Tooth wear has been described in the literature as physiologic - that is, normal, expected over the life span of an individual, and not creating a pathologic condition. It has also been described in pathologic terms as caused by stress, corrosion, and friction, utilizing a variety of mechanisms and affected by a host of endogenous and exogenous factors. From a clinician’s point of view, when should we decide to restore a tooth or change the conditions in the mouth to protect the teeth; and what should we consider using to either prevent or restore abnormal - i.e, pathologic - tooth wear?
This review in Part One (Northwest Dentistry, September-October 2009) looked at what is normal, non-pathologic tooth wear and etiologies associated with all forms of tooth wear. Part Two will discuss the effects of tooth wear in enamel and dentin, when it may be advisable to intervene in the wear processes diagnosed on specific patients, and what methods of prevention and restoration can be utilized to restore or maintain the dentition. This review will not look at the need for full mouth reconstruction due to wear.
Mechanisms of Wear
This section will describe the oral mechanisms that protect or break down or are overwhelmed by the various etiologies that effect tooth wear, as well as the mechanisms of the etiology and how they affect teeth.
Saliva provides numerous protective functions for the teeth. Saliva provides normal hydration to the tooth; it lubricates the food bolus, enabling easier chewing and swallowing. Saliva also provides some bacterial protection and helps to control the demineralization/remineralization of tooth surfaces. Salivary proteins such as acidic proline-rich proteins, statherins, histatins, and cystatins have affinity for mineral surfaces, inhibit calcium phosphate precipitation, and protect the integrity of the enamel surfaces.90,91 Any disease process or acidic challenge that overwhelms these defenses will result in a corrosive loss of tooth structure. Salivary pellicle proteins, as well as the salivary calcium and phosphate and the plaque fluid, retard demineralization of tooth surfaces. The bicarbonate/carbonate buffer system in the saliva neutralizes acids.92 Salivary pellicle will protect the enamel from short-term erosion of organic acids93 and can form within three minutes. However, dietary acids such as citric acid are not inhibited from dissolution of the enamel.94
In an in vitro study, challenges to enamel were made with an acid below pH 5.0 for 10 and 20 minutes and for three or six exposures each time frame. The net mineral loss was the same. However, the increased frequency of acid exposure increased the total demineralization results. The conclusion was that frequent acid attacks could overwhelm the ability of the saliva to remineralize the enamel.95 Erosive depth clearly depends upon pH values of the acid and the time of exposure.96
Once enamel has been softened by acid attack, oral soft tissues can abrade the enamel more easily.97 However, when low pH acids are used together with attrition, the enamel wear is lower than in neutral pH situations due to a smoothing effect of erosion of contacting surfaces.98 The greater the load and the more time acid is applied to enamel, the greater the wear.99
In an analysis of cementum with surface root caries that had been exposed to fluoride, it was reported that fluoride was detected in the outer 25 micron of the cementum. However, the fluoride did not penetrate into the dentinal structure.100 Cemental structure participates in the remineralization process.
When dentin is exposed to the oral environment, it has been found to be susceptible to acid erosion even with relatively high pH values, and it showed little likelihood of remineralization. The acid removes the dentinal smear layer and opens the dentinal tubules.101 Increasing the temperature, concentration, and exposure times of acids increases the erosion of enamel and dentin.102 Dentin rate of wear depends upon the density and tubule orientation, with peritubular dentin and better-mineralized zones of dentin more resistant to wear and erosion.
