CRITICAL REVIEWS IN ORAL BIOLOGY & MEDICINE

A Critical Review of Non-carious Cervical (Wear) Lesions and the Role of Abfraction, Erosion, and Abrasion
D.W. Bartlett* and P. Shah
Department of Prosthodontics, Floor 25, Guys Tower, St. Thomas Street, London Bridge, London SE1 9RT, UK; *corresponding author, david.bartlett@kcl.ac.uk

INTRODUCTION
wear to Tooth surface loss ora tooth cervicalrefersotherthe pathological loss of tooth tissue by disease process than dental caries (Eccles, 1982). Non-carious lesions (cervical wear) are defined as the loss of tooth substance at the cemento-enamel junction (Mair, 1992). Terms also used to describe these are cervical erosion/abrasion lesions and abfractions. The term abfraction evolved from the work by McCoy (1982), Lee and Eakle (1984), and Grippo (1991a) and describes a theoretical process whereby occlusal forces create stresses in enamel and dentin along the cervical area and predispose it to erosion and abrasion. The aim of this paper is to critically review the literature and assess whether abfraction exists as a phenomenon.

J Dent Res 85(4):306-312, 2006

ABSTRACT
The terms abfraction and abrasion describe the cause of lesions found along the cervical margins of teeth. Erosion, abrasion, and attrition have all been associated with their formation. Early research suggested that the cause of the V-shaped lesion was excessive horizontal toothbrushing. Abfraction is another possible etiology and involves occlusal stress, producing cervical cracks that predispose the surface to erosion and abrasion. This article critically reviews the literature on abrasion, erosion, and abrasion, and abfraction. The references were obtained by a MEDLINE search in March, 2005, and from this, hand searches were undertaken. From the literature, there is little evidence, apart from laboratory studies, to indicate that abfraction exists other than as a hypothetical component of cervical wear. KEY WORDS: abrasion, erosion, attrition, abfraction, tooth wear.

TOOTH WEAR
Tooth wear can be separated into attrition, erosion, and abrasion. Attrition is defined as the loss of enamel, dentin, or restoration by tooth-to-tooth contact (Pindborg, 1970). Erosion is the loss of dental hard tissues by chemical action not involving bacteria (Eccles, 1982). It is further classified, according to the source of the acid, as either intrinsic or extrinsic. Intrinsic sources of acids originate in the stomach and are associated with eating disorders, such as anorexia and bulimia nervosa (Scheutzel, 1996), or with acid reflux and regurgitation (Bartlett et al., 1996). Extrinsic sources are acids contained in dietary components, such as carbonated soft drinks and fruit, and fruit juices (Zero, 1996; Lussi et al., 2004). Abrasion is the loss of tooth substance from factors other than tooth contact (Pindborg, 1970). Perceptions relating to the relative importance of erosion, attrition, and abrasion are geographically polarized, with apparently lower recognition in North America of the potential consequences of acids in tooth wear. This apparent conflict arises from a differing interpretation of the definitions relating to the etiology of tooth wear (Bartlett et al., 1999). Non-carious cervical lesions present in a variety of forms. Historically, these have been classified according to appearance: wedge-shaped, disc-shaped, flattened, irregular, and figured areas. Generally, they vary from shallow grooves to broad dished-out lesions to large wedge-shaped defects with sharp internal and external line angles. Clinical studies and observations have shown that cervical wear lesions are often situated on the vestibular surfaces of teeth, seldom on lingual surfaces and rarely on proximal surfaces (Kitchin, 1941). They are also more pronounced on incisors, canines, and premolars and more prevalent in the maxilla than in the mandible (Kitchin, 1941). There is some suggestion that the shape of the lesion is related to its etiology (Sognnaes et al., 1972; Brady and Woody, 1977; Lee and Eakle, 1984). One group of authors suggested, in a literature review, that those lesions with sharply defined margins could be caused by abrasive factors, whereas erosion produces broader, dishshaped but shallower lesions (Levitch et al., 1994). The same authors classified palatal erosion as a non-carious cervical lesion, despite the clinical observation that this pattern of erosion is not limited to the cervical area.

