Clinical Signs of Bruxism

Attrition and Vertical Dimension

Attrition is the normal loss of tooth substance that results from friction by physiologic forces. ⁷Dental attrition is caused by tooth-to-tooth contact, resulting in loss of tooth tissue, usually starting at the incisal or occlusal surfaces. Clinical crown damage of the teeth can significantly thin the enamel structure, thus exposing the underlying structure called dentin (Figure 1). Dentin is softer and darker, increasing the risks of sensitivity, decay and discoloration. The etiology of dental attrition is multifactorial, with the most common cause being bruxism.

Figure 1.

Figure 1.

Attrition exposing dentin on tooth #25.

Due to attrition, the teeth will appear flattened from the wearing down of the occlusal surfaces of the enamel, causing enough reduction to alter the vertical dimension (Figure 2). Changes may be noticed not only by the reduction of the crown height, but also with the interproximal contact relationships. What was once a tight contact can eventually open up due to grinding the teeth down past the contact point.⁵ In this situation it eventually puts the mandible and maxilla closer together when in occlusion, bringing the nose and chin nearer to each other. This effect may also portray an older appearance. The jaw will appear sunken and deeper wrinkles of the skin around the mouth cause the lips to seemingly disappear.³⁸

Figure 2.

Figure 2.

Progression of vertical dimension from years of bruxism.

Wear Patterns

Wear facets are damage to the tooth, recognized as highly polished, smooth, flattened wear patterns on the enamel. This happens in unusual places for wear to logically occur through regular chewing. The distal corners of the maxillary central and lateral incisors are very common areas where damage from bruxism is noticed. Common canine wear facets are rounded over to the labial surface of the cusp tip, whereas normal mastication wear blends over to the lingual surface.⁵

Canines tend to show the first visual signs of bruxism because the anatomy of a canine is longer and more pointed than other tooth types. Wear facets or flat canines are obvious visual signs of grinding (Figure 3). As the canines become shorter and become in line with the occlusal line of the premolars, the force is then shared with the rest of the molars (Figure 4). Signs of attrition on molars start with the cusps flattening out and can even wear through to the dentin.³⁹

Figure 3.

Figure 3.

Facial surface exhibiting flattened, smooth, polished enamel wear on tooth #23.

Figure 4.

Figure 4.

Lingual and occlusal surfaces exhibiting polished wear on tooth #5.

First molars can show significant wear since they are one of the first permanent teeth to erupt in the oral cavity. Having the longest longevity in the mouth leaves them exposed to maximum activity over a lifetime. They withstand bruxing through mixed dentition and before orthodontics is initiated to adjust malocclusion. Usually if there are wear signs on the mandibular, there will be complementary wear signs on the maxillary. Wear facets may also show unilaterally (for a more dominant side of bruxing) or bilaterally (equal throughout the mouth).⁵

Abfractions

Abfraction is a mechanism that explains the loss of enamel and dentin caused by flexure and ultimate tissue fatigue of susceptible teeth at locations away from the point of loading. The breakdown is dependent on the magnitude, duration, frequency and location of the forces located at the cervical area of the tooth.^4,7 This happens when the tooth has flexed greatly during the grinding process and the root surface begins to break down and form a scooped or notched out appearance. It is the mechanical failure of the tooth structure.¹⁰

Chipping, Breaking, Cracks and Fractures

Putting a constant amount of force on the enamel weakens the area and can contribute to small fractures, which lead to chips and breaks.⁷ As teeth wear, the edges of the anterior teeth and the cusps or corners of the posterior teeth will begin to show micro-fractures or cracks, which usually cannot be seen on radiographic images (Figures 5‑6). Sometimes patients think these fractures are cavities because they can become stained or discolored and may be sensitive to hot and/or cold. As these fractures deepen to the constant pressure, they will eventually chip, break a corner, or damage the pulp requiring endodontic (root canal) therapy. In extreme cases the tooth may need to be extracted. The fracture begins on the outer surface of the tooth and eventually deepens until the crack enters the nerve, which leads into cracked tooth syndrome–an etiology of bruxism.^21,39

Figure 5.