The type of acid affects the erosive capability, with citric acid being more erosive than hydrochloric acid and hydrochloric acid more erosive than phosphoric acid.103 Removal of the outer, fluoride-rich layer of enamel results in a greater erosive loss of enamel when exposed to citric acid.104 In vitro testing of four different soft drinks showed that the pH, phosphate, and fluoride concentrations of the beverages correlated with the demineralization of the enamel. Calcium concentration and titratable acidity were correlated with the demineralization of the dentin.105
The tooth responses to tooth wear; whether from corrosion or friction, include the formation of reactionary and reparative dentin and obduration of dentinal tubules. The pulp also responds by forming calcific mineralized tissues, decreasing the pulpal blood supply.106 More rarely, pulpal sequelae can result from corrosion. In a clinical study, 11% of tooth wear patients were found to experience dental pulp irreversible degeneration as a result of late stage erosion (Figure 6).107
When considering the effects of friction on enamel and dentin, one should consider the physical properties of these substances to understand the mechanisms by which friction affects teeth. Enamel is a hydroxyapatite crystalline structure and has higher hardness and elastic modulus than human dentin. It is more brittle. Primary deciduous human enamel has a hardness of 4.88 GPa, compared to a hardness of between 3.3 and 3.9 GPa in permanent tooth enamel, with the lower value being perpendicular to the enamel rods. Primary deciduous enamel has a modulus of 80.35 GPa, compared to adult enamel between 87.5 GPa and 72.2 GPa, with the lower value being perpendicular to the enamel rods. Enamel is anisotropic related to the alignment of fiber-like apatite crystals.108,109
Enamel tufts wear more rapidly than surrounding well-mineralized areas of enamel. Orientation of enamel prisms affects the wear, with prisms more parallel to the surface more easily cleaved by the wear process than prisms oriented perpendicular to the surface.110 Because the enamel is hard and brittle, and because the enamel prisms are organized perpendicular to the external surface, the physical properties are maximized against opposing surfaces. As a result, enamel is built to withstand a lifetime of normal forces without being breached.111 Hypomineralization of permanent human enamel lowers both the hardness and the modulus of elasticity significantly from normal human enamel.112,113
One of the more interesting findings about permanent human molar enamel is that in a maxillary second molar, the range of hardness and modulus of elasticity varies considerably with the higher hardness and the higher elasticity found at the occlusal surface of the molar, and lower values found at the DEJ. This was correlated to the differences in the different chemistry of the hydroxyapatite. The P2O5 and the CaO were highest at the occlusal surface and lower at the DEJ, whereas Na2O and MgO showed the opposite trend. Because of these differences, the occlusal enamel on the lingual side is stiffer than on the buccal side. Conversely, the inner enamel shows the opposite. It is postulated that these differences in chemistry may be related to different function.114 Human enamel structure where inter-rod spaces are minimized shows ability for molar cusps to withstand greater horizontal tensile stress.115
Hardness of dentin is considered to be dependent upon mineral concentration.116 Mineral concentration of the dentin and its hardness have been correlated to the location on the tooth. In adult teeth, mantle dentin that is immediately adjacent to the dentin-enamel junction is softer than primary dentin underlying it. Primary adult dentin has decreasing hardness as the pulp is approached, probably due to a decrease in the hardness of the intertubular dentin matrix caused by less mineralization.117,118,119,120 The hardness and modulus of elasticity of dentin decreases as the pulp is approached in deciduous teeth as well.121
Tensile strength is a critical mechanical property for a tooth because most of the destructive occlusal forces placed on teeth are tensional or bending, causing tensile and compressive strains. The ultimate tensile strength (UTS) of dentin depends upon the dentinal tubule orientation. The UTS is lowest for tensile force that is parallel to the tubule orientation - i.e., at right angles to the collagen fibers in dentin (54Mpa) - and greatest at 90 degrees to the tubule orientation (92Mpa) (fracture parallel to the tubule direction).107,122,123 Testing for tensile strength in dentin inherently shows wide standard deviations in the sample, suggestive that tensile strength is controlled by the distribution of flaws in the dentin specimens.124
