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 will look 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.
From the Literature
The literature on tooth wear is extensive, and various descriptions of normal - i.e., physiologic - tooth wear as well as pathologic tooth wear have evolved specific terminology descriptive of its etiologies, mechanisms, and locations. Grippo suggested the latest taxonomy in 2004. In a thorough review of attrition, abrasion, corrosion, and abfraction, he describes the etiologies of tooth wear as coming from stress, corrosion, and friction, and the possibility of combining one or more of these etiologies and mechanisms.1 He defines attrition as tooth-to-tooth friction occurring on the incisal, occlusal, or proximal surfaces of teeth. Friction through attrition is endogenous, caused by parafunction and deglutition, or exogenous, caused by mastication, dental hygiene, habits, and occupational behaviors or through the use of dental appliances. Abrasion is defined as the friction between teeth and some external substance that causes friction. Gritty food substances, abrasive tooth polishes, or inappropriate (e.g., horizontal) tooth brushing with tooth paste may cause abrasion. Abfraction is a microstructural loss of tooth material in areas of greatest stress concentration from occlusal contact, and is found in the cervical regions of teeth. Suggesting multifactorial etiologies, Grippo describes stress-caused wear as microfracture/abfraction. Abfraction from exogenous wear can be caused by mastication, habits, occupational behaviors, and the use of dental appliances. Endogenous sources of stress come from parafunction, occlusion, and deglutition as etiologies for the abfraction lesion. Grippo describes corrosion as the chemical degradation of tooth structure that can be endogenous from plaque, gingival crevicular fluids, or gastric juices; or exogenous from diet, occupational exposures, and through the use of certain drugs or alcohol.1
Normal Tooth Wear
Lambrechts has studied normal in vivo tooth wear of enamel and reported that attrition — i.e., normal occlusal contact wear of human enamel — was found to be 29 micron on molars and 15 micron on premolars per year.2 In a different clinical study that measured the wear of all teeth using digitized study models, the average tooth wear loss over one year was measured as 0.04mm3 by volume or 10.7 micron by depth, which approximately doubled by year two.3 Examination of 500 patients over an 18-year period, in which study models were compared, led to the conclusion that non-pathologic tooth wear is a slow, minimally progressive process.4
In a study of Swedish children from ages 3-20 years, it was found that as children age from three to five years, there is increased attrition on deciduous teeth. Sixty-three percent of the three-year-olds had no incisal wear, whereas in the five-year-olds only 19% had no incisal wear.5 In the permanent dentition, this same study reported that the ten-, 15-, and 20-year-olds had no incisal wear in 78%, 51%, and 35% patients, respectively. Another longitudinal clinical study confirms the finding that as children age they tend to demonstrate more incisal wear.6 In a clinical study, this same author confirms that as children and adolescents get more permanent teeth, there is more incisal wear.7
Dental arch shape has been reported to affect tooth wear rates. In an anthropological study, casts of Aboriginals born between 1900 and 1940 were examined. Hypsiloid or U-shaped maxillas have more buccally directed wear, whereas parabolic or hyperbolic maxillas exhibit much heavier wear in the lingual aspects of the occlusal surfaces. The authors contrast this “as steep oblique wear vs. flat horizontal planes”.8 It has been reported that tooth wear may be a functional compensation for modifications in the anterior dentoalveolar complex.9 In this study, the changes that were described included lingual tipping of maxillary incisors with a decrease in the horizontal overlap between the maxillary and mandibular teeth. This was accompanied by a more edge-to-edge bite and incisal attrition.
Adult tooth wear is related to the craniofacial morphology of the patient as a child with the cephlometric measurements of ABN, ramal height, and gender being significant. Craniofacial morphology can bear a small but significant relationship to adult tooth wear.10
Normal tooth wear may occur as a result of the speech envelope. In a clinical study that investigated subjects with incisal tooth wear versus those with no incisal wear, subjects with incisal tooth wear had a smaller speech envelope. The study did not clearly elucidate whether the increased wear caused the smaller speech envelope or a smaller speech envelope contributed to the wear.
