My observations of masseter size and bruxism

These are my thoughts and observations when facing a patient with occlusal issues. I am unsure if they have a scientific basis or actually make sense but it will be good to learn a bit more about occlusion at Michael Melker's course in Sydney in August.

• Taking notes of the size of a patient's muscles of mastication is important in determining the functional demands on their teeth. Like any muscle, continued use results in hypertrophy. It is less obvious in the temporalis as it is located over the temporal fossa that masks the true thickness of the muscle. The masseter is the main elevator muscle of the mandible and will be enlarged in patients who clench and brux. 
• Correlate masseter size with the patent's risk of sleep apnoea. I have found that the skinny, non class 2 patients with large masseters tend to be awake clenchers. Clenchers will show less wear on their anterior and posterior teeth as the force is mainly vertical though they may display chipped teeth and cracks in their anterior and posterior teeth. As the force is not dissipated through lateral movement, all the force goes through the teeth and they tend to be the ones who crack virgin teeth.
• Clenchers may be clenchers due to aetiology i.e stress related day clenching or because their occlusion doesn't allow them to brux e.g deep bite or lateral interferences that trap them into MIP with a very steep slide into excursions. The ones who are trapped into occlusions tend to exhibit a vertical wear pattern i.e notches on the palatal surface of upper anterior teeth that the lower teeth fit into. They may display teeth splaying or mobility despite sound bone levels in an effort by the body to allow more freedom of movement.
• Clenchers tend to be the ones that complain of a sore tooth in the absence of pathology. Hypersensitivity without exposed dentine and/or tenderness to percussion without a crack or caries is what shows up the most. When clenching, if there are multiple sore teeth this may indicate a maxillary cant that is compensated by vertical elevation of one side of the mandibular occlusal plane by retrusion of the ipsilateral condyle. Take a retracted photograph with the patient's eyes facing forwards or use a fox plane to check. The patient may complain of muscular pain on the side where the maxillary teeth are higher as the elevator muscles are working harder to pull the mandible upwards. They may complain of muscular pain on the contralateral side if the lateral pterygoid is pulling the condyle forward to compensate for the occlusion. 
• They may complain of dental pain on the side where the maxillary teeth are lower as these teeth meet first in CR and will function harder in MIP. When one tooth is sore more so than the rest this is likely one that is high in occlusion or has a lateral interference. Check the occlusion with a leaf gauge and find the point of first contact. This will likely be the sore tooth.
• These patients may show asymmetric muscular hypertrophy
• The periodontal complex is a dynamic structure. The dental hard tissues are largely non dynamic from a structural point of view. 
• To an extent, the dental tissues will respond to bruxism with pulp recession and sclerosis but this does not do anything to manage forces. A crack is technically a structural solution to flexion forces but has the downside of weakening the tooth. As a crack is really the only way for the dental hard tissues to dissipate force, catastrophic fracture is the eventual outcome if the periodontium can't compensate.
• The periodontium can respond by laying down bone to buttress against lateral forces, intrude the tooth to equalise vertical forces, tilt teeth or widen the PDL space to compensate against lateral forces.
• Teeth that are mobile due to bruxism are rarely sure until the point where the mobility leads to a gross high spot on one tooth. Mobility implies that the force has been gradual enough or chronic enough for the body to compensate for the excess force. Patients who have had a sudden onset or acute exacerbation of bruxism won't have time for the bone to resorb and PDL space to widen and may complain of acute dental pain
• Patietns with exostoses or tori are less likely to have mobile teeth in response to bruxism as the physiological response is that of strengthening the teeth. This tensd to happen in patients with long term bruxism. Therefore, these tend to be the patients with large masseters, non mobile teeth and cracked or split teeth.
• I have found that patients with less hypertrophy of the masseters are the ones who exhibit pain after a worse bout of parafunction. Reason this like any other muscle. The person with the largest muscle is more likely to be able to cope with functional demands without pain. The heavy set OSA patient with large masseters is less likely to present with acute myofascial pain but will display and anterior wear pattern with altered passive eruption
• A dental midline discrepancy or a chin deviated to one side when viewed from above can be a sign of mandibular deflection into MIP. The lower jaw must move to one side moving from CR to MIP. This is usually due to an interference on the contralateral side to the deviation to closure in CR and the development of habitual muscular movement guiding the mandible into CR. Therefore these patients won't be able to reproduce these interferences easily. Using a deprogrammer or a leaf gauge will allow you to discover these. The interfering tooth is usually a maxillary posterior tooth which is lingually placed in the arch. Mandibular teeth that deviate from the arch are often there to compensate for the preexisting maxillary interference View the arch in an occlusal photograph and check for symmetry around the mid palatal line. Orthodontics to remove the interference, grinding the teeth in or building the other teeth up can correct this interference. 
• These patients will often have pain in the lateral pterygoid on the same side as the interference as the condyle is pulled forwards to move the mandible the opposite direction. They may complain of masseteric pain on the same side as the ipsilateral heavy contact activates the muscle to fire whenever it contacts.