When considering strength properties of the dentin, one must look at the various dentinal structures separately to determine the weakest structures, and their orientation in order to predict wear patterns and the effects of destructive behaviors on tooth wear. Using an atomic force microscope to determine Young’s modulus of elasticity, it has been found that the modulus of peritubular dentin is 30 GPa and that of intertubular dentin is 15 GPa.125,126 The hardness of the dentin varies greatly, being 2.3GPa for peritubular dentin and 0.5 GPa for intertubular dentin. The AFM also showed that the peritubular dentin was spatially homogeneous, whereas the intertubular dentin showed considerable spatial variation in its elasticity.127 These properties will affect how the dentin wears and fractures and how a crack can propagate. The structure of the dentin contains a hydrated matrix of collagen fibrils that is reinforced with a nanocrystalline, carbonated apatite that is called the intertubular dentin. The intertubular dentin is a matrix composed of type I collagen fibers with a carbonate rich apatite mineral phase. The mineralized fibers are isotropic by the pulp but become anisotropic in mid-dentin areas. Near the pulp the mineral phase is needle-like, but changes to plate-like near the DEJ.128 Peritubular dentin is a hypermineralized wall of the dentinal tubules and is roughly 0.5-1.5 mm in thickness.129 The collagen fibers are cross-linked by covalent bonds, providing the dentin matrix with stability and improved tensile strength. In this same study, the findings indicate that the amount of collagen cross-linking varied by tooth type, with the molars having the most, followed by premolars and canines. Incisors had the least collagen cross-linking. The authors felt that this suggests the dentin may be functionally adaptive to the stress placed against it.130
Dentin hydration can dramatically affect the physical properties. Dehydrated human dentin demonstrates lower strain values at fracture - i.e., is a more brittle material. Hydrated or rehydrated dentin (dentin that became dehydrated but is exposed to moisture to rehydrate) requires significantly greater strain at fracture.131,132 Dehydrated dentin also shows a significantly reduced stress relaxation response when a predetermined compressive load is applied to a maximum value and released.133 This partially explains the increased wear in xerostomic patients.
Because of the aforementioned properties, dentin is an excellent supporting structure for the enamel, being tough yet resilient. Dentin when exposed, however, cannot overcome wear.110 Once the enamel has been breached by wear, the dentin will wear more rapidly than the enamel. This exposes the enamel rods, unsupported and more susceptible to fracture. The lesion will progress faster given the same forces and duration once dentin is exposed.
When considering wear process, two- (e.g., opposing teeth) and three-body (e.g., opposing teeth with an abrasive slurry between them) wear testing is used to describe the wear process. Two-body wear with opposing teeth of flat and pointed specimens were tested, and the loss of tooth substance was much greater in two-body versus three-body specimens. The wear was also significantly greater on flat specimens, compared to pointed specimens.134 This finding would support that normal chewing of food will be less destructive to the teeth than will bruxing or clenching, something that is clinically self-evident.
Human enamel will wear more under dry, unlubricated conditions than under a lubricated condition, though when the load increases sufficiently, the wear will be greater.135 Enamel prisms, and specifically enamel crystals, wear by development of striations in their surface. The width of the wear striation is not related to particle size of the material being chewed because of the orientation variables of the prisms, with differential wear noted in functionally different areas of the tooth enamel.136 Introducing abrasives from toothpastes, for example, causes small surface scratches on the enamel surface to disappear and larger scratches to appear and expand. When brushing without dentifrice, the surface of the enamel is protected by a salivary pellicle. 137
Tooth brushing can create tooth wear. Hard brushes have been found to create 3.6 times as much wear as soft toothbrushes.138 Saliva has no effect on reducing eroded tooth wear from tooth brushing.139 Mean enamel wear of different dentifrices was between 0.05 to 0.40 micron after one hour of brushing with 375 g. of force. The more abrasive the dentifrice, the greater the wear, with a significant correlation made between abrasivity and wear.140 Similar ranges of enamel loss were found in an in situ clinical study.141
Acid erosion increases the susceptibility to abrasion, with dentin affected more than enamel. Dentin loss can be correlated to the abrasivity (RDA) of toothpastes used.142
In an in vitro study where the teeth were exposed to lactic acid pH 4.5 with and without cyclic tensile stress, it was found that the cyclic stress resulted in greater tooth substance loss in the cervical third of the tooth and on the mesio-buccal side (under tension) than on the disto-buccal side (under compression).143 Tensile stress in the enamel increases with an increase in the coefficient of friction.144 Teeth wear faster in the mouths of bruxers versus non-bruxers because of the increased time of force application.145 Increasing load also increases dentin loss.146 Tooth wear on abraded occlusal surfaces displays greater mean depth/breadth ratio of scooped dentin than samples taken from teeth undergoing erosion.147 Wear under stress causes microscopic pitting of the enamel, related in part to the particle size of the material creating friction on opposing surfaces.148
Interventions for Prevention and Restoration of Tooth Wear
To judge the progression of tooth wear in an individual, it is wise to make study casts to compare the various sites of tooth wear from year to year. This is helpful in deciding when to intervene. A tooth wear index (TWI) as suggested in the literature may also be used to chart existing tooth wear and track it over time. Smith and Knight have suggested an index often cited in the literature that can show progression of lesions over time.149 The index is described by scores of 0-4 in Table I.