An anthropological study compared tooth wear between modern and medieval subjects. It was assumed that medieval subjects had an abrasive diet, whereas the modern subjects had either an acidic diet or an average softer Western diet. The abrasive diet caused more substance loss of tooth structure on the occlusal surfaces, and occlusal cupping was common. The acidic diet produced less occlusal cupping than the abrasive diet but more than the Western diet. There were more buccal lesions (63%) found in subjects on the acidic diet than either of the other two diets (0% and 8%, respectively). The authors suggest that the finding of concavities on smooth surfaces is indicative of erosion
In a clinical study of 586 subjects, researchers from Wales assessed tooth wear in dentate individuals using a tooth wear index and noted that there was increased wear on the occlusal and incisal surfaces as age increased. Except for the lingual surfaces of maxillary incisors, the lingual and facial surfaces showed no significant variations in wear with aging. Males demonstrated the greatest amounts of wear compared to females.13
A clinical study of 30 patients compared the tooth wear of those patients with a chewing pattern described more as chopping, vertical chewing to those patients described as grinding, with more lateral movement to their chewing pattern. The grinding type of chewing pattern resulted in significantly more occlusal wear of posterior tooth segments compared to the chopping type.14
In a clinical study from Australia, it was reported that in those children who received optimally fluoridated water or regularly used a fluoride supplement, there was less wear noted in all sextants compared to those who did not ingest fluoride. Except in the fluoridated patients, the mandibular molar sextants did not seem protected against occlusal erosion.15
Etiology of Tooth Wear
As indicated previously by the taxonomy used to describe tooth wear, there appear to be three mechanisms and various combinations of these mechanisms by which tooth wear occurs. Friction, corrosion, and stress can all contribute singly or in combinations to create the types of wear reported in the literature and found in dental practices treating dentate populations. In mathematically describing wear, the equation states that wear is proportional to the normal force times the distance, so movement becomes another factor to consider in determining etiology.
Erosive wear, now called corrosion, is typically seen in young adolescents due to diet. Ingestion of large quantities of acidic soft drinks, many with a pH of 2.3, are capable of demineralizing teeth.16 While saliva can provide some buffering capacity for such acidic drinks, in large quantities the acid will have an effect on tooth enamel. Exercise dehydration will also decrease the salivary protection and increase tooth wear.17 The use of a sports drink will not itself cause significant erosion, as found in clinical observational studies.18,19 Over-consumption of acidic soft drinks in young children can clearly lead to faster erosion of deciduous teeth than permanent teeth.20 In a British study of 14-year-old students where consumption of carbonated drinks was from one to three cans per day, it was found that the tooth wear as measured by a tooth wear index had no correlation to salivary flow rate or buffering capacity. There was a correlation with acid regurgitation.21
Sites of erosive tooth wear may be saliva-dependent, as was found in a survey of 450 patients with tooth wear. In this study, non-carious cervical lesions were associated with occlusal attrition in 27.71% of the facial sites, compared to 2.61% of the lingual sites. The most common site for non-carious cervical lesions was in the maxillary incisors. The least common was in mandibular molars.22
Liquid flow rates affect the severity of dental erosion. In a study that measured flow in vitro, it was found that erosive depth increased with increased time of exposure, total volume, increased flow rate, and decreased outlet diameter.23 Drinking acidic drinks through a straw directed at the teeth increases the erosive depth. Tooth surface pH is affected by the method of drinking. Holding an acidic drink orally shows the greatest pH drop, followed by a long-sipping method, followed by gulping, which showed the least drop in pH.24 After acids have demineralized enamel, licking with the tongue could have an ability to remove more enamel than if no tongue licking is present.25
Corrosion can be caused by a variety of medical conditions. Gastro-esophageal reflux (GERD) patients commonly show marked erosion of the lingual surfaces of the maxillary anterior teeth, incisal surfaces of maxillary and mandibular teeth, and the occlusal surfaces of mandibular molars26,27,28,29,30,31(Figure 1). Asthma has been shown to cause corrosion (erosion) on the occlusal surfaces and less on the lingual surfaces, as seen in GERD.32 Chronic alcoholism is expected to cause a corrosive (erosive) type of wear associated with bruxing and clenching. It is expected to see more rapid cupping of the occlusal cups tips and general occlusal wear.33 Bulimia and other eating disorders also cause increased corrosive wear of the teeth because of the stomach acid affecting the teeth34,35 (Figure 2).
