Abstract
Introduction: The aims of this study were to analyze the association among (sleep and awake) bruxism, (static and dynamic) occlusion and temporomandibular joint modifications in healthy adults. Materials and methods: 60 healthy subjects (33 females and 27 males), 30 of them with bruxism, were investigated. Bruxism type, joint pain, muscle pain and/or fatigue, centric relation, dental wear, static and dynamic occlusion were analyzed. Results and discussion: Muscle pain and fatigue sensation of the masticator apparatus were higher in subjects with bruxism than in those without bruxism (3.23 vs 1.46). Joint noises and joint pain occurred with increasing frequency in subjects with bruxism. Sleep bruxism is associated with mandible lateral shift during mouth opening, joint pain and non-functional lateral guidance. A lack of occlusal involvement was found in the etiology of awake bruxism. Conclusions: Sleep bruxism is related with non-functional occlusion, while awake bruxism showed no occlusal interaction, suggesting the necessity of a different therapeutic approach.
Keywords: sleep bruxism, awake bruxism, functional and non-functional occlusion.
1.INTRODUCTION
Temporomandibular joint disorders (TMDs) are frequently encountered in dental practice. Approximately 60-70% of adults show at least one symptom, but only 25% of them are seeking treatment, especially for muscle or joint pain. Opposite to its high incidence among adults, the therapeutic approach remains intensively debated, due to its multifactorial etiology. Parafunctions are known to be an etiological factor for TMDs, at least a favorizing, if not a determining one [1,2]. Bruxism is cited as a major factor, followed by chewing gum [3,4]. Bruxism has been approached as a single entity, without distinction between awake and sleep bruxism and no differentiation of the involvement of each form in the etiolgy of disfunction [5]. However, several authors have reported significant differences between awake and sleep bruxism in terms of clinical symptoms and etiology [6]. Similarly with TMDs, bruxism has a poorly known etiology, which hinders a successful therapeutic approach. The role of occlusion as a causative factor for bruxism is intensely debated in the literature. Until recently, the determinant role was imputed to occlusal factors, which include disfunctional occlusion [7]. Some studies have shown the association between passive interferences and sleep bruxism [8]. Ramfjord has shown that occlusal interferences may occur in every patient with bruxism. The author asserts that re-establishing occlusal harmony through electromyography is followed by reduction in the tension of masticator muscles and harmonization of muscle activity [9]. Dawson has shown that elimination of occlusal interferences in subjects with bruxism determines a decreased, even completely stopped clenching movement in some cases. Other authors have contested the role of occlusion in the etiology of awake or sleep bruxism. Lazic et al., following a T-Scan II analysis, reported no association between sleep bruxism and occlusal alterations [10]. Kato et al. found out a similar prevalence of sleep bruxism in subjects with or without interferences, bruxing activity having not decreased following occlusal therapy [11]. Further on, according to our knowledge, no precise differentiation and no comparison between awake and sleep bruxism and occlusion have been performed. A meta-analysis associates awake bruxism with central disturbances, respectively Down syndrome, autism, anxiety, suggesting the involvement of the limbic system in its physiopathology [12]. There is a scarcity of data regarding the etiology, diagnostic and treatment of awake bruxism [13,14]. It is important to assign separately the role of each etiologic factor of awake or sleep bruxism for establishing a specific successful therapeutic approach.
However, the literature is insufficient or conflicting concerning occlusion and its etiological role in bruxism. Nevertheless, a determining and also favorizing role in the etiology of TMDs is assigned to parafunctional and vicious habits: bruxism, sleep habit position (e.g. on the belly), postural changes, unilateral mastication. Hence, the aims of this study were to analyze the possible association among awake and sleep bruxism, static and dynamic occlusion and temporomandibular joint structural and functional modifications in healthy adults.
