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DISCOVERY! |
Department of Oral Function, Section of Oral Kinesiology, Academic Centre for Dentistry Amsterdam (ACTA), Louwesweg 1, 1066 EA Amsterdam, The Netherlands; f.lobbezoo{at}acta.nl
Martin A. Taubman, Editor
KEY WORDS: tooth wear • temporomandibular pain • oral movement disorders • bruxism • sleep disorders
INTRODUCTION
Faces don’t lie. Indeed, many things can be read from a person’s face, like feelings of sorrow, agony, and pain. Dentists know that such non-verbal information and chair-side narratives are equally important outcomes of taking an oral history. At the same time, the dentition is worthy of observation at speaking distance as well. People always think that dentists secretly study the dentition of the person to whom they are speaking, so that they can learn, for example, about the shade of the person’s teeth. Speaking for myself, however, I am not interested in tooth color as much as in the visible wear of the dentition.
Tooth wear is a growing problem in our aging population, and can be caused, at least in part, by grinding of the teeth. Grinding is one of the possible manifestations of bruxism, an oral movement disorder. The term "bruxism" is derived from the Greek words "vrigmos ódodon" and includes both grinding and clenching. People seem to engage in bruxism as if to fight off pain. In the Bible (Matthew 13), Jesus explains the parable of the weeds in the field as follows: "As the weeds are pulled up and burned in the fire, so it will be at the end of the age. The Son of Man will send out his angels, and they will weed out of his kingdom everything that causes sin and all who do evil. They will throw them into the fiery furnace, where there will be weeping and gnashing of teeth." Apparently, the purported causal link between bruxism and negative emotions like pain has been common knowledge for about 2,000 years!
The Belgium Royal Museums of Fine Arts in Brussels display a small, 166 x 92 mm, 16th century oil painting by Pieter Brueghel the Elder that features the face of a Flemish farmer (Fig.
). The peasant has his eyes forcefully closed and his mouth wide open, as if he is yawning intensively. Indeed, the panel is called "The yawner" or "Head of a yawning man". However, three decades ago, David Marsden of the Institute of Neurology, Queen Square, London, recognized blepharospasm (i.e., a tonic spasm of the orbicularis oculi muscle, resulting in closure of the eyelids) and a dystonically opened mouth in the farmer’s face. This combination of blepharospasm and oromandibular dystonia represents the segmental movement disorder, "Meige syndrome". Since Marsden’s observation, this disorder is also called "Brueghel syndrome". Interestingly, it is still considered possible that the farmer in Brueghel’s painting is actually yawning. Brueghel was very knowledgeable about the peasant men and women of his time, including their good and bad qualities. It is therefore not unlikely that the yawning man represents the Capital Sin of Idleness. My personal contribution to this discussion is that this farmer was an obstructive sleep apnea (OSA) patient, and consequently suffered from excessive daytime sleepiness (see below: Sleep Disorders with Dental Implications). For me, this face doesn’t lie!
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TEMPOROMANDIBULAR PAIN
In our clinic for oral kinesiology at ACTA, patients often report with temporomandibular pain (TMP). For this condition, many etiological theories have been proposed and rejected. Currently, the multifactorial, biopsychosocial etiological model is being considered. As a working hypothesis, a disturbance between load and load-bearing capacity is thereby used. Bruxism is frequently put on the load side of the balance. However, even though this is a common clinical feeling of dentists—including myself—solid evidence for a causal relationship between bruxism and TMP is lacking (Lobbezoo and Lavigne, 1997). To prove causality, longitudinal studies are necessary. Such time-consuming studies must meet several criteria, including a sufficient number of observations (i.e., a number that respects the natural fluctuation in both bruxism and TMP), and the use of proper techniques to quantify the conditions under study. For TMP, a standardized clinical examination may be sufficient. Also, a diary may be used to quantify TMP, as long as the investigators remember that self-reported data have their limitations. Daytime clenching may be quantified with a diary as well, but for sleep bruxism, electromyographic or even polysomnographic recordings are required. This obviously limits the feasibility of longitudinal studies on the purported causal relation between bruxism and TMP. So far, only a few case studies on this subject, with instrumental techniques used to quantify sleep bruxism, have been published (e.g., van Selms et al., 2004). Thus, large-scale studies are badly needed.
ORAL MOVEMENT DISORDERS
Above, I introduced bruxism as an oral movement disorder. For me, the story of this group of clinical conditions started in 1993. After completing my PhD thesis on the jaw-stretch reflex, under the solid supervision of Frits Bosman, Hilbert van der Glas, and Andries van der Bilt at the Utrecht University in The Netherlands, I had the privilege to spend three post-doctoral years at the Université de Montréal, Québec, Canada, in the laboratory of Gilles Lavigne. This inspired pioneer in sleep disorders in dental patients guided my first steps in the field of sleep bruxism and other oral movement disorders. Together with his colleagues Jacques Montplaisir, a psychiatrist and specialist in sleep medicine at the Hôpital du Sacré-Coeur, and Jean-Paul Soucy, a nuclear radiologist at the Hôpital Notre-Dame, we performed a series of interesting studies.