Received May 11, 2005; Accepted November 8, 2005

306

J Dent Res 85(4) 2006

Critical Review of Abfraction

307

PREVALENCE OF CERVICAL WEAR

The prevalence of cervical wear has been reported to vary between 5 and 85% (Bergstrm and Lavstedt, 1979; Levitch et al., 1994; Piotrowski et al., 2001; Aw et al., 2002; Oginni et al., 2003; Borcic et al., 2004). This large variation reflects the relatively few studies reporting the prevalence of cervical wear alone. Most studies report general levels of tooth wear in children and adolescents (Smith and Robb, 1996; Bartlett et al., 1998; Bardsley et al., 2004). From these studies, it is accepted that tooth wear is an almost universal condition, but that severe dentin exposure on non-cervical sites is relatively uncommon, at 2-4% (Lussi et al., 1991; Millward et al., 1994; Smith and Robb, 1996; Hugoson et al., 1996; Bartlett et al., 1998; Deery et al., 2000; Al Dlaigan et al., 2002; Dugmore and Rock, 2004; Bardsley et al., 2004). A few studies reporting the prevalence of tooth wear include data on cervical wear (Smith and Robb, 1996; Bartlett et al., 1998). These studies support the findings of others that cervical wear involving loss of enamel is common, but that exposure of dentin is less frequent, with quotes ranging between 2 and 6%. From the few studies reporting the prevalence of cervical wear, maxillary teeth seem to be more frequently affected, perhaps because of their lingual tilt (Levitch et al., 1994). Almost exclusively, the prevalence is reported on the buccal surfaces and rarely on the lingual surfaces of teeth (Khan et al., 1999). The teeth most commonly affected, from a study of 1002 patients from 4 dental practices in Croatia, are premolars and molars, with incisors being the least affected (Borcic et al., 2004). Enamel wear in the Croatian study was observed to be common, at around 60-70%, while dentin exposure varied between 0.6 and 5.6% of sites. In this sample, the prevalence and severity of cervical wear lesions appeared to increase with age, and this finding is supported by two other studies of 428 and 1007 adults recruited in practices in Turkey and the southeast of England, respectively (Smith and Robb, 1996; Akgul et al., 2003). Another study reported 10-35% of tooth sites with enamel cervical wear in a cluster sample of 210 adolescents in South London (Bartlett et al., 1998). Sangnes and Gjermo (1976) reported similarly high levels of enamel wear in the cervical region in 533 subjects. From these studies, it seems that cervical tooth wear of enamel is common, but this inference is based on relatively few epidemiological studies compared with the investigations on the prevalence of tooth wear as a whole (Table 1).

THE ROLE OF ABRASION IN THE ETIOLOGY OF CERVICAL WEAR

The role of abrasion has been investigated in the laboratory and clinically. Most of the early laboratory Table 1. The Prevalence of Cervical Enamel Wear with Size of Sample and Prevalence of studies were based on the hypothesis that Enamel Wear brushing with toothpastes containing abrasives will wear teeth. However, the Size of Prevalence of values of less than 1 m obtained in more Author Reference Sample Wear of Enamel recent laboratory and in situ studies suggest that the amount of enamel wear by Bergstrm and Lavstedt Community Dent Oral Epidemiol, 1979 818 30% toothpastes may not be clinically Smith and Robb J Oral Rehabil, 1996 1007 N/A significant (Svinnseth et al., 1987; Joiner et Bartlett et al. Br Dent J, 1998 210 20-30% al., 2004). There has been comparatively Piotrowski et al. J Am Dent Assoc, 2001 32 100% little work on dentin and abrasion, because Aw et al. J Am Dent Assoc, 2002 57 100% the tissue is more complex and more Oginni et al. Int Dent J, 2003 106 62.3% difficult to measure (Ashmore et al., 1972). Borcic et al. J Oral Rehabil, 2004 1002 13% Early clinical work suggested that the

orientation of the toothbrush influenced the wear of the teeth. From these studies, horizontal brushing was suggested as causing two to three times as much wear compared with vertical brushing (Mannerberg, 1960). This evidence was derived from scratches seen on replicas of teeth taken from 32 dental nurses. Prolonged contact time between bristles and tooth surface assessed in a laboratory study was reported to increase this further (Bjorn and Lindhe, 1966). Manly et al. (1965), in a laboratory study, reported that wear is, to some extent, dependent upon the force and frequency applied to the brush. The hypotheses of these early studies reflected the understanding at the time that cervical wear was caused by abrasion. A large cross-sectional study of 818 subjects showed an increase in the frequency of cervical lesions in patients (12% of the total) who brushed twice daily, compared with those who brushed less frequently (Bergstrm and Lavstedt, 1979). The results were supported by a smaller study on 100 military personnel of whom fewer than 50 had some cervical wear (Radentz et al., 1976). Although males might be expected to apply greater force during brushing, this may not influence the prevalence of cervical lesions when the genders are compared (Radentz et al., 1976; Sangnes and Gjermo, 1976; Bergstrm and Lavstedt, 1979). If the force during toothbrushing was important, it might be expected that lesions would be observed more frequently on the side of the mouth opposite the hand holding the brush (Kitchin, 1941; Sangnes and Gjermo, 1976). One study of 106 subjects reported that more lesions were found on the left side of right-handed subjects, but the difference was not statistically significant (Oginni et al., 2003). Another study on the effect of handedness on gingival cleaning and abrasion found no association with abrasion of the gingival tissues (Niemi et al., 1987). Overall, there appears to be little evidence for the effect of which hand holds the brush and the outcome on the tissues. However, other older laboratory studies indicate that the force of brushing varies with the brushing technique, the groups of teeth brushed, the stiffness of the bristles, the age of the brusher, and also individual brushing habits (Bjorn and Lindhe, 1966; Kakudo et al., 1969). Some studies suggest that toothpaste has more relevance to abrasion than does the toothbrush (Litonjua et al., 2004a). Very small and insignificant changes on the tooth surface are caused by the toothbrush itself (Manly et al., 1965; Bjorn et al., 1966; Volpe et al., 1975; Bergstrm and Lavstedt, 1979). The initial lesions have been described as small scratches on the tooth surface (Mannerberg, 1960). There is some suggestion that softer brushes result in greater abrasion than do harder brushes, since they carry more paste (Dyer et al., 2000). But the