2.MATERIALS AND METHODS
The analytical, cohort, observational, crosssectional, prospective study was approved by the Institutional Review Board of the "Iuliu Hatieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania on 19.04.2018 (approval number: 184). The subjects - enrolled between May-June 2018 at the Prosthodontic Department of the Faculty of Dental Medicine - have been informed on the structure and objectives of the study and have signed an informed consent. A number of 60 healthy subjects, students of the Faculty of Dental Medicine, of various nationalities (M:F ratio=0.81, mean age 23,1±2.04 years), was divided into two groups: a study group, including 30 subjects with (awake and sleep) bruxism, and a control group, comprising 30 subjects without bruxism. Bruxism was diagnosed by anamnesis, by associating signs and symptoms and by the presence of dental wear. No polysomnography was used to diagnose the sleep disorder. The inclusion criteria comprised: clinically healthy subjects, no ongoing orthodontic treatment, with bruxism (study group). Exclusion criteria: associated general pathology, chronic treatment with anti-inflammatory or anxiolytic drugs, orthodontic appliances, trauma, fractures of facial bones, joint surgery or congenital joint disease, ongoing dental treatments, extended prosthodontic restorations (bridges with more than three units) which could interfere with mandible movements. Examination of each subject included anamnesis, a questionnaire, and clinical inspection of the dento-maxillary apparatus. A single examiner performed all observations, respecting the same protocol for each subject. Clinical anamnesis, recording general data (age, gender, nationality), comprised a questionnaire with five questions concerning the presence of bruxism. The Fonseca questionnaire was applied, with improvement of the 8th question for differentiation of the bruxism type:"Do you clench or grind your teeth?" by division into two sections:"Do you clench or grind your teeth during daytime, when you are awake?" and "Do you clench or grind your teeth during sleep?" Additional questions regarding personal perception of occlusion were added ("Do you feel comfortable with your occlusion?"); presence of joint pain, muscle pain or fatigue in the morning, at awakening, constant use of anti-inflammatory or anxiolytic drugs. Answers were marked with numbers from 1 to 5 (1=never, 5=always).
The clinical phase, the main tool of diagnosis, assessed dental wear, ranging it into four groups, according to its distribution: lower incisors, upper incisors, lower and upper incisors, frontal and lateral teeth (generalized).
Occlusal examination involved two stages: static (Angle class and sagittal, vertical and transversal analysis in incisors, canines and first molars, left and right) and dynamic (anterior and lateral guidance, centric relation). Physiologic and pathologic variations were noted.
The centric relation is the mandibular jaw position in which the head of the condyle is situated in the highest position within the glenoid fossa [15]. Bimanual manipulation for centric relation examination was used according to Dawson, with the patient in dorsal decubitus position and neck in light extension. The following functional situations were found: point centric (maximum intercuspation corresponds to centric relation); long centric (between maximum intercuspation and centric relation, at a sagittal slide of 0.2-1.2 mm). Pathologic, non-functional situations were considered when a transversal slide between maximum intercuspation or when a sagittal slide higher than 2 mm were found.
Anterior guidance was considered functional if a contact existed between the marginal edges of the lower incisors and the palatal surfaces of the upper incisors, and if the movement was supported by two pairs of antagonistic incisors on both sides of the midline [16]. The movement should be linear, symmetric, with similar intensity, until it achieves an edge-to-edge contact, with disocclusion on the posterior teeth.
Anterior guidance was considered nonfunctional when an open bite occurrs in maximum intercuspation position, which determines the posterior teeth to perform the guidance with overloading of the joints and masticator muscles and occurrence of dental wear [17,18].
Interferences and premature contacts were marked using 40 micrometers Bausch articulating paper on both the active and passive side.
Functional lateral guidance was considered as:
- canine guidance, when the movement is supported by canines on the working side;
- lateral group function, when lateral guidance is supported by canines and all lateral teeth on the working side;
- antero-lateral guidance, when lateral guidance is supported by the canine along with one or two consecutive incisors on the same side with the movement.
The absence of antagonistic canines in maximum intercuspation is a prerequisite for a non-functional lateral guidance. Hence, all such clinical situations were classified as nonfunctional lateral guidance.
Functional guidance implies disocclusion of all teeth that do not participate to the movement, from the beginning until the end. The presence of obstacles along the movement was recorded using 40 micrometers Bausch articulating paper. Active and passive interferences and premature contacts were recorded.
The temporomandibular joint was examined by inspection, palpation and auscultation, the following data being noted: joint pain during movement, asymmetry in mobility or surface, range of motion, joint noises (crepitus, clicking).
The trajectory of mouth opening and closing was classified as [19]:
- normal, with no deviation during movement; - sinusoidal, with mandible shift towards the movement side and recurrent by the end of the movement;
- deviated, with mandible shift from the opening and accentuated shift towards the end of the maximum opening, with no recovery.
The values of the mandible movement range [20], maximum opening, and maximum lateral right and left, maximum protrusion [21] were recorded using a caliper.
Data was analyzed using MedCalc Software version 17.4 program with statistical significance at p<0.05.
3.RESULTS
Out of the total number of 60 studied subjects, 33 were females and 27 were males. Mean age was 23.9 years in subjects with bruxism and 22.3 years in subjects with no bruxism, 18 subjects with bruxism were females and 12 were males, whereas there was an equal gender distribution in subjects with no bruxism (Table 1).
Out of the total number of subjects with sleep bruxism, 11 had both sleep and awake bruxism.
The nationalities of subjects with bruxism were diversified. Subjects with Romanian nationality prevailed (56.7%), but we have encountered also French (26.7%), other Europeans (13.3%) and non-European (3.3%) citizens.