A raw score has no meaning without understanding the age of the patient and what a normal pattern of wear would look like over time. The wear normally expected in a 60-year-old patient would be abnormal if seen in a 20-year-old. There are indices that do include age. However, they are complicated mathematical models used to predict what wear should be.150 One paper does describe an average of tooth wear using this index on tables for each tooth for 45-54-year-olds, 55-64-year-olds, 65-74-year-olds, 75-plus-year-olds, male subjects, and female subjects. These averages may be useful in comparing tooth wear index scores among individual patients.13
Once the assessment of tooth wear is made, a diagnosis of pathology including probable etiologies of the tooth wear should be recorded. If the wear is normal for the age of the patient, no further action beyond recording is necessary.
If the wear is considered pathologic, some form of intervention is recommended to prevent further wear, minimize damage, or protect the teeth. Interventions depend upon the etiology of the wear, and, because wear can be multifactorial, a range of interventions may be necessary. Abrahamsen151 has described a methodology used to determine which etiologies may be causing the tooth wear. He suggests hand-held study casts are necessary to make the determination so that the occlusal aspects can be clearly seen.
1. If the wear is greater in the anterior than the posterior and the wear facets match up on opposing casts, the wear is from bruxism.
2. Where there is more anterior than posterior wear and the lingual surfaces of the maxillary anterior teeth are worn smoothly from gingival tissue, and the lingual surfaces of maxillary posterior teeth seem affected, the cause is from acid regurgitation. In this situation, the worn surfaces of the casts will not match up.
3. If the posterior teeth have greater wear than the anterior teeth and cupping or cratering is present with the mandibular first molar most severely affected, the cause is from swishing of acidic drinks. In this instance, the worn surfaces of the casts do not coincide and the edges of the enamel look sharp.
4. If the posterior teeth have greater wear than the anterior teeth and cupping or cratering is present but there is even posterior wear on all of the upper and lower teeth, the wear is created by fruit mulling, where acidic fruits are kept in contact with the teeth for extended periods while chewing.
5. If the anatomic details on the teeth appear faded with a sandblasted appearance, or the facial surfaces of the lower canines and premolars have cervical notches, the cause is from toothbrush/dentifrice abrasion. In this case, the worn surfaces of the casts will not match up.
6. This author also suggests a miscellaneous category, but does not enumerate it. Abfraction lesions and other forms of tooth wear not described above would fit into this ill-defined category. Since abfraction is caused in part by occlusal stress, the tooth with the facial non-carious cervical lesion (NCCL) would also have an occlusal wear facet that would fit the opposing teeth.
Recommendations for Treatment
After an acid attack, saliva can remineralize dentin, and takes approximately 30 minutes to do so.152 Erosion and abrasion of enamel surfaces exposing dentin increases susceptibility to both erosion and abrasion alone or in combination and can be correlated to the abrasivity of the dentifrice used.153 A mild toothpaste with low abrasivity is recommended together with a soft bristle brush. Horizontal tooth brushing must be eliminated.
