Bruxism is a controversial phenomenon. Both its definition and the diagnostic procedure contribute to the fact that the literature about the aetiology of this disorder is difficult to interpret. There is, however, consensus about the multifactorial nature of the aetiology. Besides peripheral (morphological) factors, central (pathophysiological and psychological) factors can be distinguished. In the past, morphological factors, like occlusal discrepancies and the anatomy of the bony structures of the orofacial region, have been considered the main causative factors for bruxism. Nowadays, these factors play only a small role, if any. Recent focus is more on the pathophysiological factors. For example, bruxism has been suggested to be part of a sleep arousal response. In addition, bruxism appears to be modulated by various neurotransmitters in the central nervous system. More specifically, disturbances in the central dopaminergic system have been linked to bruxism. Further, factors like smoking, alcohol, drugs, diseases and trauma may be involved in the bruxism aetiology. Psychological factors like stress and personality are frequently mentioned in relation to bruxism as well. However, research to these factors comes to equivocal results and needs further attention. Taken all evidence together, bruxism appears to be mainly regulated centrally, not peripherally.

Summary  The management of bruxism has been the subject of a large number of studies. A PubMed search, using relevant MeSH terms, yielded a total of 177 papers that were published over the past 40 years. Of these papers, 135 were used for the present review. Apparently, research into bruxism management is sensitive to fashion. Interest in studying the role of occlusal interventions and oral splints in the treatment of bruxism remained more or less constant over the years: between 1966 and 2007, approximately 40–60% of the papers dealt with this subject. The percentage of papers that dealt with behavioural approaches, on the other hand, declined from >60% in the first 2 decades (1966–1986) to only slightly >10% in the most recent decade (1997–2007). In the latter period, >40% of the papers studied the role of various medicines in the treatment of bruxism, while in the preceding decade (1987–1996), only approximately 5% of the studies dealt with the pharmacological management of bruxism. Unfortunately, a vast majority of the 135 papers have a too low level of evidence. Only 13% of the studies used a randomized clinical trial design, and even these trials do not yet provide clinicians with strong, evidence‐based recommendations for the treatment of bruxism. Hence, there is a vast need for well‐designed studies. Clinicians should be aware of this striking paucity of evidence regarding management of bruxism.

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Background: Previous randomized controlled trials have addressed the efficacy of mandibular advancement devices (MADs) in the treatment of obstructive sleep apnea (OSA). Their common control condition, nasal continuous positive airway pressure (nCPAP), was frequently found to be superior to MAD therapy. However, in most of these studies, only nCPAP was titrated objectively but not MAD. To enable an unbiased comparison between both treatment modalities, the MAD should be titrated objectively as well. Objective: The aim of the present study was to compare the treatment effects of a titrated MAD with those of nCPAP and an intra-oral placebo device. Methods: Sixty-four mild/moderate patients with obstructive sleep apnea (OSA; 52.0 ± 9.6 years) were randomly assigned to three parallel groups: MAD, nCPAP and placebo device. From all patients, two polysomnographic recordings were obtained at the hospital: one before treatment and one after approximately 6 months of treatment. Results: The change in the apnea-hypopnea index (ΔAHI) between baseline and therapy evaluation differed significantly between the three therapy groups (ANCOVA; p = 0.000). No differences in the ΔAHI were found between the MAD and nCPAP therapy (p = 0.092), whereas the changes in AHI in these groups were significantly larger than those in the placebo group (p = 0.000 and 0.002, respectively). Conclusion: There is no clinically relevant difference between MAD and nCPAP in the treatment of mild/moderate OSA when both treatment modalities are titrated objectively.

Sleep bruxism and awake bruxism are common conditions among Dutch adolescents, with self-reported prevalence rates that are slightly higher than those derived from most large-scale studies on adults. Several predictor variables were found to be exclusively associated with either form of bruxism, corroborating the common suggestion that both circadian manifestations are, at least in part, different entities.

SUMMARY There is a growing interest in bruxism, as evidenced by the rapidly increasing number of papers about this subject during the past 5 years. The aim of the present review was to provide an update of two previous reviews from our department (one about the aetiology of bruxism and the other about the possible role of this movement disorder in the failure of dental implants) and to describe the details of the literature search strategies used, thus enabling the readers to judge the completeness of the review. Most studies that were published about the etiology during the past 5 years corroborate the previously drawn conclusions. Similarly, the update of the review about the possible causal relationship between bruxism and implant failure reveals no new points of view. Thus, there is no reason to assume otherwise than that bruxism is mainly regulated centrally, not peripherally, and that there is still insufficient evidence to support or refute a causal relationship between bruxism and implant failure. This illustrates that there is a vast need for well-designed studies to study both the aetiology of bruxism and its purported relationship with implant failure.

The aim of the study was to assess the influence of four mandibular protrusion positions, at a constant vertical dimension, on obstructive sleep apnea (OSA). Seventeen OSA patients (49.2 +/- 8.5 years) received an adjustable mandibular advancement device (MAD). The patients underwent four polysomnographic recordings with their MAD in situ at, in random order, 0%, 25%, 50%, and 75% of the maximum protrusion. The mean apnea-hypopnea index (AHI) values of the patients differed significantly between the protrusion positions (P < 0.000). The 25% protrusion position resulted in a significant reduction of the AHI with respect to the 0% position, while in the 50% and 75% positions, even lower AHI values were found. The number of side effects was larger starting at the 50% protrusion position. We therefore recommend coming to a weighted compromise between efficacy and side effects by starting a MAD treatment in the 50% protrusion position.

The activity patterns of the masseter and the anterior temporal muscles were studied in twenty-one healthy male subjects while clenching at 10, 20, 30, 40 and 50% of the maximum clenching level. At low clenching levels the temporal muscle activity tended to dominate, at high levels the masseter muscle activity was stronger (P less than 0.001). The asymmetry in muscle activity also depended upon the clenching level (P less than 0.001), while at each level the masseter muscle asymmetry was greater than the temporal muscle asymmetry (P less than 0.05-P less than 0.025). By comparing the electromyographic activities of the left and right side within each subject it was found that the masseter muscle with the higher electromyographic activity tended to have the larger cross-sectional area (P less than 0.01) and at the 50% clenching level it tended to be on the side with the greater number of post-canine tooth contacts (P less than 0.001).