Bruxism is a repetitive muscular activity of the jaw characterized by grinding or clenching the teeth and by pulling or pushing the jaw. This can occur during sleep, ‘sleep bruxism’, or when awake, ‘awake bruxism’ (1). Development of this negative mechanical-physiological condition does not discriminate age, sex or ethnicity (2–5).

Worldwide epidemiological data of bruxism reported a prevalence of sleep bruxism of 15.9%, and of awake bruxism of 23.8% (6,7). In Turkey, a prevalence of sleep bruxism of 14.1%, of awake bruxism of 28.2%, and of combined bruxism of 38.8%, was reported (8). Other authors have reported a prevalence in adults of awake bruxism between 22.1 and 31%, and of 12.8% of sleep bruxism (3). Etiologic factors, including physical, biological, psychological and pathological factors are involved (6,8), albeit there is controversy regarding the influence of hereditary factors. A study in children reported a higher prevalence of bruxism (51.3%) whenever one of the parents reported a history of sleep bruxism, in contrast to children of parents with no history (30.6%) (9). Similarly, Michalowicz et al evaluated 494 monozygotic and dizygotic twins, and through questionnaires and clinical analysis they estimated the presence of signs and symptoms of bruxism (10). In their results, no significant differences in clenching or grinding the teeth were found, whether the twins had grown together or were separated. On the other hand, a case-control association study of 114 people in Japan, 48 as a control group and 66 presenting with a diagnosis of sleep bruxism made by using a portable electromyographic device, included the analysis of different variables such as temperament, character, and personality traits as well as related habits, and in parallel they genotyped 13 polymorphisms in four genes related to serotoninergic neurotransmission (SLC6A4, HTR1A, HTR2A and HTR2C). Their results established five predictors of sleep bruxism. These variables were analyzed using multivariate logistic regression stepwise analysis and the researchers reported that only carriers of the C allele of the SNP rs6313 (102C>T) of the HTR2A gene were significantly associated with an increased risk of sleep bruxism (OR=4.250, 95% CI 1.599–11.297; P=0.004). Authors of that study also concluded that a genetic factor may contribute to the etiology of sleep bruxism (11). In addition, the HTR2A gene has been associated with other psychological and systemic conditions, including schizophrenia (12), obsessive compulsive disorders (13), and depressive disorders as well as with psychosomatic symptoms (14). It was also found, in the literature, that 5HT2A is known as the 5-HT2 gene. In other studies, the interaction of serotonin (5-HT) as a neurotransmitter in behavioral responses to environmental stimuli particularly in the social environment has been reported, with this playing an important role in social responses and being associated with mood, sleep, circadian rhythm, thermoregulation, and social behavior. An association to the stress response and coping has also been reported (15,16).

Several psychological traits that have been reported in individuals with bruxism, such as anxiety and neuroticism personality trait, suggesting an anxious individual, have been linked to the rs6313 polymorphism of the 5HT2A gene (17,18). In Mexico, the Sistema Nacional de Salud (National Health System) in 2009 reported a prevalence of bruxism of 4.6% in a sample of 10,536 users of public health services; however, these data did not include information from the private sector (19). It is important to study bruxism because it is an unfavorable condition for individuals who suffer from it. Furthermore, in previous studies, discrepancies in the results have been reported. In addition, other studies of this condition (bruxism) do not develop an integral analysis. Thus, research related to bruxism is focused on its etiology, epidemiology, pathophysiology, and alterations in sleep physiology (6,20,21), and its relation with different psychological factors (2,8,22,23). Different articles include an assessment of factor inheritance (9) because of the relationship between the function of a particular gene and its expression through physical and behavioral traits (24). Regarding the rs6313 polymorphism in the HTR2A gene, it has been associated with stress, and anxiety, because of the changes these emotions have in the serotonergic system (15–18), as well as with sleep bruxism (11).

Owing to the integrated relationship between these variables, the aim of the present study was to investigate the associations between self-reported bruxism, anxiety, and neuroticism personality trait with the rs6313 polymorphism in the gene HTR2A, in a population from Northeastern Mexico.

The pathophysiological traits associated with bruxism were quantitatively measured by the SBQ (26). When the results obtained with the cutoffs established by the authors were compared, the mean of the bruxism group, 27.25 [standard deviation (SD) = 7.66], placed it in the range of the definitive clinical diagnosis of bruxism. In the data reported from the subgroups, the mean was higher in G4 than in the combined bruxism group, 32.21 (SD = 7.50). In contrast to G1, the control group, 13.91 (SD = 2.97) reflected a very low probability of symptoms associated with bruxism. With the results of this scale, we can confirm that those individuals who report combined bruxism perceive more symptoms associated with bruxism during wakefulness and during sleep, in contrast to those of the other subgroups.