308

Bartlett & Shah

J Dent Res 85(4) 2006

proposed by Davis and Winter, but has been used by several Author Reference Study Outcome different authors (Kelly and Smith, Manly et al. J Dent Res, 1965 Lab Brushing causes minimal cervical wear 1988; Bartlett et al., Bjorn et al. Odontol Revy, 1966 Lab Direction of brushing influences amount of wear 1994; Azzopardi et Padbury and Ash J Periodontol, 1974 Lab Direction of brushing influences amount of wear al., 2001). However, Radentz et al. J Periodontol, 1976 Clin Weak evidence for toothpastes causing wear the majority of labNiemi et al. J Clin Periodontol, 1987 In situ Hand grip does not alter cervical wear oratory and in situ Dyer et al. J Clin Periodontol, 2000 Lab Abrasion from brush and toothpaste produced 1 m of wear studies support the Joiner et al. J Clin Periodontol, 2004 In situ Abrasion from brush and toothpaste produced 1 m of wear hypothesis that a Litonjua et al. J Oral Rehabil, 2004b Lab Axial loading of teeth did not increase cervical wear after brushing combination of erosion and abrasion increases wear (Jaeggi toothbrush acts only as a device to carry the abrasive paste to and Lussi, 1999; Hooper et al., 2003; Amaechi et al., 2003; the tooth surface. Even if the toothpaste does cause wear, the Azzopardi et al., 2004; Attin et al., 2004). amount has been estimated to be a few microns rather than the The combined etiology of cervical wear is further more extreme wear seen clinically (Saxton and Cowell, 1981). supported by an investigation analyzing study casts from 264 Further doubts about toothbrush abrasion causing cervical wear individuals and involving data from saliva and dietary were reported by Volpe et al. (1975) in a study of 120 subjects questionnaires (Bader et al., 1996). The case-controlled study using 2 dentifrices. The results showed no correlation between reported that cervical wear is a multifactorial process in both development of cervical lesions and abrasivity of the initiation and progression. There is only one clinical study that toothpastes. In conclusion, from results of laboratory and has investigated the progression of cervical wear lesions (Lussi clinical studies, there is little evidence to suggest that cervical and Schaffner, 2000). This six-year longitudinal clinical study wear lesions are solely caused by abrasion (Table 2). reported the results for 55 people with cervical wear, and the authors observed that both consumption of dietary acids and THE COMBINED ROLE OF EROSION AND ABRASION frequency of toothbrushing correlated to increased wear. If the combination of erosion and abrasion is cumulative, it One of the first papers to introduce the concept that abrasion is might be expected that, theoretically, reversal is possible. Two accelerated with acid-softening or dissolution was a classic different groups of researchers (Jaeggi and Lussi, 1999; Attin et laboratory investigation by Davis and Winter (1980). This work al., 2004), using in situ studies, reported that if the tooth has been supported by numerous laboratory studies showing that surface is not exposed to mechanical abrasion while in the the combined effect of erosion and abrasion is greater than the softened state, remineralization can reverse the softening after a effect of either operating on its own (Azzopardi et al., 2001; prolonged period of exposure to saliva. From this laboratory Eisenburger et al., 2003). One laboratory study comparing study, they surmised that a delay of at least one hour before abrasion with erosion demonstrated a 50% increase in wear brushing, but after an acid challenge, can increase the (Eisenburger et al., 2003). Despite this evidence, one study resistance of the tooth surfaces to abrasion (Jaeggi and Lussi, reported no statistically significant difference in wear after 5 1999; Attin et al., 2000). In conclusion, there is overwhelming erosive/abrasive cycles on extracted teeth (De Menezes et al., evidence from laboratory and clinical studies that erosion and 2004). This study immersed bovine root dentin in common abrasion are linked in cervical wear (Table 3). Conversely, dietary drinks for 5 min and subjected the specimens to 5000 there is little evidence to suggest that cervical wear is caused brushing stokes with a remineralizing phase. The remineralizing solely by erosion or abrasion. phase consisted of inorganic mineral ions, including potassium chloride and calcium phosphate, and was the likely reason why ABFRACTION the acids effect was reduced. The choice of 5000 cycles was first Abfraction means to break away (Braem et al., 1992). There remain many lesions that cannot be Table 3. References Supporting the Role of Erosion and Abrasion in Cervical Wear explained by toothbrush abrasion or erosion alone for example, single-tooth lesions with unaffected Author Reference Study teeth on either side. In addition, some studies have found no association between the incidence of lesions Davis and Winter Br Dent J, 1980 Lab and horizontal toothbrushing (Bevenius et al., 1993). Kelly et al. J Dent, 1988 Lab It is suggested that abfraction is the cause of such Bader et al. Community Dent Oral Epidemiol, 1996 Case-control lesions. Abfraction lesions present primarily at the Jaeggi and Lussi Caries Res, 1999 In situ cervical region of the dentition and are typically Hooper et al. J Clin Periodontol, 2003 In situ wedge-shaped, with sharp internal and external line Eisenburger et al. Caries Res, 2003 Lab angles. Attin et al. Caries Res, 2004 In situ Engineering studies have demonstrated that when Azzopardi et al. Br Dent J, 2004 In situ teeth are loaded in a horizontal direction, the effect of Lussi and Schaffner Caries Res, 2000 Prevalence the stress becomes concentrated in the cervical De Menezes et al. Clin Oral Investig, 2004 Lab region, causing flexure (Hammadeh and Rees, 2001;
Table 2. References Supporting the Role of Cervical Wear and Abrasion