The mean age was 23.1 years, significantly higher in subjects with sleep bruxism (23.9 years), compared to those with no bruxism (22.3 years). Sleep bruxism was not influenced by gender or nationality. Muscle pain and fatigue sensation of the masticator apparatus had a score of 3.23 in subjects with bruxism and of 1.46, respectively, in those with no bruxism. The self-reported comfort of occlusion had a score of 3.02 in subjects with sleep bruxism and of 4.2 in those without bruxism. In subjects with bruxism, joint noises and joint pain occurred with increasing frequency.
Occlusal analysis and joint evaluation in subjects with bruxism is shown in Table 2.
Statistical analysis shown that sleep bruxism is significantly associated with mandible lateral shift during mouth opening, with joint pain during examination (p=0.05). Angle class in subjects with and without sleep bruxism is similar. Non-functional anterior guidance is not related to sleep bruxism. Sleep bruxism is associated with non-functional lateral guidance (p=0.04). Interferences or premature contacts during lateral guidance are not influenced by bruxism. Angle class is not associated with sleep bruxism.
Dental wear was encountered especially at the lower and upper incisors; lower incisor wear was significantly associated with sleep bruxism. No subject had generalized dental wear.
Awake bruxism was found in 6 females and 5 males, respectively in 7 Romanian and 4 French subjects. The mean age in subjects with awake bruxism was 23.8 years, similar to those with sleep bruxism and significantly higher than in those without bruxism. Subjects with awake bruxism had a personal occlusal satisfaction score of 3, lower than those without awake bruxism, which showed a score of 3.75. The score of pain and muscle fatigue is 3.27 in subjects with awake bruxism, of 2.14 in subjects without awake bruxism and of 1.46, respectively, in those with no bruxism. Clinical examination of occlusion in subjects with awake bruxism is shown in Table 3.
Statistical analysis shown no correlation between joint noises and awake bruxism but, alternatively, a significant association of awake bruxism with joint pain during examination (p=0.05). Angle class is not associated with awake bruxism. Non-functional anterior guidance is not related to sleep bruxism (p=0.027). Modifications during lateral guidance do not influence the onset of awake bruxism. Dental wear in subjects with awake bruxism was found in the frontal teeth, namely in the lower and upper (5 cases), and only in the lower ones (4 cases). No subject had generalized dental wear.
4.DISCUSSION
The present study analyzed the association between sleep and awake bruxism with occlusal and joint alterations. All subjects had at least one occlusal modification, independently of bruxism. Our results show the absence of any correlation between bruxism and gender, dismissive of the bruxism type, which is also shown by other authors [22-24]. Nonetheless, Wetselaar P et al. showed, in a study published in 2019 on adult Danish subjects, a significant association between female gender and sleep bruxism, respectively awake bruxism [25]. Sousa HCS et al. encountered a higher prevalence of sleep bruxism in male adolescents [26]. Different data reported by several authors suggests the necessity of continuing research on a higher number of subjects, representative for that population. We have identified no correlation between nationality and bruxism, nor does the literature offer information on this topic. Clinical examination of the temporomandibular joint showed a significant association between joint pain and sleep and awake bruxism (p=0.05). Our results show that bruxism is a predisposing factor for TMDs, which include also pain in the dynamic examination of the joint [27]. Related to this, sleep bruxism has been similarly reported by Henrikson et al. [28] in subjects with TMDs. In a study performed on 522 subjects, Van Selms et al. established a relationship between sleep/ awake bruxism and joint pain, irresponsive to subject's psychological state [29], while Nogueira et al. have shown a 5.28 times increased risk of developing TMDs in subjects with bruxism compared to those without bruxism [30]. In a study published in 2018, Prado et al. shown that teenagers with no joint crepitus of sleep or awake bruxism had signs of sleep or awake bruxism [31]. In this study, we have noticed that young subjects with sleep or awake bruxism had an enhanced frequency of joint clicking (60-63.3%) compared to those without bruxism (43.3-49%). Future studies on various age groups would be necessary to establish the joint damage caused by bruxism. We have encountered Angle class distribution in subjects with sleep bruxism similar with the values reported in literature [32], but no relationship could be established between Angle class and bruxism. Clinical examination of static occlusion shown that subjects from all groups had Angle class I (between 72.7-80%), followed by Angle class II (6.7-18.2%) and Angle class III (9.1-13.3%). We have encountered a higher percentage of subjects with Angle class I than the value reported in literature, with a prevalence of 50-60% [32,33,34], but variation also depends on subject's age. In our study, some subjects had finished orthodontic treatment, which corrected the malocclusion. Also, our study showed a statistically significant association between mandible lateral shift during mouth opening and sleep bruxism (p=0.05), yet not sustained in awake bruxism. The existing studies do not reveal information regarding this association, evidencing only the relationship between bruxism and TMDs [29,30], which suggests the need of future studies.