The psychological traits evaluated were anxiety and neuroticism, as these, besides being associated with bruxism, have been associated with the 5HT2A (rs6313) SNPs. To measure anxiety symptoms, the BAI version adapted to the Mexican population was used (27). Regarding symptoms of anxiety in the control group, mean = 8.38 (SD = 8.27), and bruxism, mean = 12.44 (SD = 9.96) from the subgroups, the highest score was reported by the combined bruxism, mean = 14.80 (SD = 10.30). These results confirm that the more the symptoms of bruxism, the higher the level of anxiety. The correlation between symptoms of anxiety and self-reported bruxism was r=0.393, P=0.01. Personality trait neuroticism was assessed with the Eysenck Personality Questionnaire Revised-abbreviated (EPQR-A), using the adapted Spanish version (28). The results for neuroticism in the control group were mean = 2.28 (SD = 1.49), and for bruxism, mean = 2.82 (SD = 1.71). For the subgroups, the highest score was in the combined bruxism group, mean = 3.26 (1.49). Bilateral correlation between levels of neuroticism and self-reported symptoms of bruxism was r=0.337 (P=0.01) and between neuroticism-anxiety, r=0.528 (P=0.01). The neuroticism trait indicates a tendency of the individual to present anxiety. These results indicate a greater tendency for neuroticism trait in individuals with more symptoms of self-reported bruxism and anxiety. The inherited context is controversial because some studies on families report a significant association when several members clench or grind their teeth as in the study performed by Lobbezoo et al (9). That study included 39 children aged 3 years and through a questionnaire they established whether any family members clenched or grinded their teeth. Their results reported a 51.3% higher prevalence of bruxism when one of the parents reported a history of sleep bruxism, in contrast to those children of parents with no history (30.6%). Regarding research on twins, the study performed by Michalowicz et al (10), who evaluated 494 pairs of twins between 16 and 80 years (M = 46.4±12.3), identified no significant difference in grinding or clenching teeth in either types of monozygotic and dizygotic twins. Rintakoski et al, included 1,141 pairs of twins between 23 and 27 years of age (M = 24) (30). The diagnosis of bruxism was performed asking the question ‘Do you grind your teeth?’, giving five response options: Nightly, weekly, occasionally, or once a week, never, and I do not know; in order to classify patients according to their frequency of symptoms, ‘weekly bruxism’, ‘rarely bruxes’ and ‘never bruxes’. Their results indicated that the genetic factor determines 52% of the variance for bruxism during sleep in both sexes.

Furthermore, research suggesting a genetic association is scarce, as in the case-control study of Abe et al (11), which investigated the association of genetic, psychological, and behavioral factors with sleep bruxism in a Japanese population. It included 114 individuals between 20 and 70 years of both sexes; 66 diagnosed with sleep bruxism and 48 as controls. It was through questionnaires adapted in Japanese, such as the Epworth Sleepiness Scale (ESS), that it was possible to assess the presence or absence of snoring, apnea/hipopnea, and restless legs. By using the NEO-FFI questionnaire, personality traits were assessed together with the Temperament and Character Inventory (TCI). Those authors also included a questionnaire to assess the presence of familial aggregation with stressful events in the past, the habit of grinding during daytime, TMD and daytime headache, with the option of a dichotomous (yes/no) answer. As well as the presence of daily habits such as the amount of cigarettes smoked, alcohol ingestion, and caffeine intake, their results reported that only the presence of restless legs was associated with sleep bruxism (P=0.036). Regarding genotype, they found a significant association of the C allele carrier of the SNP rs6313 (102C>T) from gene HTR2A with an increased risk of sleep bruxism (OR=4.250; 95% CI 1,599–11,297; P=0.004); thus, they stated that the genetic factor may contribute to the etiology of sleep bruxism. Particularly stress and anxiety of symptoms were assessed via a short dichotomous question-type questionnaire, making it difficult to establish the level of stress and/or anxiety and its difference with the control group. In the present study, with the results of the psychometric instruments used at hand, the presence of anxiety and neuroticism traits in individuals with bruxism was confirmed.

In order to perform genotype analysis, the sample was divided by generations and four groups were established according to self-reported signs and symptoms. The Hardy-Weinberg test was used in this sample; however, when performing the analysis of genotypic homogeneity (genotypes C/C, C/T and T/T) vs. the four groups, (3×4), no trend was observed between the SNP rs6313 and the individuals from the different analyzed groups (F=4.517, P=0.612). In contrast to the subjects from Japan, in this population from northeastern Mexico, there was no significant genetic association found, which is explained by the close relationship between genetic factors and the environment and by its influence to cause individual differences in genes related to personality traits, cognitive skills, and specifically, bruxism (31,32). However, out of the four groups, the farthest from significance was the control group with P=0.82, unlike the combined bruxism group with P=0.10. For this reason, the latter group was considered for odds ratio analysis, determining that combined bruxism has a higher relative risk of neuroticism traits (OR=15.0; CI 1.52–148.32), and a higher relative risk of anxiety symptoms in grade 3-moderate (OR=3.56; 1.27–10.03), and in grade 4-severe (OR=8.40; CI 1.45–48.61). In this study, through the use of psychometric scales, a positive correlation between anxiety and neuroticism psychological traits in subjects with self-reported symptoms of bruxism, can be confirmed, additionally noting that the highest score was reported by subjects who self-reported combined bruxism. Thus, the association between greater perception of symptoms of bruxism with sensitivity to symptoms of anxiety and neuroticism trait is strengthened. Furthermore, these data were confirmed by separating the sample by generations and by genotypic homogeneity. This evaluation found that combined bruxism has a higher relative risk of developing traits of neuroticism and anxiety symptoms in grade 3-moderate and grade 4-severe individuals. No significant difference was found in the association between patients with bruxism (sleep, waking or combined) and the rs6313 polymorphism HTR2A gene. Polymorphisms associated with either normal or pathological traits are population-related; thus, it may be that either this is not related to bruxism in our population or it may be due to the heterogeneity of the Mexican population as well as the size of the sample.