J Dent Res 85(4) 2006

Critical Review of Abfraction

309

Lee et al., 2002; Rees et al., 2003). McCoy (1982) proposed that bruxism may be the primary cause of angled notches at the cemento-enamel junction. The author postulated that tooth flexure from tensile stresses led to cervical tooth breakdown. Later, Lee and Eakle (1984) hypothesized that the primary etiological factor in wedge-shaped cervical erosions was the impact of tensile stress from mastication and malocclusion. The wear is suggested to be created by a combination of bending and barrelling deformations that cause alternating tensile and compressive stresses, which lead to a weakening of the enamel and dentin. The cyclic tension and compression may reach a fatigue limit and result in cracking or breakage of the tooth structure. At the same time, the opposite region comes under compressive stress. When the direction of the force changes (e.g., in bruxism), the tooth bends in the opposite direction, and the stresses correspondingly reverse at this cervical area. This bending of the tooth from side to side results in fatigue and fracture of the most-flexed zone. The interocclusal forces create physical microfractures, or abfractions, at the cervical region, which, in turn, result in wear. It has been reported that enamel is weak in tension (Powers et al., 1973), and the tensile phase of deformation therefore may cause disruption, allowing water and other small molecules to penetrate between the prisms and prevent reestablishment of interprismatic bonds on release of the stress (Levitch et al., 1994). Lee and Eakle (1996) suggested, in a review, that the cervical fulcrum area of a tooth might be subject to unique stress, torque, and moments resulting from occlusal function, bruxing, and parafunctional activity. These flexural forces would then disrupt the normally ordered crystalline structure of the thin enamel and underlying dentin by cyclic fatigue, leading to cracks, chips, and rupture (Spranger, 1995; Lee and Eakle, 1996; De Las Casas et al., 2003). Ultimately, the enamel breaks away at the cervical margin and progressively exposes the dentin, in which the process continues. Grippo (1991b, 1992) subsequently coined the term abfraction and defined it as the pathological loss of tooth substance caused by biomechanical loading forces that result in flexure and failure of enamel and dentin at a location away from the loading. Grippo (1991b) suggested that abfraction is the basic cause of all non-carious cervical lesions, whereas Lee and Eakle (1984) proposed a multifactorial etiology, with a combination of occlusal stress, abrasion, and erosion. Spranger (1995), in a review of the literature, supported the multifactorial nature of the cervical area. The authors suggested that the wear was related to the anatomy, the distribution of forces calculated from elastic deformation studies, development of caries, and occlusion and parafunction. But much of the evidence for abfraction has been derived from finite element studies (Rees, 1998; Piotrowski et al., 2001; Rees et al., 2003; Geramy and Sharafoddin, 2003; Rees and Hammadeh, 2004). These computerized numerical procedures use discrete triangular elements, joined together to form nodes. The elements are ascribed certain physical properties, and a series of theoretical applied loads produces complex algebraic equations that are used to assess the impact of forces applied along the length of the model. Rees and coauthors (Rees, 1998; Rees and Jacobsen, 1998; Rees and Hammadeh, 2004) used this concept to estimate the effect of repeated loading on restoration of cervical cavities. The

hypothesis suggests that continual occlusal loading produced displacements and stresses under the buccal cervical enamel and dentin, increasing crack initiation and encouraging loss of the restoration. The same authors subsequently investigated the effect of stress formation on unrestored teeth (Rees and Jacobsen, 1998). Lateral forces applied to the occlusal surfaces of premolars increased stress concentrations along the buccal cervical areas. Contradictory evidence from the finite element studies suggests that the lingual walls of teeth should be equally as susceptible to cervical wear as are the buccal walls (Rees, 2002), but this is not supported by the clinical findings, where lingual lesions are comparatively rare (Radentz et al., 1976). Further finite element studies showed that exposed dentin could be eroded by acid undermining enamel, causing more breakdown and increasing wear (Rees and Hammadeh, 2004). Although mathematical prediction models attempt to assess the impact of the periodontal ligament and the associated tissues, the actual role of the ligament in absorbing occlusal forces remains difficult to prove. Certainly, the theory behind abfraction seems to be plausible. Clinical and laboratory studies do not necessarily support such a simple etiology. A controlled study on extracted premolars with axial and non-axial loading indicated that no relationship between the direction of the load and the creation of cervical lesions could be established (Litonjua et al., 2004b). The same group investigated the effects of continuous and noncontinuous loading on cervical wear on extracted premolars (Litonjua et al., 2004b). The authors reported that there was no evidence of microfracture, and that the application of occlusal load may not have a role in the progression of cervical lesions. In contrast, Staninec et al. (2005), in a laboratory study on thin sections of enamel and dentin taken from the cervical area of extracted unworn teeth, showed increased loss of mineralized tissue after stress and immersion in acid. The combination of erosion and stress upon the sections increased wear evenly over the length to a greater extent than when stress was applied singularly. But a clinical study investigating matching occlusal contacts to cervical wear lesions in 32 subjects reported no correlation between lesion dimensions and facet areas on the teeth (Piotrowski et al., 2001). These authors reported that control teeth had less gingival recession than did affected teeth, and therefore proposed that the lesions were more likely a result of toothbrushing than occlusal stress. Another recent study, from the articulated casts of 299 dental students, observed no correlation between occlusal wear and cervical lesions (Estafan et al., 2005). A study on 52 modern skulls, collected between 1920 and 1958, showed that attrition was a common finding, but of the 415 teeth examined, only 15 were found to have cervical wear lesions (Horning et al., 2000). The authors reported that, from the skulls, there was little evidence of occlusal forces causing either bone formation in the periodontal ligament or abfraction. One paper reported the results of a study on 122 subjects with cervical wear (Khan et al., 1999). Cervical wear was compared with the appearance of the occlusal surface on the same tooth, and within the same subject, different occlusal lesions could be attributed to erosion or attrition. The study showed increased frequency of attrition on the occlusal surfaces in those with cervical wear. But they also showed an equal frequency between erosion on the occlusal surface with cervical wear lesions. The numbers of sites exhibiting an

