Effects of bruxism. Bruxism may cause muscle hypertrophy and severe damage to the dentition. The parafunctional forces applied during bruxism have also been suggested in the aetiology of dental implant failure, periodontal tissue damage and tooth fracture. Hypothetically the repetitive overloading of the TMJ and muscles by bruxing movements may cause tissue damage leading to TMD. It is possible that muscle overload may initiate or reactivate TrP in susceptible individuals.
In order to be able to establish a cause and effect relationship between bruxism and POMP the evidence needs to be examined with several criteria as basic tenets; bias, chance and confounders are absent, the association is consistent, bruxism must precede POMP, some type of relation exists between the degree of bruxism and the severity of the POMP (i.e. a dose–response) and the association makes epidemiological sense (Lobbezoo and Lavigne, 1997). We will presently examine whether occlusal discrepancies induce muscle hyperactivity and if occlusal discrepancies or muscle hyperactivity can cause POMP.
Bruxism and orofacial pain. Excessive bruxism with insufficient relaxation, as in jaw clenching, is thought to lead to muscle ischaemia and pain. In this context the most widespread belief is that POMP is induced by repetitive tooth clenching, grinding or abnormal posturing of the jaw. These habits are, however, extremely common and statistically have not been proven to induce POMP. Evidence for masticatory muscle hyperactivity in the aetiology of POMP is largely indirect, and relies mostly on experimental tooth clenching.
Masticatory muscle pain has been studied experimentally using two general approaches. Exogenous models of pain involve the injection of algesic substances into muscle and are discussed later in this section. Endogenous models of experimental pain have been studied extensively and involve the persistent contraction or exercise of masticatory muscles (Christensen, 1971, 1981; Scott and Lundeen, 1980; Clark et al, 1984, 1991; Bowley and Gale, 1987; Choy and Kydd, 1988; Buchner et al, 1992; Gay et al, 1994; Lund and Stohler, 1994; Svensson and Graven-Nielsen, 2001; Turp et al, 2002; Shiau et al, 2003; Ariji et al, 2004; Glaros and Burton, 2004). These experiments have produced inconsistent, non-specific and inconclusive results questioning the role of muscle hyperactivity/overload in POMP.
Obviously these intensive experimental exercises are not identical to the chronic parafunctional activities, which occur in patients. For example chronic low level clenching induces muscle pain but again only in a subset of patients (Glaros et al, 1998). Population studies suggest that tooth grinding may cause myalgia (Macfarlane et al, 2001, 2003b; Lobbezoo et al, 2006). It has also been found that self reported clenching is more consistently associated with POMP than grinding although there was no cause and effect relationship established (Velly et al, 2003). The reliability of self reported bruxing habits is problematic; 85–90% of the population will report that at some time they have ground or clenched their teeth (Bader and Lavigne, 2000). Many patients who self report tooth grinding admit that this was first brought to their attention by their dentist (Marbach et al, 1990). The reliability of clinician judgements of bruxism has been found to be extremely poor (Marbach et al, 2003). Notwithstanding, self reported clenching is frequently associated with POMP (Huang et al, 2002; Johansson et al, 2006). However, the directionality of a possible cause and effect remains unproven and in addition bruxism and POMP may be clinical manifestations of a shared neuropathology.
Whilst the models described have not totally elucidated the mechanisms underlying POMP they have consistently shown that pain following experimental muscle contraction is of short duration and self-limiting. Thus, sustained or repeated abnormal loading of the masticatory apparatus as in these experiments is of a doubtful primary role in POMP.
