The frequencies of tobacco use, the amount smoked, and perceived bruxism were overall associated as has been reported selleck chemicals earlier (Rintakoski et al., 2010). Independent of genetic background, smoking, and bruxism were associated with identical twin pairs. Further, in the present study, nicotine dependence was associated with more frequent bruxism, even in the presence of a history of major depression and alcohol dependence. The few earlier studies on this topic have all used self-reports of bruxism obtained by questionnaires or interviews for the epidemiological analyses (J. Ahlberg et al., 2004; K. Ahlberg et al., 2005; Johansson et al., 2004; Lavigne et al., 1997; Molina et al., 2001; Ohayon et al., 2001), with a more detailed sleep laboratory examination only in the study of Lavigne et al.

(1997), albeit only on 15 bruxing subjects. Using questionnaires may cause difficulties in defining the actual prevalence of bruxism: It may be even more common among populations than surveys indicate but not recognized as a behavior by individuals because of its potential subconscious nature. However, any underreporting is unlikely to be associated with smoking status or nicotine dependence. It is commonly agreed that sleep bruxism, defined as a stereotyped movement disorder occurring during sleep and characterized by tooth grinding and/or clenching, is in normal subjects detected in about 8% of the adult population (Lavigne, Manzini, & Kato, 2005) The prevalence for bruxism in our study is within the range, as also reported earlier (Hublin et al., 1998).

Bruxism has been associated with stress, anxiety, orofacial pain, and sleep problems. It may also damage teeth and lead to costly treatments. On the other hand, bruxism may as part of sleep arousal mirror reflux disease or sleep apnea (Lavigne et al., 2005). Nevertheless, the pathophysiology of bruxism has remained far from clear. Bruxism has been diagnosed for research purposes using multiple axes: subjective perception by questionnaires and interviews (including a bed partner report of grinding sounds) and objective assessment by extraoral and intraoral examination for secondary clinical signs of bruxism (e.g., masseter hypertrophy, pain on palpation of the masticatory muscles, tooth wear facets, and/or shiny spots on restorations) and/or by electromyographic (EMG) or polysomnographic (PSG) recordings.

Clinical signs of bruxism, however, AV-951 may reflect a problem in the past rather than the present, and even EMG and PSG may only provide a timely indication of a fluctuating phenomenon (Lavigne et al., 2005; Van der Zaag, Lobbezoo, Visscher, Hamburger, & Naeije, 2008). It is commonly accepted that PSG is necessary when physiological events adherent to bruxism episodes are investigated, but it should be borne in mind that most of the epidemiological data on bruxism are gathered from subjects by questionnaire or interview.