310
Table 4. Studies Comparing Abfraction with Cervical Wear Author Xhonga Lee and Eakle Braem et al. Levitch et al. Rees and Jacobsen Khan et al. Horning et al. Piotrowski et al. Lee et al. Rees et al. De Las Casas et al. Geramy and Sharafoddin Rees and Hammadeh Litonjua et al. Estafan et al. Staninec et al. Reference

Bartlett & Shah

J Dent Res 85(4) 2006

Study Clinical Hypothesis Case report Lit review Lab study Clinical Comparative Comparative Lab Lab Lab Lab Lab Lab Clinical Lab

Outcome Occlusion related to cervical wear Discussion document Occlusal forces related to cervical wear Occlusal forces related to cervical wear Occlusal forces related to cervical wear Cervical wear related to erosion and attrition Lack of anatomical evidence for abfraction Cervical wear lesions not related to occlusal forces Finite element analysis supports occlusion and cervical wear Finite element analysis supports occlusion and cervical wear Finite element analysis supports occlusion and cervical wear Finite element analysis supports occlusion and cervical wear Finite element analysis supports occlusion and cervical wear Occlusal forces not related to cervical wear No relationship between occlusion and cervical wear Bending forces and acids cause wear

J Oral Rehabil, 1977 J Prosthet Dent, 1984 J Prosthet Dent, 1992 J Dent, 1994 J Dent, 1998 Aust Dent J, 1999 J Periodontol, 2000 J Am Dent Assoc, 2001 J Dent, 2002 Eur J Oral Sci, 2003 Comput Methods Biomech Biomed Eng, 2003 Quint Int, 2003 Eur J Oral Sci, 2004 J Oral Rehabil, 2004b J Prosthet Dent, 2005 J Dent Res, 2005

association between attrition and cervical wear were relatively low, and the authors did not report the results of any statistical tests. The results of the study add support to the multifactorial nature of cervical wear. Weak support was obtained from a clinical case study where strain gauges were used in three subjects (Nohl and Setchell, 2000). In the healthy subjects, increased strain developed along the cervical areas, but there was no information available to compare the results with those from controls. There is some evidence supporting the association between occlusal stress and cervical wear, but most of this is derived from finite element analysis and laboratory studies, with little direct data to confirm this clinically. In conclusion, there appears to be little evidence to correlate occlusal stress positively to cervical wear (Table 4).

bruxists as compared with non-bruxists (Xhonga, 1977). In this study on 30 subjects, the authors reported a significant association (p > 0.001) between the presence of occlusal and cervical wear. However, the authors grouped the subjects into bruxists and non-bruxists, based upon the appearance of occlusal wear. They defined erosion as wear occurring along the cervical margin. Therefore, those in the bruxist group, by selection, had more wear and consequently were more likely to develop cervical wear. There was no attempt to compare the location of the cervical with that of the occlusal wear lesions. This comparison was undertaken by Estafan et al. (2005), who compared cervical wear lesion with the occlusal contacts and observed no correlation between these factors in their study.