Methamphetamine and Ecstasy (methylenedioxymethamphetamine) use also results in increased tooth wear.36,37,38 Snorting of methamphetamine leads to higher tooth wear in the maxillary anterior teeth, whereas continued methamphetamine use can lead to over-consumption of carbonated drinks, clenching, and grinding. Thus the effects of corrosion, attrition, and stress abfractions can all be found.37 These drug users also typically have extensive smooth-surface caries.
Syndromes in which xerostomia occurs demonstrate excessive tooth wear. In a case report, it was reported that in four subjects with congenital dysfunction of the major salivary glands, excessive tooth wear was present. Syndromes included Sjogren’s, Prader-Willi, and congenital rubella. Patients with medication-induced xerostomia also demonstrated increased tooth wear.39 Normal salivation provides many protections to the teeth including lubrication, buffering capacity, clearance of acidic substances by swallowing, pellicle formation, and the capacity for remineralization of demineralized tooth substance.39,40
Corrosion and attrition are often combined in mouths of bruxers.41 Simultaneous erosion and abrasion results in 50% more wear than by alternating erosion and abrasion singly.42 In a six-year clinical study in which erosion and wedge-shaped defects presumably caused by toothbrush abrasion were followed, there was a definite progression of the lesions despite dietary and hygiene counseling. Using multiple linear regression statistics, the authors found that nutritional acids and age were significant risk factors and explained 28% of the variability. Using the same statistical technique, the authors reported that tooth brushing and age contributed to 21% of the variability found in the progression of wedge-shaped defects.43 Extrinsic factors that are environmental have been suggested as causing erosive tooth loss. The exposure to acid fumes, swimming in pools with low pH, and dietary contributions have been described as contributing to corrosion.44 Endogenous factors are also described as causing corrosion. Erosion from dietary acids or gastric acids is described as smooth lesions appearing cupped on the occlusal or incisal surfaces and concave on facial or lingual surfaces.45 Progression of these lesions is stated to be intermittent, with periods of activity and inactivity. Prevalence has been reported as occurring in 80% of children and 43% of adults.46
Tooth wear because of attrition or abrasion is frequently also seen with some corrosion47 (Figure 3). In a clinical study of 100 patients, 98% had evidence of erosion and attrition, while 82% had signs of abrasion as well.
A reported in vitro study showed that the degree of load, the time of applied stress, and the use of an acid environment all altered the wear found on premolars. The lower the load, the lower the frictional loss of tooth structure. The greater the amount of time the force was applied, the greater the tooth loss. The citric acid medium actually decreased the loss comparing the same time and load. The authors described the outcome as simulating a three-body wear in neutral pH conditions, whereas two-body wear in the acidic environment due to increased polishing.48
In a clinical study with a sample size of seven, bite force and dento-facial morphology were described in patients exhibiting severe dental attrition. The patients were all male. They had high bite force levels in the incisal regions of 63% of the molar bite force and all had a rectangular facial morphology. The maxillary dental arch also was described as more rectangular than normal.49 In another Swedish study, with a sample size of 54 adults with advanced occlusal wear, it was reported that the level of maximum bite force was high compared to normal populations. The craniofacial structure is characterized by “deviation in the vertical direction, a small angle between the mandibular-palatal planes and a small gonial angle” compared to Swedish norms.50
