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Quantitative Polygraphic Controlled Study on Efficacy and Safety of Oral Splint Devices in Tooth-grinding Subjects

¹ Département de Restauration, Prosthodontics Postgraduate Program, Faculté de médecine dentaire, Université de Montréal, C.P. 6128, Succursale Centre-ville, Montréal (Québec) H3C 3J7, Canada; and
² Centre d’étude du sommeil, Hôpital du Sacré-Cœur de Montréal, Canada;

Correspondence: ^* corresponding author, Gilles.Lavigne{at}Umontreal.ca

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS & METHODS RESULTS DISCUSSION REFERENCES

 
The efficacy of occlusal splints in diminishing muscle activity and tooth-grinding damage remains controversial. The objective of this study was to compare the efficacy and safety of an occlusal splint (OS) vs. a palatal control device (PCD). Nine subjects with sleep bruxism (SB) participated in this randomized study. Sleep laboratory recordings were made on the second night to establish baseline data. Patients then wore each of the splints in the sleep laboratory for recording nights three and four, two weeks apart, according to a crossover design. A statistically significant reduction in the number of SB episodes per hour (decrease of 41%, p = 0.05) and SB bursts per hour (decrease of 40%, p < 0.05) was observed with the two devices. Both oral devices also showed 50% fewer episodes with grinding noise (p = 0.06). No difference was observed between the devices. Moreover, no changes in respiratory variables were observed. Both devices reduced muscle activity associated with SB.

Key Words: sleep bruxism • tooth grinding • bite splint • randomized controlled study

	INTRODUCTION

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The oral device known as the occlusal splint (OS) is frequently used in the management of sleep bruxism (SB) to protect teeth from damage (e.g., wear or fracture) resulting from forceful jaw muscle contractions or to reduce concomitant orofacial pain, if present (Pierce et al., 1995; Okeson, 2003). However, the efficacy of the OS in reducing jaw muscle activity remains controversial. Some studies reported a reduction in SB motor activity (electromyographic [EMG] recording) when comparisons were made with recordings from the baseline night, whereas others showed no effect (Solberg et al., 1975; Okeson, 1987; Rugh et al., 1989; Okkerse et al., 2002; Sjöholm et al., 2002). It should be noted that these studies did not include a palatal-control device (PCD), which covers the palatal area without protecting the tooth. The absence of a PCD prevents any conclusion that occlusal tooth coverage explains OS action. The use of a PCD, in a limited number of SB subjects, was reported to reduce or have no effect on SB motor activity (Cassisi et al., 1987; Hiyama et al., 2003).

SB is a parasomnia, an excessive motor activity with tooth-grinding, that intrudes upon a subject’s otherwise normal sleep (Thorpy, 1997; Lobbezoo and Naeije, 2001). Evidence from recent controlled studies suggests that most SB episodes are secondary to a cascade of physiological events related to sleep arousal (Okura et al., 1996; Macaluso et al., 1998; Kato et al., 2001, 2003). The predominant sequence is as follows: a transient (3–10 sec) brain and heart activation, a rise in muscle tone of jaw openers-suprahyoid muscles, then rhythmic contractions of jaw-closer muscles with occasional tooth-grinding. The incidence of sleep arousals in SB subjects is within the normal range ( 14 arousals/hr of sleep) (Mathur and Douglas, 1995; Boselli et al., 1998; Lavigne et al., 2001a). However, SB episodes associated with sleep arousals are characterized by a rapid onset of tachycardia and an important rise in electroencephalographic or electromyographic activities (Kato et al., 2001). The influences of OS on sleep arousal are unknown.

Sleep apnea (i.e., cessation of breathing in sleep with hypoxemia and risk of hypertension, daytime sleepiness) is a health hazard found twice as often in the general population reporting tooth-grinding than in the normal population (Krieger, 2000; Ohayon et al., 2001). The safety of using OS in subjects with SB and sleep apnea needs to be assessed. In a recent preliminary study, it was noticed that, out of 10 subjects with a clear diagnosis of sleep apnea, the use of OS aggravated respiratory disturbances (e.g., from a lower to a more severe diagnostic category) in four of them (Gagnon et al., 2004). However, it was reported by others that OS had no effect on the mean index of respiratory disturbances per hour of sleep. Since individual subject variation was not shown in these studies, we do not know if some of them had an aggravation (Sjöholm et al., 1994; Mehta et al., 2001; Gotsopoulos et al., 2002).