CONCLUSION MULTIFACTORIAL ETIOLOGY OF CERVICAL WEAR

Stress corrosion and piezoelectric effects have also been theorized to have an effect on cervical wear (Grippo and Simring, 1995). More recently, new terms have been introduced to describe cervical tooth wear. Biodental engineering factors (Grippo and Masi, 1991) have been defined as the effect of piezoelectricity at the cervical area, and stress corrosion (Grippo and Simring, 1995) has been used to describe a multifactorial physiochemical degradation of the CEJ area. Also, dental compression syndrome (McCoy, 1999) is tooth deformation related to malocclusion, parafunctional habits, and temporomandibular joint disorders. Several factors indicate a multifactorial etiology of cervical wear (Osborne-Smith et al., 1999). Cervical wear has been reported on the lingual surfaces of teeth in sites where toothbrush access is limited (Lee and Eakle, 1984). Cervical wear has been reported adjacent to restorations that remain unaffected (Braem et al., 1992), and, generally, mobile teeth are not as frequently affected as non-mobile teeth (Grippo, 1992). The hypothesis that occlusion has some influence has been recognized with increased incidence of cervical wear in Tooth wear is a universal consequence of aging (Smith and Robb, 1996). The cause of pathological levels of tooth wear is difficult to diagnose and is generally a result of abrasion, attrition, and erosion (Smith and Knight, 1984). It is therefore difficult to select specific etiologies and make assumptions based on theories that assume that they do not co-exist with each other. Therefore, cervical wear lesions, like other forms, are probably created by a combination of erosion, abrasion, and attrition. There is strong support that erosion and abrasion are important in the development of wedge-shaped lesions along the cervical margins of teeth, but, as yet, there is insufficient evidence to confirm that abfraction truly exists. More research, particularly clinical, is needed to establish the validity of abfraction existing as an entity. Much stronger evidence suggests that the result of cervical wear is a combination of erosion, abrasion, and attrition.

REFERENCES
Akgul HM, Akgul N, Karaoglanoglu S, Ozdabak N (2003). A survey of the correspondence between abrasions and tooth brushing habits in Erzurum, Turkey. Int Dent J 53:491-495. Al Dlaigan YH, Shaw L, Smith AJ (2002). Dental erosion in a group of

J Dent Res 85(4) 2006

Critical Review of Abfraction

311

British 14-year-old, school children. Part III: Influence of oral hygiene practices. Br Dent J 192:526-530. Amaechi BT, Higham SM, Edgar WM (2003). Influence of abrasion in clinical manifestation of human dental erosion. J Oral Rehabil 30:407413. Ashmore H, Van Abbe NJ, Wilson SJ (1972). The measurement in vitro of dentine abrasion by toothpaste. Br Dent J 133:60-66. Attin T, Buchalla W, Gollner M, Hellwig E (2000). Use of variable remineralization periods to improve the abrasion resistance of previously eroded enamel. Caries Res 34:48-52. Attin T, Siegel S, Buchalla W, Lennon AM, Hannig C, Becker K (2004). Brushing abrasion of softened and remineralised dentin: an in situ study. Caries Res 38:62-66. Aw TC, Lepe X, Johnson GH, Mancl L (2002). Characteristics of noncarious cervical lesions: a clinical investigation. J Am Dent Assoc 133:725-733. Azzopardi A, Bartlett DW, Watson TF, Sherriff M (2001). The measurement and prevention of erosion and abrasion. J Dent 29:395400. Azzopardi A, Bartlett DW, Watson TF, Sherriff M (2004). The surface effects of erosion and abrasion on dentine with and without a protective layer. Br Dent J 196:351-354. Bader JD, McClure F, Scurria MS, Shugars DA, Heymann HO (1996). Case-control study of non-carious cervical lesions. Community Dent Oral Epidemiol 24:286-291. Bardsley PF, Taylor S, Milosevic A (2004). Epidemiological studies of tooth wear and dental erosion in 14-year-old children in North West England. Part 1: The relationship with water fluoridation and social deprivation. Br Dent J 197:413-416. Bartlett DW, Smith BG, Wilson RF (1994). Comparison of the effect of fluoride and non-fluoride toothpaste on tooth wear in vitro and the influence of enamel fluoride concentration and hardness of enamel. Br Dent J 176:346-348. Bartlett DW, Evans DF, Anggiansah A, Smith BG (1996). A study of the association between gastro-oesophageal reflux and palatal dental erosion. Br Dent J 181:125-131. Bartlett DW, Coward PY, Nikkah C, Wilson RF (1998). The prevalence of tooth wear in a cluster sample of adolescent schoolchildren and its relationship with potential explanatory factors. Br Dent J 184:125-129. Bartlett D, Phillips K, Smith BG (1999). A difference in perspectivethe North American and European interpretations of tooth wear. Int J Prosthodont 12:401-408. Bergstrm J, Lavstedt S (1979). An epidemiologic approach to toothbrushing and dental abrasion. Community Dent Oral Epidemiol 7:57-64. Bevenius J, LEstrange P, Karlsson S, Carlsson GE (1993). Idiopathic cervical lesions: in vivo investigation by oral microendoscopy and scanning electron microscopy. A pilot study. J Oral Rehabil 20:1-9. Bjorn H, Lindhe J (1966). On the mechanics of toothbrushing. Odontol Revy 17:9-16. Bjorn H, Lindhe J, Grondahl HG (1966). The abrasion of dentine by commercial dentifrices. Odontol Revy 17:109-120. Borcic J, Anic I, Urek MM, Ferreri S (2004). The prevalence of non-carious cervical lesions in permanent dentition. J Oral Rehabil 31:117-123. Brady JM, Woody RD (1977). Scanning microscopy of cervical erosion. J Am Dent Assoc 94:726-729. Braem M, Lambrechts P, Vanherle G (1992). Stress-induced cervical lesions. J Prosthet Dent 67:718-722. Davis WB, Winter PJ (1980). The effect of abrasion on enamel and dentine after exposure to dietary acid. Br Dent J 148:253-256. De Las Casas EB, Cornacchia TP, Gouvea PH, Cimini CA Jr (2003). Abfraction and anisotropyeffects of prism orientation on stress distribution. Comput Methods Biomech Biomed Engin 6:65-73. Deery C, Wagner ML, Longbottom C, Simon R, Nugent ZJ (2000). The prevalence of dental erosion in a United States and a United Kingdom sample of adolescents. Pediatr Dent 22:505-510. De Menezes M, Turssi CP, Hara AT, Messias DC, Serra MC (2004). Abrasion of eroded root dentine brushed with different toothpastes. Clin Oral Investig 8:151-155. Dugmore CR, Rock WP (2004). The prevalence of tooth erosion in 12-yearold children. Br Dent J 196:279-282.