In part, these studies dealt with the role of neurotransmitter systems (especially the dopaminergic one) in the etiology of sleep bruxism (for a review, see Lobbezoo and Naeije, 2001). Dopaminergic medicines that are mainly indicated for use in the treatment of Parkinson’s disease, such as the catecholamine precursor L-dopa and the dopamine D2 agonist bromocriptine, were found effective in reducing the number of bruxism events per hour of sleep. After my post-doctoral period, I continued my work in the field of oral movement disorders with Machiel Naeije, a biophysicist and chair of the department of Oral Function of ACTA, in close collaboration with Hans Hamburger, a neurologist and specialist in sleep medicine at the Slotervaart General Hospital, Amsterdam, The Netherlands. Among other findings, we encountered a lasting reduction of sleep bruxism after three months’ treatment with a low dose of pergolide, a dopamine D1/D2 receptor agonist (van der Zaag et al., 2007). Since this intriguing observation was made in a single patient, we are currently conducting a long-term randomized clinical trial in our laboratory, using a specific dopamine D2 receptor agonist with fewer possible side-effects than those that we have been using so far.
Dentists should note that dopaminergic medicines cannot be prescribed for bruxism patients on a routine basis, especially not by the dentists themselves. At least one medical specialist should be involved, to monitor not only the desired effects, but also the undesired side-effects. An even more important reason to be cautious with these types of medicines is the fact that high doses may lead to the development of oral dyskinesias. In an excellent overview of the literature, Blanchet et al.(2005) defined these movement disorders as abnormal, involuntary, uncontrollable movements predominantly affecting the tongue, lips, and jaw. Interestingly, the accompanying jaw movements resemble bruxism, so this movement disorder can be considered a secondary, iatrogenic type of bruxism. Hence, we have an interesting paradox at hand: Primary, idiopathic bruxism may benefit from a treatment with dopaminergic substances, while this treatment, in turn, may cause iatrogenic bruxism as part of an oral dyskinesia.
The chronic use of other types of medicines may also cause oral movement disorders (Blanchet et al., 2005). For example, neuroleptics like haloperidol may cause tardive dyskinesia, a disorder that may resemble bruxism. Discontinuing the offending medicine does not usually ameliorate this disorder, as is mostly the case after withdrawal from dopaminergic medicines. In fact, tardive dyskinesia sometimes surfaces only after the neuroleptics have been discontinued.
Where oral dyskinesias are relatively mild, oro-mandibular dystonias are much more intense (Blanchet et al., 2005). Again, bruxism-like contractions of the masticatory muscles may be present, and the facial expressions are sometimes so extreme that the disorder is misattributed to a psychogenic cause. Oro-mandibular dystonia may also be caused by the chronic use of neuroleptics, and is then called tardive dystonia. This form of dystonia is relatively mild, and there is a chance—albeit small—of remission after the offending medicine is discontinued. The primary form of oro-mandibular dystonia, however, is more frequently encountered, and may be caused by severe neurodegenerative disorders like Huntington’s disease, disorders of the basal ganglia, or trauma.
Treatments of oral dyskinesias and oro-mandibular dystonias are mostly palliative (e.g., benzodiazepines, intramuscular botulinum toxin injctions, etc.), and must be performed in close collaboration with medical specialists. The role of dentists, however, is important as well: They may be the first to recognize the movement disorder. Their discussions with the treating medical specialists are also of importance: Together, dentists and medical specialists should create a situation in which the dyskinetic or dystonic patient can be treated for his/her (sometimes extensive) dental problems, which may, at least in part, be caused by the movement disorder. Certain dental procedures may lead to oral movement disorders, but the evidence is limited (for a review, see Blanchet et al., 2005). More research is needed for further elucidation of the dental aspects of oral movement disorders.
BRUXISM
Undoubtedly, bruxism is the most frequently occurring oral movement disorder. It may occur in people both while awake and during sleep. Both forms probably have different etiologies, and their diagnosis and treatment require different approaches. Treatment is indicated when bruxism causes pain in the masticatory system (e.g., TMP), or leads to damage such as tooth wear or fractures of teeth, restorations, or even of implants. Most studies thus far have dealt with sleep bruxism, because it is more easily quantified. A recent example from our laboratory is a randomized clinical trial with occlusal stabilization splints (van der Zaag et al., 2005). In a placebo-controlled, parallel design, some patients benefited more from such appliances than others; no group effect was observed. This suggests that caution is required when splints are indicated, apart from their obvious role in protecting against tooth wear. More randomized trials are needed to prove or reject the efficacy of this (and other) treatment options for (sleep) bruxism.