The objective of the present study was to assess, by the use of a short-term controlled-random design, whether OS reduced SB motor activity, influenced sleep variables (e.g., duration and quality of sleep, number of arousals), and are safe with regard to respiratory parameters (e.g., apnea/hypopnea, snoring) in young healthy SB subjects.

	MATERIALS & METHODS

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Population
Five young women and four men (mean age ± SEM, 23.7 ± 0.9 yrs; range, 20–29 yrs) with a history of tooth grinding were selected for this study. All participants signed a consent form and received financial compensation for inconvenience related to the study. The institutional ethics committee approved the study.

Subjects were recruited by referrals from clinicians and by advertising on the University campus. A history of tooth-grinding events occurring 3 times or more a week, as reported by the patient’s sleep partner over the preceding 6 mos, was the main criterion for selection (Lavigne et al., 1996; Thorpy, 1997; Lobbezoo et al., 2001). The presence of tooth wear ranging from class 2 through class 4 (Johansson et al., 1993) on at least 3 occlusal surfaces and/or masseter muscle hypertrophy upon voluntary clenching and/or symptoms of morning orofacial jaw muscle fatigue were also noted when all subjects were examined.

To be eligible to participate in the study, SB subjects were required to be between 18 and 45 years of age, have a good comprehension of French, be able to sign a consent form, and agree to spend at least 4 nights at the sleep research laboratory. The first night was for habituation and was not included in the statistical analysis. The second night was used to record jaw muscle activity and tooth-grinding sounds to establish baseline levels and to rule out other sleep disorders. At least 4 phasic (3 muscle contractions at a frequency of 1 Hz) or mixed (phasic and tonic contractions) episodes of SB per hour of sleep with 2 audible tooth-grinding events per night had to be present to confirm a subject’s eligibility to participate in the study (Lavigne et al., 2001a,b). During baseline recording, patients who showed signs of other sleep disorders—such as periodic leg movements during sleep (> 10 events per hour of sleep), electroencephalographic (EEG) epileptiform activity, sleep apnea (> 5 apnea or hypopnea events per hour of sleep)—and snoring were excluded. Also excluded were patients reporting pain, those who had been treated with any type of oral device in the preceding 6 mos, those wearing a partial denture, missing more than 2 posterior teeth (third molars excluded), presenting gross malocclusion, or taking medication or alcohol on a regular basis. Finally, a negative history of medical, neurological, motor, or psychiatric disorders was required for subjects to be included in the study.

Experimental Procedure and Occlusal Splint Fabrication
This crossover study evaluated two oral devices (Fig. 1): a hard acrylic U-shaped occlusal splint and a palatal device (e.g., not interfering with the occlusion in any mandibular movements). The OS was used as the treatment and the PCD as the active control. The technician scoring sleep and oromandibular activity data was blind to the type of device used.

View larger version (91K): [in this window] [in a new window]   Figure 1. Photographs of the occlusal splint (a,b) and palatal control device (c,d) on model and in mouth, respectively.

The first night of sleep laboratory recording was for habituation. The second night was used for sleep disorders diagnosis and to establish baseline data. A computer-generated sequence then randomly assigned which of the two oral devices was to be worn first by each patient. Patients were given two weeks to get used to the splint. The subjects then spent a third night at the laboratory, wearing their first splint, for the collection of polygraphic data. The second splint was given on the next morning and was worn by the subject for two weeks. Further laboratory recordings were made on the fourth night, with subjects wearing their second splint. Patient compliance was checked on an irregular basis by a ‘phone call to the patient to ensure that he/she was using the oral device as requested.