Dyer D, Addy M, Newcombe RG (2000). Studies in vitro of abrasion by different manual toothbrush heads and a standard toothpaste. J Clin Periodontol 27:99-103. Eccles JD (1982). Tooth surface loss from abrasion, attrition and erosion. Dent Update 9:373-374, 376-378, 380-381. Eisenburger M, Shellis RP, Addy M (2003). Comparative study of wear of enamel induced by alternating and simultaneous combinations of abrasion and erosion in vitro. Caries Res 37:450-455. Estafan A, Furnari PC, Goldstein G, Hittelman EL (2005). In vivo correlation of noncarious cervical lesions and occlusal wear. J Prosthet Dent 93:221-226. Geramy A, Sharafoddin F (2003). Abfraction: 3D analysis by means of the finite element method. Quintessence Int 34:526-533. Grippo JO (1991a). Abfractions: a new classification of hard tissue lesions of teeth. J Esthet Dent 3:14-19. Grippo JO (1991b). Tooth flexure (letter). J Am Dent Assoc 122(7):13. Grippo JO (1992). Noncarious cervical lesions: the decision to ignore or restore. J Esthet Dent 4 Suppl:55-64. Grippo JO, Masi JV (1991). Role of biodental engineering factors (BEF) in the etiology of root caries. J Esthet Dent 3:71-76. Grippo JO, Simring M (1995). Dental erosion revisited. J Am Dent Assoc 126:619-630. Hammadeh M, Rees JS (2001). The erosive susceptibility of cervical versus occlusal enamel. Eur J Prosthodont Restor Dent 9:13-17. Hooper S, West NX, Pickles MJ, Joiner A, Newcombe RG, Addy M (2003). Investigation of erosion and abrasion on enamel and dentine: a model in situ using toothpastes of different abrasivity. J Clin Periodontol 30:802-808. Horning GM, Cohen ME, Neils TA (2000). Buccal alveolar exostoses: prevalence, characteristics, and evidence for buttressing bone formation. J Periodontol 71:1032-1042. Hugoson A, Ekfeldt A, Koch G, Hallonsten AL (1996). Incisal and occlusal tooth wear in children and adolescents in a Swedish population. Acta Odontol Scand 54:263-270. Jaeggi T, Lussi A (1999). Toothbrush abrasion of erosively altered enamel after intraoral exposure to saliva: an in situ study. Caries Res 33:455461. Joiner A, Pickles MJ, Tanner C, Weader E, Doyle P (2004). An in situ model to study the toothpaste abrasion of enamel. J Clin Periodontol 31:434-438. Kakudo Y, Hieda T, Matsuzawa S, Ishida A, Yoshihara M (1969). Relations between brushing force and the number of strokes during tooth brushing in pre-school children and primary school pupils. J Osaka Dent Univ 3:187-199. Kelly MP, Smith BGN (1988). The effect of remineralizing solutions on tooth wear in vitro. J Dent 16:147-149. Khan F, Young WG, Shahabi S, Daley TJ (1999). Dental cervical lesions associated with occlusal erosion and attrition. Aust Dent J 44:176-186. Kitchin PC (1941). The prevalence of tooth root exposure and the relation of the extent of such exposure to the degree of abrasion in different age classes. J Dent Res 20:565-581. Lee HE, Lin CL, Wang CH, Cheng CH, Chang CH (2002). Stresses at the cervical lesion of maxillary premolara finite element investigation. J Dent 30:283-290. Lee WC, Eakle WS (1984). Possible role of tensile stress in the etiology of cervical erosive lesions of teeth. J Prosthet Dent 52:374-380. Lee WC, Eakle WS (1996). Stress-induced cervical lesions: review of advances in the past 10 years. J Prosthet Dent 75:487-494. Levitch LC, Bader JD, Shugars DA, Heymann HO (1994). Non-carious cervical lesions. J Dent 22:195-207. Litonjua LA, Andreana S, Bush PJ, Tobias TS, Cohen RE (2004a). Wedged cervical lesions produced by toothbrushing. Am J Dent 17:237-240. Litonjua LA, Bush PJ, Andreana S, Tobias TS, Cohen RE (2004b). Effects of occlusal load on cervical lesions. J Oral Rehabil 31:225-232. Lussi A, Schaffner M (2000). Progression of and risk factors for dental erosion and wedge-shaped defects over a 6-year period. Caries Res 34:182-187. Lussi A, Schaffner M, Hotz P, Suter P (1991). Dental erosion in a population of Swiss adults. Community Dent Oral Epidemiol 19:286290. Lussi A, Jaeggi T, Zero D (2004). The role of diet in the aetiology of dental