If muscle hyperactivity is clearly related to POMP, bruxers should report more muscle pain. Some preliminary results suggest that a majority of patients with bruxism have pain levels and sleep quality comparable with POMP patients (Lavigne et al, 1991). Myalgia is reported in only 20–30% of bruxers and it unclear if this is a myofascial pain or a form of post exercise muscle soreness (PEMS) (Lavigne et al, 1996; Bader and Lavigne, 2000). Recent studies show that only gender, joint clicking and other non-painful TMD symptoms are significantly related to nocturnal EMG activity or bruxism (Ahlberg et al, 2004; Baba et al, 2005). Moreover, 19.7% of POMP patients report peak pain in the morning whilst in bruxers this is 83.3%, suggesting that the latter may indeed be a form of PEMS (Lavigne et al, 1996; Camparis and Siqueira, 2006). In addition, the bruxers with morning pain have less tooth-grinding episodes than those without (Bader and Lavigne, 2000; Rompre et al, 2007). This may be due to a protective mechanism that reduces muscle activity in the presence of pain. Alternatively the high bruxers with no pain may have undergone an adaptive process (Bader and Lavigne, 2000). Comparing bruxers with and without TMD no significant differences in bruxism levels or sleep patterns were present (Camparis et al, 2006). In contrast a study on adult bruxers revealed frequent complaints of orofacial and bodily pain and 65% reported frequent headaches in the morning (Bader et al, 1997). However, the patients in this study (Bader et al, 1997) reported more comorbid features such as anxiety and tension than those in previous studies (Lavigne et al, 1996).
In summary, available data do not support the traditional concept of POMP induced or maintained by muscle hyperactivity (Lund et al, 1991). Moreover, examining the available data vis-a-vis the ideal criteria for establishing a cause and effect relationship casts serious doubts on the validity of the hypothesis that muscle hyperactivity leads to POMP. Bias and confounders such as anxiety, EMG activity from the muscles of facial expression and the separation of rhythmic masticatory muscle activity from actual grinding or clenching are not consistently excluded or accounted for. Daytime or sleep bruxism may be different in their effects on the masticatory system but these have not been separated in studies. The association between bruxism and POMP is inconsistent; experimental models show a high degree of selectivity and no prolonged muscle pain. No dose–response is present as demonstrated by the facts that bruxers do not report extremely high levels of POMP and high activity bruxers in fact complain less of morning muscle pain than do low level bruxers. Finally the association makes little epidemiological sense; TMD are rare in children in whom bruxism is most common and TMD/POMP peaks in young adults when bruxism is shown to be decreasing in frequency. There is little evidence to support SB in the aetiology of POMP but the role of bruxing and clenching habits particularly in the daytime are as yet unclear (Lobbezoo et al, 2006). In addition, we have little data on the ability of such bruxing habits to activate or initiate TrP in masticatory muscles in a similar way that has been suggested for myofascial pain in other regions (Simons, 2004). Based on the above the vicious cycle theory is untenable and an alternative model is needed to explain motor changes in patients with muscle pain and disorders.
The pain-adaptation model. The pain-adaptation model is based on data from persistent musculoskeletal pain conditions (including that of POMP) and proposes that the observed changes in motor function are secondary to persistent pain and mediated at the spinal level (Lund et al, 1991). Changes in masticatory muscle function, secondary to experimental muscle pain as described above, support this model and confirm clinical complaints of dysfunction in muscular TMD patients (Svensson and Graven-Nielsen, 2001). Injection of hypertonic saline into the jaw muscles induces pain with a significant reduction in jaw movements and in EMG activity during the agonist phase accompanied by a small increase in antagonist muscle activity (Graven-Nielsen et al, 1997; Svensson et al, 1998a). The pain-adaptation model suggested that pain will induce inhibition of alpha motorneurons during jaw closing and facilitate these during antagonist (opening) activity (Lund et al, 1991). This model therefore accurately fits the currently available data. More recently the ‘Integrated Pain Adaptation Model’ has been suggested (Murray and Peck, 2007) which proposes that the existing Pain Adaptation Model is a subset of a broader model that could be called the Integrated Pain Adaptation Model. This model is based on the premise that pain acts as a homeostatic emotion requiring a behavioural response; an optimized recruitment strategy of motor units that represents the individual’s integrated motor response to the sensory-discriminative, motivational-affective and cognitive-evaluative components of pain. This recruitment strategy aims to minimize pain and maintain homeostasis.
If muscle dysfunction is not the cause of pain but rather part of the spectrum of a ‘pain-adaptation’ response then some of the parafunctions including some of the bruxing habits can no longer be considered as a primary aetiological mechanism of pain in POMP (Lund et al, 1991). However, the precise association between bruxism and POMP remains unclear at this stage.