disorders Center. The target group in this study are patients between the age of 6 years and 18 years. The legal guardians of the patient, or the patient if they are 18-year-old, will be asked to sign a consent form to be included in the study. They will also be asked to complete a questionnaire to obtain demographic information, as well as, a modified version of the DC/TMD questionnaire to screen for self-reported bruxism [18]. Patients must present a laboratory-based polysomnography to confirm the diagnosis of both OSA and sleep bruxism. Subjects will be excluded if they are ≤5 or ≥18, or have craniofacial anomaly, ASA III, history of epilepsy, night terrors, major neurologic disorder, dyskinetic jaw movements persisting in sleep (dystonia, tremors, chorea, dyskinesia),  major sleep disorder, major psychiatric disorder, attention-deficit/hyperactivity disorder (ADHD), history of psychoactive medications, and edentate patients.

Polysomnographic recording:

  • The subjects will be selected from the sleep laboratory at the University of Kentucky Sleep disorders Center. The subjects will spend one night in a sleep laboratory and polysomnographic (PSG) recording and scoring will be performed by a registered polysomnographic technologist. The recording variables included are electroencephalograms (EEGs), right and left electrooculogram; electromyogram (EMG) of the masseter, submental and anterior tibialis muscle; and electrocardiogram. A position sensor will be used to record body position. Variables for sleep breathing includes airflow (nasal/oral thermistor), chest and abdominal effort, and SpO2 measured by pulse oximetry. Sleep bruxism will be scored by PSG recordings that includes EMG traces placed on the masseter muscle and AV. The masseter side selected for analysis will be randomized across subjects. The primary investigator will be calibrated with a registered polysomnographic technologist. The polysomnographic recordings will be read and analyzed by the primary investigator.

Assessment of breathing and masseter muscle activity:

  • According to the standard criteria of ICSD-3, obstructive sleep apnea diagnosis is given when an AHI threshold of 1 event or more is recorded during a PSG. Sleep rhythmic masticatory muscle activity with sleep bruxism (RMMA-SB) and other oromotor activities EMG recordings will be conducted from an adapted published criterion [19-21]. EMG traces will be placed on the masseter muscle to record sleep bruxism. RMMA episodes will be scored according to the three types of: phasic (3 or more EMG bursts of the masseter muscle, each lasting between 0.25 to 2 seconds.), tonic (or more EMG bursts of the masseter muscle lasting longer than 2 seconds) or mixed (both phasic and tonic bursts). A diagnosis of sleep bruxism will be given in the presences of >2 episodes of RMMA-SB per hour and/or >25 RMMA-SB EMG bursts per hour. Observed sleep related oromotor activities other than RMMA-SB, (e.g., face scratching, swallowing or coughing), will be classified as a sleep oromotor activity. Unidentified events by AV recordings will be excluded.

Classification of temporal associations between sleep bruxism and sleep apnea-hypopnea events:

  • The temporal classification is adapted from a study conducted by Saito. et al. [14]. The two temporal patterns considered in the study are as follow: (i) when a sleep apnea-hypopnea event terminates and a sleep bruxism event commences is called P1 (AHE to SB), (ii) when a sleep bruxism event terminates and a sleep apnea-hypopnea commences is called P2 (SB to AHE). Overlapping events will be considered as the nearest pattern that resembles that pattern. A sleep bruxism event will be scored with a window of 5-minute after or before the sleep apnea hypopnea event.

Statistical analysis:

  • Data analysis: Mean distribution of the two patterns will be calculated for all the participants. The paired t-test will be conducted to analyze the temporal association between sleep bruxism and sleep apnea-hypopnea events. Statistical significance is set at a P-value <0.05. Descriptive statistics (i.e. frequencies and percentages) will be conducted and analyzed. Dependent variables are RMMA-SB episodes and RMMA-SB bursts. Independent variables are AHI, AI, BMI, gender, and age.
  • Power analysis: A priori power analysis conducted with GPower indicates that a total of 27 participants is needed to detect a correlation of moderate effect size (r= .30).