Diet plays a critical role in corrosion. The chemical factors that affect the corrosion of the tooth are the pKa values of the acid, the adhesion and chelating properties, and calcium, phosphate, and fluoride content. The behavioral factors of eating habits, life style choices, and excessive consumption of acids affect corrosion. The biological factors of flow rate, buffering capacity of the saliva, salivary composition, pellicle formation, tooth composition, fluoride exposure, and dental and soft tissue anatomy all can affect corrosion. Reducing the frequency and contact of acids can be used to control corrosion,154 as can the addition of protective agents such as fluoride155, calcium phosphates,156 and regular oral hygiene practices used to promote health by plaque removal, and control of the oral micro biota. Fluoride used in toothpaste (1,450 ppm NaF) is able to remineralize enamel acid dissolution from carbohydrates applied for 30 seconds each for one, three, or five times a day.157
Patients most at risk for corrosion in combination with frictional wear suffer from dehydration, caffeine addiction, GERD, asthma, diabetes mellitus, hypertension, and other conditions leading to xerostomia. Routine examination is recommended for the salivary glands, oral mucosa, skin, and eyes for evidence of salivary hypofunction. A self-management plan should be developed to control or alleviate the xerostomia, limiting the damage of erosion and abrasion of the teeth.158 Common aids include the use of remineralizing materials including fluorides in toothpastes, gels, and varnishes; and calcium phosphates in solution (Recaldent, Bonlac Bioscience Int. Pty Ltd, Melbourne, Australia, sold as MI paste for professional use), and also in sugarless chewing gums (Trident with Recaldent, Cadbury Adams USA LLC, Parsippany New Jersey); xylitol chewing gums; use of non-alcohol rinses (Oral Balance, Laclede Inc., Rancho Dominguez, California); wetting agents including artificial saliva (Moi-Stir, Kingswood Laboratories, Indianapolis, Indiana; MouthKote, Parnell Pharmacueticals Inc, San Rafael, California; Xerolube, Colgate Oral Pharmacueticals, Canton, Massachusetts).159
Fluoride, barium sulfate, silver nitrate, and especially oxalate cause a precipitation in the dentinal tubules, occluding them and preventing fluid flow.160 All of these agents present in a variety of products can be used to desensitize teeth where exposed dentin is present.
When corrosion lesions are sensitive and the lesion depth is minimal, dentin bonding agents have been applied to protect the area from further acid erosion and will provide some level of protection, though for how long is unknown.161
Clinically it may be difficult to know an NCCL is from erosion only. The clinician may look at the exposed enamel and notice a matte finish to the surface, indicative of acid demineralization, but not in all cases will erosion appear this way because of subsequent abrasion.
Some erosive lesions will be very sensitive to touch or air. These lesions probably do not have a smear layer and probably do not have sclerotic dentin. Other lesions may have sclerotic dentin. This is significant if the depth of the lesion is at or beyond an ideal cavity depth for the restorative material that would be used. Once the progression of a corrosive lesion has shown consistent progression and dietary counseling has not changed the pattern of wear, it is time to intervene with a restoration to protect the tooth from additional corrosion that may threaten the pulp. If no sclerotic dentin is present, and there is no abfraction component from occlusal stress, the lesion may be bonded utilizing a three-part etch, rinse, prime, and bond system, followed by composite resin (Figure 7, the restored patient seen in Figure 3).
If amalgam is preferred, a cavity preparation with 900 cavosurface margins may be prepared. Bonding the amalgam utilizing a three-step etch, rinse, prime, and bond system together with a dual or chemically cured resin cement is recommended to decrease microleakage and post-operative discomfort (Figure 8).162,163,164,165,166 In some patients where the corrosion process continues unabated, the loss of tooth substance around the restoration will become evident and additional protection may be required. Extreme cases of corrosion may require a crown or veneer to protect the teeth. (See Figure 9, the restoration of the patient in Figure 2.)
In a sampling of white subjects, worn anterior teeth and premolars were compared to unworn teeth. It was found that there was a 1.01 mm difference in length between the worn and unworn central incisors; a 0.93 mm difference between worn and unworn canines; and 0.31mm between worn and unworn lateral incisors. The study showed a clear loss of tooth structure from attrition of significant magnitude to consider restoration.167 Esthetic restoration of worn anterior teeth is often considered to improve the length lost to attrition. Anterior tooth attrition is frequently due to bruxing, clenching, and paranormal functional habits, as well as habits such as biting thread or fishing line, chewing fingernails, chewing on objects such as pencils, rather than from normal chewing. Some patients will exhibit a pattern of wear caused by lower anterior teeth fitting into the wear pattern of upper teeth in latero-protrusive motion. This can be caused by constant light rubbing over many hours of the day, creating a keyhole effect. Worn incisal tips on canines are a common finding as people with canine guidance age (Figure 4).
