In today’s blog we continue to explore the different bruxism phenotypes.
Perhaps one of the biggest reasons for the confusion in the literature was the failure to differentiate sleep bruxism from bruxism occurring when awake.
Approximately one third of patients with SB also exhibit concomitant wake-time bruxism. The latter has an estimated prevalence of 12% in children and >20% in adults [1]. Psychosocial factors like stress, anxiety-hypervigilance and personality traits have significant influence on AB whereas there is less evidence to support their role in the pathogenesis of SB. The Polyvagal Theory (Porges, 1995)[2] which describes the development of the mammalian social engagement system and the involvement of the myelinated vagus, provide insights that suggest AB may be an effective adaptive strategy employed by certain individuals under stress to increase their ‘vagal brake’. The stoic socio-cultural environment (rewarding self-control, discouraging the open expression of emotions, keeping your mouth shut and your teeth together!) rather than genetics are thought to be responsible for significant racial differences in the higher prevalence of oral tori/bony exostoses in Asians [3, 4].
In the lead up to our July symposium, I wish to begin dismantling the misconceptions surrounding Sleep Bruxism and the unsupported views held by some local dentists regarding its management. This is the first in a series of weekly blogs covering various aspects of clinical practice and I hope the insights I have gained over the course of my career, will encourage you to re-evaluate commonly accepted, non-evidence based dogma so prevalent in dentistry….