Polysomnographic Recordings and Scored Variables
Sleep recordings were made on each of the 4 nights from 10:30 p.m. to 7:00 a.m. The setting of the recordings has been described elsewhere (Lavigne et al., 1996; Lobbezoo et al., 1997). In summary, the following surface electrodes were used: 2 electroencephalograms (C₃A₂, O₂A₁), one electrocardiogram (EKG) and bilateral electro-oculograms (EOGs), and electromyograms (EMGs) from the masseter, sternocleidomastoid, anterior tibialis, and one site for chin/suprahyoid activities. Data were collected and amplified with a sampling rate of 128 Hz and kept for further scoring with the use of sleep recording and scoring software (Harmonie, Stellate System, Montréal, Canada). Audio and video signals were recorded in parallel. Information on sleep quality, total duration, efficiency, percentages of stage duration, number of micro-arousals per hour, number of awakenings per hour, and sleep latency was calculated. Moreover, the frequency of SB episodes per hour of sleep, the number of bruxism bursts per hour, and the number of episodes with sounds were estimated. A detailed analysis of SB muscle activity was also performed for the right masseter. For each SB episode, the total episode duration, number of bursts, number of bursts/sec, mean amplitude of the bursts (RMS calculation), sum of burst duration, mean burst duration, and mean interval between bursts were calculated (Lavigne et al., 1997). The sleep scoring was done according to the standard criteria of Rechtschaffen and Kales (1968), and the final diagnosis of SB was made according to previously published criteria (Lavigne et al., 1996).

Respiratory function was assessed by nasal airflow measures through a thermistor sensor (Thermocouple, Protech, Woodville, WA, USA) and a thoracic and abdominal belt. The number of apnea-hypopnea events per hour of sleep was computed. The presence of swallowing events was estimated indirectly with the use of video signals and laryngeal movements as recorded over the thyroid cartilage with a piezoelectric sensor (Opti-Flex, Newlife Technologies, Midlothian, VA, USA). This method is a valid and non-invasive technique currently used in sleep medicine (Miyawaki et al., 2003). An index of the number of swallowing events per hour was computed based on data from the piezoelectric sensor.

Statistical Analysis
We used repeated-measures ANOVA to evaluate treatment effects. The baseline data were then compared with data from either the occlusal or palatal nights by paired comparisons. Friedman two-way ANOVA followed by Wilcoxon signed-ranks tests for paired comparisons were used when the data distribution was not normal. We performed sign tests to evaluate whether subjects did or did not improve with the splints.

	RESULTS

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The influence of the oral devices on sleep variables was that both reduced the percentage of time that subjects spent in deep non-REM sleep (stages 3 and 4, Table). However, simple contrast analysis revealed trends only when baseline recordings were compared with those with OS (14.9% to 10.6%; p = 0.057) and PCD (14.9% to 11.0%; p = 0.085). Although the duration of stages 3 and 4 was slightly lower during the nights with oral devices, no other sleep variables (e.g., efficiency, sleep latency, incidence of micro-arousals or awakenings) differed among the 3 recorded conditions. The presence of the splints did not induce an increase in the respiratory variables, apnea and hypopnea index, which remained low for the whole study. A non-statistically significant increase in the number of swallowing events per hour was observed with the OS (67%; p = 0.12).

View larger version (14K): [in this window] [in a new window]   Figure 2. Comparison among baseline (B), occlusal splint (OS), and palatal control device (PCD) nights for the number of (a) bruxism episodes per hour, (b) episodes with tooth-grinding noise, and (c) bursts per hour. Median is shown for episodes/hr, since the data distribution was not normal; otherwise, means ± SEM are shown (nine subjects). * p 0.05 when compared with baseline value (details in Table).

View larger version (15K): [in this window] [in a new window]   Figure 3. Individual data distribution for the number of bruxism episodes per hr for baseline (B), occlusal splint (OS), and palatal control device (PCD) nights. The median is circled. A decrease more important than night-to-night variability (25%) was observed for six and five patients, respectively, when occlusal splint and palatal control device nights were compared with the baseline night.

	DISCUSSION

TOP ABSTRACT INTRODUCTION MATERIALS & METHODS RESULTS DISCUSSION REFERENCES

 
This study gives support for the use of an oral device to reduce SB motor activity. More importantly, it shows that oral devices (with or without tooth coverage) reduced jaw muscle activity in SB subjects. Although a similar frequency of sleep arousals was noted across sleep conditions, most EMG variables were significantly reduced with the use of both devices. Interestingly, in our young SB subjects, there was no obvious exacerbation of sleep respiratory variables with OS and PCD.