Restoration of these anterior defects, when not associated with significant posterior tooth wear, may be required to break the patient of the habits creating the wear, thereby protecting the teeth from further wear. The least invasive method to restore these defects is by application of bonded composite resin.168,169 Because many of the exposed dentinal defects will have sclerotic dentin, bonding to the dentin can be complicated by the significant mineralization of the dentin. Increased etching time as well as preparation to expose fresh dentin have been suggested to improve retention. Overlap of the restoration on enamel surfaces is also suggested to improve retention and improve esthetics. In the studies cited, anterior guidance was altered to achieve posterior disclusion.
Restoration of teeth affected by bruxing where canine guidance is restored can be seen in the above four figures. The patient wanted the midline diastema closed. To do so and maintain appropriate tooth proportionality, the centrals and laterals had to be lengthened. By altering the lateral guidance, the additions, in the form of veneers, were durable enough to protect the teeth and maintain the integrity of the restoration (Figures 10-13).
Bruxism is thought to affect 5-20% of a normal population.170 Normal loss of enamel due to natural wear is estimated to be about 10-20 micron per year averaged.2,3 Bruxers exhibit three to four times the normal wear.171 Interocculsal appliances are recommended to limit wear, especially in the mouths of nocturnal bruxers.172 Severe occlusal wear seen in posterior teeth and anterior teeth may require protection from fracture, restoration of lost vertical dimension, improvement in occlusal guidance by restoration of all the teeth with combinations of crowns and/or onlays, or veneers to restore appropriate function, esthetics, and guidance, lessening the stress on the individual teeth and the periodontal support mechanisms.
Localized posterior wear creating sensitivity and/or fremitus - i.e., visible or palpable tooth mobility due to occlusal pressure - can be adjusted to help resolve the tooth sensitivity.173
Abfraction lesions created by occlusal stress and in combination with either toothbrush abrasion and/or corrosion may or may not be sensitive. Localized occlusal adjustment is recommended to decrease the effect of the stress (especially lateral occlusal stress) which may be the etiology creating the NCCL, thereby removing the flexure of the tooth from creating greater concentrations of stress.174 If the lesion depth has reached an ideal cavity depth of 1-1.5mm, it may be time to consider restoration of the defect to protect the pulp, after the occlusion has been adjusted to remove lateral stress on the tooth.
These lesions are frequently restored with bonded composite resin restorations. However, the loss of this restoration is high if the clinician relies solely on bonding to retain the restoration.175,176 Many authors recommend some form of mechanical undercut as well as bonding. In addition, layering of the initial composite material solely on dentin, then covering with a second or third layer that covers the enamel, may limit the effect of the polymerization shrinkage of the composite. This will improve longevity, and limit post-operative sensitivity and microleakage. Layering composite material over a resin-modified glass ionomer also seems to improve the retention.177
Use of a three-step etch, prime, and bond is recommended to improve retention as well.178,179,180 As mentioned above, a bonded amalgam restoration can also be placed after preparation of ninety-degree cavosurface margins and some convergence of occlusal and gingival walls.
If the lesion appears to have sclerotic dentin, it is recommended to double the etching time to improve the bond to this hypermineralized dentin.181 The different bonding systems have bond strengths which are significantly different, with the three-step etch, prime, and bond exhibiting the best retentive value to sclerotic dentin.182
Dentists should monitor tooth wear in individual patients, especially when they perceive some unusual wear patterns. When tooth wear does not seem to fit the age and occlusion of the patient, its progression should be monitored. Once a pattern of pathologic tooth wear has been identified, attempts should be made to intervene and disrupt the suspected etiologies, whether from corrosion, friction, or stress. Year-to-year comparisons of study casts can be used to assist in the diagnosis and determination of etiology. Prevention and preservation of existing tooth structure is the goal, using interventions with the least invasiveness while also restoring tooth contours as needed to protect the teeth from further pathologic wear, and ultimately to prevent fracture of the tooth. n
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*Dr. Larson is Associate Professor, Department of Restorative Sciences, Division of Operative Dentistry, University of Minnesota School of Dentistry, Minneapolis, Minnesota 55455. Email is firstname.lastname@example.org.