Figure 5.

Jagged, chipped and thinning enamel on the incisal edge.

Figure 6.

Figure 6.

#9 – small chips
#10 – flat, smooth incisal

Periodontal Recession and Bone Loss

Periodontal patients can be the most challenging group of patients to control the repercussions of grinding. Bruxism can be a serious, aggravating factor in periodontal disease because it can interfere with the normal recovery time of the periodontium. Regeneration of the tissue is constantly taking place, and adding bruxism disturbs the circulation by interfering with the functional adaptability and regeneration of the periodontal tissues. Bruxism and periodontal disease in all stages contributes additional stress and strain on the diseased tissues. This increases the risks for tissue breakdown and reduces the rate of regeneration. Disturbances caused in the periodontium by altering the circulation can cause interference with the nutrition of the periodontal tissues.^40,41

When patients grind their teeth, they add axial and bone-in stress. Axial stress is excessive force applied vertically to the teeth and periodontum.⁷ Bone-in stress is the response of the bony structure to applied force. Application of excessive pressure stimuli to bone may cause the formation of thicker and more numerous trabeculae. If tissue components cannot compensate for excessive stress, bone resorption will occur. Localized bone destruction or an isolated periodontal pocket may occur with bruxing.³⁸

Mobility

If mobility is caused by bruxing, there usually will not be any signs of periodontal pocketing. The periodontal ligament may respond to increased occlusal forces by resorbing some of the bone of the alveolar resulting in mobility.⁴ With bruxing, the teeth are forcefully rocked back and forth in the socket, which can cause temporary mobility, progressing to risks of permanent mobility.⁵ Tooth mobility with sleep bruxism is greater in the morning and is significant when found in teeth with little or no evidence of periodontal disease. Such teeth may exhibit a dull percussion sound and patient may report soreness when biting on the tooth or teeth.⁵

Buccal Exostosis and Tori

Bony out-growths that form where there is an excessive amount of stress and tension placed on the teeth’s underlying structures are called tori or exostosis. With excess strain and tension placed on the teeth and jaws, the body’s defense is to produce extra boney material to support the teeth. This bone grows and becomes visible under the soft tissue. They are commonly seen in patients who clench or grind their teeth. Exostosis of the maxilla and/or mandible may be the result of bruxism. Exostosis tends to recur if bruxism continues after their removal.^5,44

Force and Wear

The masseter muscle is considered one of the strongest single muscles in the body and can produce substantial force.⁴⁴ In the natural relaxed state the maxillary and mandibular teeth are separated by about 2‑3 mm of space. Teeth usually come into contact with each other when chewing and swallowing, using a force of less than 25 pounds of pressure, with food to buffer direct contact with chewing. When bruxism is involved, there is an abnormal increase in magnitude, frequency and duration elevating the pounds of pressure to increase to the maximum biting force of 200 to 300 pounds of pressure.^5,16,41,46 The grinding force compared to regular mastication is three to ten times more powerful–enough to crack a walnut.^10,46 Functional tooth contact during a 24-hour period is approximately 20 minutes. Excessive forces generated by bruxism extends for more than 20 minutes.¹⁶ Normal tooth wear in non-bruxers is considered to be ~29um (micrometer) in molars and ~15um in premolars per year. Dental enamel loss of ~10-40 um occurs from friction of normal biting or chewing, while the forces generated for mastication are between 20-120 Newtons (N). When bruxing, the load can be as high as 1000 N, changing normal physiologic wear to severe wear, leading to fatigue failure and fractures.⁴

Audible Occlusal Sounds

Bruxism many times is diagnosed from a bed partner or someone observing the patient during a napping time who is disturbed due to the noise produced by grinding. The audibility is determined by the tooth-to-tooth friction, the area in which the grinding occurs and the force of the grinding.⁵ The sounds can be described as crunchy, chewing on gravel, rocks or marbles.