The present study has obvious limitations that require caution to be exercised when the data are interpreted. First, all SB subjects were young and were tooth grinders (not clenchers); they may then not represent SB in the general population. Second, the subjects were also very motivated to participate in the study, since their dentists had recommended an occlusal splint and their sleep partner was complaining of tooth-grinding sounds. Motivation may be a potential bias. There might be a deceptive bias regarding oral device design, since the PCD did not offer tooth protection. To prevent this, we clearly explained that both designs had been used in a previous study and that both were suggested to be effective. Third, the period of habituation to each oral device was short (2 wks), which may have prevented us from observing long-term influence. Interestingly, other studies have reported that OS induce a reduction in oromotor activity that persists up to 6 mos (Sheikholeslam et al., 1986; Pierce and Gale, 1988). Fourth, the OS used in the present study was made for the maxilla. A study design with OS made on the mandible may have given different results. Fifth, the sample size of the study was small, although a sufficient statistical power was obtained for most important outcomes (e.g., SB oromotor variables). The power was low only to show a statistical difference for the swallowing-laryngeal movement. For this variable, a sample size of 25 subjects would have been needed for the difference greater than 60% between the baseline and OS night to reach a power of 80% at an alpha level of 0.05. Regarding the sleep respiratory disturbance index, even with low power we felt comfortable with the observed result, since the difference (0.4 vs. 0.8) is well below the diagnostic criteria of 5 apnea and hypopnea episodes per hour of sleep (Krieger, 2000).

In our study, although SB subjects had similar sleep efficiency, with or without oral devices, the nights with the OS and PCD showed that stages 3 and 4 (so-called "restorative sleep") were nearly 1/3 shorter (trend only). This is contrary to another report showing that OS has no influence on slow-wave activity (SWA: a measure that is similar to stages 3 and 4) (Nagels et al., 2001). Since our study was short-term, it could be possible that, with time, the duration of stages 3 and 4 with oral devices tends to normalize toward values usually observed in young normal sleepers (17–21%) (Boselli et al., 1998; Landolt and Borbely, 2001).

The most interesting finding of this study is that the use of oral devices in SB subjects reduces the frequency of SB oromotor events and tooth-grinding-related activities. Only one patient showed an exacerbation of SB with the OS. This was not unexpected, since others have found that nearly 20% of SB patients had more muscle contractions with such oral devices (Clark et al., 1979). SB is an exaggerated muscular response (e.g., frequency and amplitude) in ongoing "usual sleep arousal response" in otherwise normal sleeper (Okura et al., 1996; Macaluso et al., 1998; Kato et al., 2001, 2003; Lavigne et al., 2001a, 2002). We have found in this study, as well as in a previous one, that the frequency of sleep arousals in these young SB subjects remains within the range observed in normal subjects (<14 arousals/hr of sleep) (Mathur and Douglas, 1995; Boselli et al., 1998). However, the use of an oral device could then reduce the strength of sleep arousal reaction in preventing excessive muscle activation, an hypothesis currently under investigation in our laboratory. We recently suggested that SB activity may contribute to the recovery of airway patency in sleep (Lavigne et al., 2003). It could then be possible that the palatal thickness ( 1 mm) of an oral device modifies tongue position during sleep. This obviously needs more attention, since, during the light sleep of normal young subjects, the posterior displacement of the tongue and soft palate contributes to reduced airway patency (Trudo et al., 1998). The common rationale for the use of OS is to prevent tooth damage from SB-tooth-grinding, and since both devices reduced the oromotor activity, the mechanism of action is to be further investigated.

	ACKNOWLEDGMENTS

 
This study was supported by Canadian Institutes of Health Research and Québec FRSQ grants. We also thank A. Petersen and F. Bélanger for editing this paper and Dr. Y. Gagnon for his clinical expertise.

Received for publication May 14, 2003. Revision received November 26, 2003. Accepted for publication March 2, 2004.

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Journal of Dental Research, Vol. 83, No. 5, 398-403 (2004)
DOI: 10.1177/154405910408300509


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This Article Abstract Figures Only Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Dubé, C. Articles by Lavigne, G.J. Search for Related Content PubMed PubMed Citation Articles by Dubé, C. Articles by Lavigne, G.J. Social Bookmarking                         What's this?