Many studies have been completed regarding occlusal forces, but the degree of sophistication in measurement has changed significantly over time. An initial finding was that “The functional chewing forces are small compared to static isometric closing forces that the stomatognathic system can exert.”51 Anderson first reported masticatory force in 1956 using four subjects. He reported that normal force varied by the consistency of the food being chewed (carrot versus meat versus biscuit) between about 16-32 lbs ((71-142N).52 More recently, it also has been reported that the magnitude of masticatory forces ranges from 2-40 pounds (9-180N) with a duration of from 0.25-0.33 seconds.53 Maximal biting force has been measured in young subjects and falls between 115-120 lbs (516-532N).54 The presence of restorations did not affect the bite force. Gender differences do occur. The mean maximal bite force for men has been measured as 190 lbs (847N) versus 134 lbs (597N) for women.55 In patients who brux, maximal bite force has been measured at 205 lbs (911N) in the molar region of men versus 128 lbs (569N) in the incisor region of women.56 This difference between anterior and posterior biting force has been measured as less than these reported values elsewhere, with 79-82 lbs (353-365N) in the molar region and 12-14 lbs (56-64N) in the premolar region and 14 lbs (65N) at the incisors.57 Whatever the actual values, it is apparent that the most extreme forces are in the most posterior teeth. When these forces are calculated as a force per area and then converted to international units, a force of 205 pounds affecting a point of contact 1/32 inch square places 45.23 MPa of force. Normal chewing force using the same area of contact results in a force of 8.826 KPa, well below the ultimate tensile strength of 42.1 MPa of enamel and 61.6 MPa of superficial dentin.58
When posterior teeth are lost and the proprioception is altered, the maximal bite force also goes down.59,60 Nocturnal bite force of bruxing is different from daytime maximum bite force. In a study that measured those differences, nocturnal bruxing forces were reported as a mean of 49 lbs (220N) and a maximum force of 93 lbs (415N) versus a voluntary daytime force of 174 lbs (775N).61 However, nocturnal bruxing forces were timed as duration of 7.1 seconds versus a normal chewing duration of 0.25-0.33 seconds. This means that the longer duration of bruxing with greater force than used for chewing will cause greater damage and wear to teeth because the longer time of force application causes a longer contact path on the tooth.
Clenching force on one tooth is reported to be up to ten times greater on the canine than maximum biting forces distributed in a balanced way.62,63 Maximum biting forces exerted by the muscles are exerted in the maximum intercuspal position and are distributed according to distance from the condyles, with the second molar taking 55% of the maximum force and the incisors taking 20% of the force.64 Bruxing and clenching forces can reduce the protection afforded by salivary lubrication by reducing the film thickness sufficiently to increase frictional contact and increase the wear of the opposing surfaces.110 Clenching causes very little if any wear, but undoubtedly contributes to stress. Wear requires movement. Damage can occur only if the force exceeds the strength of the material or through a fatigue process (Figure 4).
What effects do these forces — whether from normal chewing, single tooth bruxing, multiple tooth bruxing, or clenching - do to the teeth? In a photoelastic study using about 4.4 lbs (2kg) of force on a tooth in a vertical load, it was found that distal incline planes or slopes of cusps and lingual incline planes or slopes of the buccal cusps received the greatest force on mandibular molars. The magnitude of the stress is increased considerably when the occlusion was flat plane.65 The total force is the same; the distribution of this force changes. A vertical force contacting an inclined surface is resolved into a force normal to the surface and one parallel to the surface. As the incline becomes horizontal, the normal force increases and the parallel force decreases, but the total force is the same.
Using extracted teeth prepared for endodontic access with MOD cavity preparations, teeth were stressed with a load, either continuously or cyclically. Continuous loading resulted in progressive cuspal displacement both time- and load-dependent. It took 20 minutes for the tooth to recover from the deformation. Cyclic loading resulted in cumulative increase in cusp displacement, but only to a very small extent: ≈1 micron. The conclusion is that continuous loading as in clenching can be more destructive than cyclic loading as in chewing because of an increase in the fatigue of the stressed teeth over time.66
An interesting anthropological study did a finite-element analysis of 29 intact molars wherein a cleavage type load was applied. They reported that first maxillary molar functional and non-functional cusps dissipate loads equally well. In maxillary second and third molars the non-functional cusps resist loads better. Mandibular molar functional cusps all dissipate force equally well.