Interferences on the closing path in centric relation were found in 50% of the subjects with sleep bruxism, compared to 27% in those without sleep bruxism (p>0.05), and no differences in subjects with awake bruxism. The role of interferences in centric relation in the onset of bruxism is not supported by the actual studies [8], although Nassif NL et al. published in 1999 positive results in reducing bruxism activity in subjects who received occlusal appliances for repositioning the mandible in a corrected centric relation position [35].
The main aim of this study was to identify the dynamic occlusal modifications which could generate or favor the onset of bruxism. For an individualized analysis, subjects were grouped into subjects with sleep, awake or no bruxism. We have noted for each group, the passive and active interferences or the premature contacts during anterior and lateral guidance. A statistically significant association between sleep bruxism and non-functional lateral guidance was identified (p=0.04), with no contact between mandibular canine and maxillary canine during maximum intercuspation. In subjects with awake bruxism, the absence of passive propulsive interferences is statistically significant (p=0.027), suggesting the absence of occlusion involvement in the etiology of awake bruxism. Safari et. al., in a similar study (2013), have found passive interferences in subjects with bruxism, with no differentiation between sleep or awake bruxism or between passive propulsive interferences and passive lateral guidance interferences, as done in our study. However, their results support the involvement of malocclusion as a favoring factor for bruxism (155). Authors like Yalçn Yeler et al. [36] identified no association between self-reported sleep bruxism and occlusal changes, but their study was different, due to the computerized analysis of the occlusion, compared to the clinical analysis performed in other studies.
Bruxism is one of the major causes of dental wear, whose gravity and distribution depend on the intensity and frequency of the bruxing activity [37,38]. In our subjects, dental wear was located only at the frontal teeth, more among the lower incisors and less among the upper incisors. The absence of dental wear in posterior teeth could be related to the young age of the studied subjects, which may induce reduced consequences of bruxism. Our study analyses exhaustively the associations between the occlusal modifications and the presence of sleep or awake bruxism in young subjects. We found out that several occlusal modifications that can be regarded as an etiological factor of bruxism.
There are some limitations of the present study, as the reduced number of subjects did not allow data analysis on subgroups. It would be interesting to analyze the occlusal and joint modifications during their evolution, after the occlusal treatment, associated with pain relievers for joint pain. Furthermore, the study does not account the psychological aspects that might influence bruxism, as shown by literature reports.
5.CONCLUSIONS
This study supports the hypothesis of bruxism involvement in the onset of TMDs, due to the significant association between sleep and awake bruxism and joint pain. Within the limitations of this study, related to the reduced number of studied subjects and their young age, the results indicate a significant association between sleep bruxism and non-functional lateral guidance, showing the role of malocclusion in the etiology of sleep bruxism. Alternatively, a lack of occlusal evolvement in the etiology of awake bruxism was observed.
As a conclusion, the present study emphasizes the sharp difference between the two types of bruxism: sleep bruxism, with malocclusion involvement, and awake bruxism, with no occlusal interaction. This suggests the necessity of a different therapeutic approach for the two pathologies, customized on specific etiologic factors.
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Abstract
The role of occlusion as a causative factor for bruxism is intensely debated in the literature. [...]recently, the determinant role was imputed to occlusal factors, which include disfunctional occlusion [7]. [...]the aims of this study were to analyze the possible association among awake and sleep bruxism, static and dynamic occlusion and temporomandibular joint structural and functional modifications in healthy adults. 2.MATERIALS AND METHODS The analytical, cohort, observational, crosssectional, prospective study was approved by the Institutional Review Board of the "Iuliu Hatieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania on 19.04.2018 (approval number: 184). The Fonseca questionnaire was applied, with improvement of the 8th question for differentiation of the bruxism type:"Do you clench or grind your teeth?" by division into two sections:"Do you clench or grind your teeth during daytime, when you are awake?" and "Do you clench or grind your teeth during sleep?" Additional questions regarding personal perception of occlusion were added ("Do you feel comfortable with your occlusion?"); presence of joint pain, muscle pain or fatigue in the morning, at awakening, constant use of anti-inflammatory or anxiolytic drugs. [...]all such clinical situations were classified as nonfunctional lateral guidance.
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Details
1 Assistant, "Iuliu Haţieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania
2 Lecturer, "Iuliu Haţieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania
3 Associate professor,"Iuliu Haţieganu" University of Medicine and Pharmacy, Cluj-Napoca, Romania