A focused review about the etiology of bruxism (Lobbezoo and Naeije, 2001) concluded that there is no (or hardly any) role for morphological factors in the etiology of bruxism, while psychological factors (e.g., stress) and pathophysiological factors (e.g., disturbances in central neurotransmitter systems) seem, to a greater or lesser extent, to be involved in the etiology of this oral movement disorder. In addition, Gilles Lavigne’s laboratory performed another interesting series of studies on the role of arousals in sleep bruxism. Arousals, i.e., abrupt changes from a deeper sleep stage to a lighter one, or even toward wakefulness, turned out to be frequently followed by bruxism events (Kato et al., 2001). Our own observations (unpublished) show that the reverse can also occur.
SLEEP DISORDERS WITH DENTAL IMPLICATIONS
Sleep disorders like snoring and OSA may also have dental implications. OSA is characterized by repetitive obstructions of the upper airway, often resulting in oxygen desaturation and, thus, arousal from sleep. It is a serious condition, with excessive daytime sleepiness and life-threatening cardiovascular diseases as its possible consequences. While the diagnosis and treatment of OSA obviously belong to the domain of medical specialists, dentists can be asked to make an intra-oral device that is specifically designed to keep the upper airway open by pulling the lower jaw forward during sleep. Many studies of the efficacy of such devices have been performed, and in our laboratory, results from a pilot study support the possible effectiveness of the so-called mandibular advancement device in the treatment of moderate OSA in particular (Aarab et al., 2005). It should be noted, however, that many aspects of such treatment are still unclear, such as possible adverse reactions, compliance, and efficacy after long-term usage.
CONCLUDING REMARKS
Above, I have sketched the central position of oral movement disorders like bruxism within the discipline of Oral Kinesiology. Considerable research is still needed to advance this field, especially regarding the purported causal relationship between bruxism and temporomandibular pain, the dental implications of oral movement disorders, and the diagnosis, etiology, and treatment of (sleep) bruxism and OSA. Hence, there is an abundance of challenges for all of us at the interface of wear and tear!
ACKNOWLEDGMENTS
Part of the work described in this paper was supported by the Canadian Medical Research Council (CMRC), the Fonds de la Recherche en Santé du Québec (FRSQ), and the Netherlands Institute for Dental Sciences (IOT). I am grateful to all my former and present colleagues in Utrecht, Montréal, and Amsterdam, as well as to my ’collaborative friends’ around the world, without whom I could never have realized the various research projects. This paper is based on the author’s remarks, "Tussen slijten en verbijten", delivered on March 10, 2006, on the occasion of the public acceptance of his full professorship of Oral Movement Disorders at the Faculty of Dentistry, University of Amsterdam, The Netherlands.
Received March 24, 2006; Last revision November 14, 2006; Accepted November 14, 2006
REFERENCES
Aarab G, Lobbezoo F, Wicks DJ, Hamburger HL, Naeije M (2005). Short-term effects of a mandibular advancement device on obstructive sleep apnea: an open-label pilot trial. J Oral Rehabil 32:564–570.[ISI][Medline]
Blanchet PJ, Rompré PH, Lavigne GJ, Lamarche C (2005). Oral dyskinasia: a clinical overview. Int J Prosthodont 18:10–19.[ISI][Medline]
Kato T, Rompré P, Montplaisir JY, Sessle BJ, Lavigne GJ (2001). Sleep bruxism: an oromotor activity secondary to micro-arousal. J Dent Res 80:1940–1944.
Lobbezoo F, Lavigne GJ (1997). Do bruxism and temporomandibular disorders have a cause-and-effect relationship? J Orofac Pain 11:15–23.[Medline]
Lobbezoo F, Naeije M (2001). Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil 28:1085–1091.[ISI][Medline]
van Selms MK, Lobbezoo F, Wicks DJ, Hamburger HL, Naeije M (2004). Craniomandibular pain, oral parafunctions, and psychological stress in a longitudinal case study. J Oral Rehabil 31:738–745.[ISI][Medline]
van der Zaag J, Lobbezoo F, Wicks DJ, Visscher CM, Hamburger HL, Naeije M (2005). Controlled assessment of the efficacy of occlusal stabilization splints on sleep bruxism. J Orofac Pain 19:151–158.[ISI][Medline]
van der Zaag J, Lobbezoo F, van der Avoort PG, Wicks DJ, Hamburger HL, Naeije M (2007). Effects of pergolide on severe sleep bruxism in a patient experiencing oral implant failure. J Oral Rehabil (in press).
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