In 1984, Lee and Eakle proposed a theory that tensile stresses from occlusal forces caused cervical erosive lesions (also called non-carious cervical lesions, NCCL).68 Grippo later called such lesions “abfraction” (taken from engineering vocabulary). Abfraction occurs from the loading forces placed on teeth during static events such as swallowing or clenching and cyclic events such as chewing or bruxing. He states that the flexing and fatiguing of the weakest point in the distribution of the stress along the enamel-dentin boundaries, at the cervical margin, cause this type of lesion69 (Figure 5).
In a clinical study that examined the performance of dentinal adhesives in non-carious cervical lesions, Heymann et al agreed that the results showing failures of Class V composites in part are explained by the flexure of the teeth resulting in restoration loss.70 In subsequent publication, other authors supported the concept of “abfraction” by reporting development of subgingival non-carious cervical lesions.71 There are those who disagree with the concept of abfraction, stating that there is no correlation between occlusal/ incisal wear and development of NCCL;72 that stresses may be dissipated by periodontal ligament and alveolar bone;73 that using a more sophisticated model of enamel prism anisotropy (orientation) in stress concentration alters stress distribution to the cervical in mathematical modeling;74 and that in vitro simulation using tooth brushing with and without non-axial forces resulted in no difference in tooth wear in the cervical margins.75 Bader et al, in a case-controlled clinical study, provided evidence that development and progression of non-carious cervical lesions was multifactorial and that multiple mechanisms may initiate and allow progression of these lesions.76 Previous in vitro studies cited here have shown that NCCL progress in an acidic environment worsens when greater stress is introduced.42 While no direct evidence can be presented, abfraction lesions theoretically may not progress except in acidic conditions. It is also reasonable to conclude that abfraction lesions may progress due to toothpaste abuse (horizontal tooth brushing with any abrasive toothpaste) as it has been shown to do in vitro.77,78
The finite element models studying this concept demonstrate that there is adequate force transmitted through the cusps or cusp inclines to the CEJ to exceed the known strength of enamel.79 If a restoration is present (Occ, MO, DO, MOD) and depending on the width and depth of the restoration, it can increase the cervical stresses exceeding the tensile and shear stresses of enamel.80 A finite element study correlated to the strains seen in human teeth showed that strains were concentrated near the CEJ regardless of load direction. As measured in this study, the asymmetrical strains developed in the cervical regions of teeth in response to oblique occlusal forces are consistent with asymmetric non-carious cervical lesions.81
In a clinical study of 14 years, the progression of non-carious cervical lesions was positively correlated (r2 =0.98) to occlusal volume loss and was significant. The volume loss reported over 14 years was 0.9-11.5mm3 for cervical lesions and between 0.39-7.79 mm3 for occlusal wear.82 A recent clinical study showed a significant correlation between the presence of non-carious cervical lesions and occlusal attrition.83
Multifactorial etiologies have been accepted to explain the development and progression of abfraction lesions.84,85,86 Other etiologies most frequently cited are corrosion,77 and toothbrush (toothpaste) abrasion.87 The lesions were characterized in a clinical study using 171 teeth from 57 patients. Ninety-one percent of the lesions occurred with axial depths between 1-2mm; 49% had occluso-gingival widths of 1-2mm; 74% had angular shape of 45-135 degrees. Commonly (76%) the lesions had sclerotic dentin, and 73% had little to no sensitivity. Seventy-five percent of the patients presented with an Angle Class I occlusion on the involved side, with 60% group function on excursive movement. Eighty-two percent of the teeth had wear facets, and 99% had little to no mobility.88 The lack of mobility has been confirmed by another study that looked at periodontal support. In this study the authors reported that abfractions are less likely to occur in patients who are periodontally compromised due to tooth movement.89 While abfraction cannot be totally discounted, it is probably by itself a small instigating mechanism requiring other mechanisms such as corrosion or friction to advance in size.
Part Two of this article will describe the oral mechanisms that protect or break down or are overwhelmed by the various etiologies that affect tooth wear, as well as the mechanisms of the etiology and how they affect teeth.
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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.