312

Bartlett & Shah

J Dent Res 85(4) 2006

erosion. Caries Res 38(Suppl 1):34-44. Mair LH (1992). Wear in dentistrycurrent terminology. J Dent 20:140144. Manly RS, Wiren J, Manly PJ, Keene RC (1965). A method for measurement of abrasion of dentin by toothbrush and dentifrice. J Dent Res 44:533-540. Mannerberg F (1960). Appearance of tooth surface as observed in shadowed replicas in various age groups, in long-term studies, after toothbrushing, in cases of erosion and after exposure to citrus fruit juice. Odontol Revy 11(Suppl):70-86. McCoy G (1982). The etiology of gingival erosion. J Oral Implantol 10:361-362. McCoy G (1999). Dental compression syndrome: a new look at an old disease. J Oral Implantol 25:35-49. Millward A, Shaw L, Smith A (1994). Dental erosion in four-year-old children from differing socioeconomic backgrounds. ASDC J Dent Child 61:263-266. Niemi ML, Ainamo J, Etemadzadeh H (1987). The effect of toothbrush grip on gingival abrasion and plaque removal during toothbrushing. J Clin Periodontol 14:19-21. Nohl FS, Setchell DJ (2000). Surface strains induced by measured loads on teeth in vivo: a methodological study. Eur J Prosthodont Rest Dent 8:27-31. Oginni AO, Olusile AO, Udoye CI (2003). Non-carious cervical lesions in a Nigerian population: abrasion or abfraction? Int Dent J 53:275-279. Osborne-Smith KL, Burke FJ, Wilson NH (1999). The aetiology of the noncarious cervical lesion. Int Dent J 49:139-143. Padbury AD, Ash MM Jr (1974). Abrasion caused by three methods of toothbrushing. J Periodontol 45:434-438. Pindborg JJ (1970). Pathology of the dental hard tissues. 1st ed. Copenhagen: Munksgaard. Piotrowski BT, Gillette WB, Hancock EB (2001). Examining the prevalence and characteristics of abfractionlike cervical lesions in a population of US veterans. J Am Dent Assoc 132:1694-1701. Powers JM, Craig RG, Ludema KC (1973). Frictional behavior and surface failure of human enamel. J Dent Res 52:1327-1331. Radentz WH, Barnes GP, Cutright DE (1976). A survey of factors possibly associated with cervical abrasion of tooth surfaces. J Periodontol 47:148-154. Rees JS (1998). The role of cuspal flexure in the development of abfraction lesions: a finite element study. Eur J Oral Sci 106:1028-1032.

Rees JS (2002). The effect of variation in occlusal loading on the development of abfraction lesions: a finite element study. J Oral Rehabil 29:188-193. Rees JS, Hammadeh M (2004). Undermining of enamel as a mechanism of abfraction lesion formation: a finite element study. Eur J Oral Sci 112:347-352. Rees JS, Jacobsen PH (1998). The effect of cuspal flexure on a buccal Class V restoration: a finite element study. J Dent 26:361-367. Rees JS, Hammadeh M, Jagger DC (2003). Abfraction lesion formation in maxillary incisors, canines and premolars: a finite element study. Eur J Oral Sci 111:149-154. Sangnes G, Gjermo P (1976). Prevalence of oral soft and hard tissue lesions related to mechanical toothcleansing procedures. Community Dent Oral Epidemiol 4:77-83. Saxton CA, Cowell CR (1981). Clinical investigation of the effects of dentifrices on dentin wear at the cementoenamel junction. J Am Dent Assoc 102:38-43. Scheutzel P (1996). Etiology of dental erosionintrinsic factors. Eur J Oral Sci 104:178-190. Smith BG, Knight JK (1984). A comparison of patterns of tooth wear with aetiological factors. Br Dent J 157:16-19. Smith BG, Robb ND (1996). The prevalence of toothwear in 1007 dental patients. J Oral Rehabil 23:232-239. Sognnaes RF, Wolcott RB, Xhonga FA (1972). Dental erosion. I. Erosionlike patterns occuring in association with other dental conditions. J Am Dent Assoc 84:571-576. Spranger H (1995). Investigation into the genesis of angular lesions at the cervical region of teeth [review]. Quintessence Int 26:149-154. Staninec M, Nalla RK, Hilton JF, Ritchie RO, Watanabe LG, Nonomura G, et al. (2005). Dentin erosion simulation by cantilever beam fatigue and pH change. J Dent Res 84:371-375. Svinnseth PN, Gjerdet NR, Lie T (1987). Abrasivity of toothpastes. An in vitro study of toothpastes marketed in Norway. Acta Odontol Scand 45:195-202. Volpe AR, Mooney R, Zumbrunnen C, Stahl D, Goldman HM (1975). A long term clinical study evaluating the effect of two dentifrices on oral tissues. J Periodontol 46:113-118. Xhonga FA (1977). Bruxism and its effect on the teeth. J Oral Rehabil 4:6576. Zero DT (1996). Etiology of dental erosionextrinsic factors. Eur J Oral Sci 104(2 Pt 2):162-177.