Timetable:

October2019

Submit research draft of MS protocol

Review committee meeting

November 2019

Obtain approval from Master of Science protocol review committee

IRB submission and making any necessary modifications

January-August 2020

Patient recruitment and data collection

September-October 2020

Statistical analysis

November 2020-December 2020

Prepare manuscript

December 2020

Send manuscript to committee

Abstract submission for AAOP

Abstract submission for AADSM

January 2021

Manuscript modification and finalization

April 2021

Defense date

May 2021

Deliver complete manuscript to graduate school

Present poster at AAOP

Present poster at AADSM

Uncategorized References

1. Lobbezoo, F., et al., Bruxism defined and graded: an international consensus. J Oral Rehabil, 2013. 40(1): p. 2-4.

2. Lobbezoo, F., et al., International consensus on the assessment of bruxism: Report of a work in progress. J Oral Rehabil, 2018. 45(11): p. 837-844.

3. De Leeuw LR, K.G., Orofacial Pain. Guidelines for Assessment, Diagnosis, and Management, 5th edition. 2013.

4. Medicine, A.A.o.S., International Classification of Sleep Disorders, 3rd edn. 2014.

5. Mayer, P., R. Heinzer, and G. Lavigne, Sleep Bruxism in Respiratory Medicine Practice. Chest, 2016. 149(1): p. 262-71.

6. Herrera, M., et al., Bruxism in children: effect on sleep architecture and daytime cognitive performance and behavior. Sleep, 2006. 29(9): p. 1143-8.

7. Standards and indications for cardiopulmonary sleep studies in children. American Thoracic Society. Am J Respir Crit Care Med, 1996. 153(2): p. 866-78.

8. Section on Pediatric Pulmonology, S.o.O.S.A.S.A.A.o.P., Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics, 2002. 109(4): p. 704-12.

9. Marcus, C.L., et al., Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics, 2012. 130(3): p. e714-55.

10. Luz Alonso-Alvarez, M., et al., [Consensus document on sleep apnea-hypopnea syndrome in children (full version). Sociedad Espanola de Sueno. El Area de Sueno de la Sociedad Espanola de Neumologia y Cirugia Toracica(SEPAR)]. Arch Bronconeumol, 2011. 47 Suppl 5: p. 0, 2-18.

11. Wise, M.S., et al., Executive summary of respiratory indications for polysomnography in children: an evidence-based review. Sleep, 2011. 34(3): p. 389-98AW.

12. Franklin, K.A. and E. Lindberg, Obstructive sleep apnea is a common disorder in the population-a review on the epidemiology of sleep apnea. J Thorac Dis, 2015. 7(8): p. 1311-22.

13. Dehlink, E. and H.L. Tan, Update on paediatric obstructive sleep apnoea. J Thorac Dis, 2016. 8(2): p. 224-35.

14. Saito, M., et al., Temporal association between sleep apnea-hypopnea and sleep bruxism events. J Sleep Res, 2013.

15. Dutra, K.M., et al., Oro-facial activities in sleep bruxism patients and in normal subjects: a controlled polygraphic and audio-video study. J Oral Rehabil, 2009. 36(2): p. 86-92.

16. Tan, M.W.Y., et al., Prevalence of Sleep Bruxism and Its Association with Obstructive Sleep Apnea in Adult Patients: A Retrospective Polysomnographic Investigation. J Oral Facial Pain Headache, 2019. 33(3): p. 269-277.

17. Saito, M., et al., Weak association between sleep bruxism and obstructive sleep apnea. A sleep laboratory study. Sleep Breath, 2016. 20(2): p. 703-9.

18. Ohrbach, R., Diagnostic Criteria for Temporomandibular Disorders: Assessment Instruments. Version 15May2016. www.rdc-tmdinternational.org Accessed on October 9, 2019.

19. Carra, M.C., N. Huynh, and G. Lavigne, Sleep bruxism: a comprehensive overview for the dental clinician interested in sleep medicine. Dent Clin North Am, 2012. 56(2): p. 387-413.

20. Carra, M.C., et al., Overview on Sleep Bruxism for Sleep Medicine Clinicians. Sleep Med Clin, 2015. 10(3): p. 375-84, xvi.

21. Yamaguchi, T., et al., Comparison of ambulatory and polysomnographic recording of jaw muscle activity during sleep in normal subjects. J Oral Rehabil, 2012. 39(1): p. 2-10.

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