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J Am Dent Assoc, Vol 134, No 7, 845-850.
© 2003 American Dental Association
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CLINICAL PRACTICE

Noncarious cervical lesions and abfractions

A re-evaluation



LUIS A. LITONJUA, D.M.D., M.S., SEBASTIANO ANDREANA, D.D.S., M.S., PETER J. BUSH, B.S., THOMAS S. TOBIAS, D.D.S. and ROBERT E. COHEN, D.D.S., Ph.D.


   ABSTRACT
TOP
 ABSTRACT
DEFINITION AND CONCEPTS IN...
 EVIDENCE IN SUPPORT OF...
 THE RESTORATIVE CHALLENGE
 CONCLUSIONS
 REFERENCES
 
Background. The concept of abfraction is controversial. The authors present the fundamental basis of abfraction and review studies that describe the condition.

Types of Studies Reviewed. The authors used data on masticatory forces, enamel and dentin properties, as well as stress studies related to abfraction, for background information. They also analyzed the genesis of the abfraction theory, experimental evidence, case presentations, clinical investigations and restorative studies.

Results. The theory of abfraction is based primarily on engineering analyses that demonstrate theoretical stress concentration at the cervical areas of teeth. While some recent stress studies support earlier findings, others have provided significant deviating information. Few controlled studies exist that demonstrate the relationship between occlusal loading and abfraction lesions. The role of occlusal loading in noncarious cervical lesions (as shown by clinical data) appears to be part of a multifactorial event that may not necessarily follow the proposed classic abfraction mechanism, and other mechanisms or factors may explain cervical restoration failure just as well.

Clinical Implications. There is little direct evidence supporting the theory of abfraction as the primary factor in the formation of noncarious cervical lesions. Controlled clinical trials are necessary to elucidate more fully the etiology of those lesions.

Abrasion is the wearing away of structure through an abnormal mechanical process. Dental abrasion implies the wearing away of tooth structure caused by incorrect brushing.1 It is well-recognized that noncarious cervical lesions may be caused by toothbrush abrasion. In the last 20 years, however, some authors have asked whether such lesions may be due to another mechanism such as occlusal loading. We conducted this literature review to evaluate the evidence that the proposed mechanism induces cervical lesions.

The term ‘abfraction’ was coined from the Latin words ‘ab,’ or away, and ‘fractio,’ or breaking.

During mastication, every chewing stroke is associated with axial and horizontal forces caused by occlusal morphology and the cyclic movement pattern of the mandible.2 Bite and masticatory force investigators,3–10 however, have reported varying results due to different experimental conditions. Other researchers have studied the compressive and tensile strength of enamel and dentin by applying static or continuous force.11–22 In general, the compressive strength of enamel is greater than that of dentin, while the tensile strength of dentin is greater than that of enamel. The tensile strengths of enamel and dentin are much lower than are their respective compressive strengths.14,15


   DEFINITION AND CONCEPTS IN A HISTORICAL PERSPECTIVE
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 ABSTRACT
 DEFINITION AND CONCEPTS IN...
EVIDENCE IN SUPPORT OF...
 THE RESTORATIVE CHALLENGE
 CONCLUSIONS
 REFERENCES
 
In the early 1980s, McCoy23,24 questioned the role of toothbrush abrasion in the etiology of what previously had been referred to as "cervical erosion," proposing that bruxism may be the primary cause of angled notches at the cementoenamel junction, or CEJ. Citing engineering studies,25–27 McCoy postulated that tooth flexure from tensile stresses led to cervical tooth breakdown and Class V amalgam restoration failure. Using engineering studies similar to those used by McCoy, Lee and Eakle28 later hypothesized that the primary etiologic factor in wedge-shaped cervical erosion is tensile stress from mastication and malocclusion. They said that water or other small molecules could penetrate the broken hydroxyapatite chemical bonds and make the tooth susceptible to chemical erosion and toothbrush abrasion (FigureGo). Based on the premises of McCoy23,24 and Lee and Eakle,28 Grippo29,30 subsequently coined the term "abfraction" from the Latin words "ab," or away, and "fractio," or breaking. He defined it as the pathological loss of tooth substance caused by biomechanical loading forces that results in flexure and failure of enamel and dentin at a location away from loading. Grippo presented clinical cases to support the formation of abfraction lesions, although he did not provide diet, periodontal and toothbrushing histories.



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  		Figure. Tooth flexure model seen at the cervical dentinoenamel junction of a maxillary tooth. Tensile stresses (back-to-back arrows) are concentrated at the cervical areas as a result of eccentric occlusion (single arrow). Disruption of chemical bonds between enamel and dentin hydroxyapatite crystals cause a fracture, and small molecules prevent re-establishment of chemical bonds. Adapted from the Journal of Prosthetic Dentistry, Vol. 52, WC Lee and WS Eakle, Possible Role of Tensile Stress in the Etiology of Cervical Erosive Lesions of Teeth, 374-80, Copyright 1984, with permission from Elsevier.28

 
The engineering studies cited by McCoy23,24 and Lee and Eakle28 employed finite elemental analysis, or FEA, or photoelastic methods—techniques that used computerized geometric or plastic models, respectively. Those models showed that eccentrically loaded teeth flex25 and demonstrated internal stress distribution as possible failure planes.26 The technique also revealed that stress flowed around enamel, concentrating stress at the CEJ and generating tensile stresses that pull apart enamel prisms and increase susceptibility to chemical erosion.27 While more recent investigations31,32 support cervical stress, others could not reach the same conclusions because the modeling of enamel properties20 and the dentinoenamel junction20,33 both may play a critical role in altering stress distribution. Other analyses revealed the important role of the periodontal ligament and the load distribution into the surrounding bone,34–38 both of which were not included in previous models. Dramatic variations of stress exist when removing or including the periodontal ligament and alveolar bone; therefore, it is imperative to model both when undertaking FEA of teeth, especially when examining stresses at the cervical region.38 This may not preclude other factors such as the complex deformation of the mandible during functional loading.39 Nevertheless, careful assessment should be made when those engineering principles are interpreted in the oral cavity, since those engineering methods have inherent limitations that may prevent them from generating accurate data.40–42

In the ensuing years, reviews43–49 generally cited the same works,23,24,28–30 with their findings supported by clinical observations, as well as other engineering studies. Investigators attributed cervical restoration failures to abfraction and proposed treatment options. Although authors generally noted that more studies were indicated to further characterize the abfraction phenomenon, they labeled lesions as abfractions when V- or wedge-shaped notches could not be explained readily by toothbrush abrasion.

More recently, authors have introduced new terms describing tooth wear. "Biodental engineering factors"50 have been defined as the effect of piezoelectricity at the cervical area, and "stress corrosion"51 has been used to describe a multifactorial physiochemical degradation of the CEJ area. In addition, "dental compression syndrome"52–55 is tooth deformation related to malocclusion, parafunctional habits and temporomandibular joint disorders.


   EVIDENCE IN SUPPORT OF A MULTIFACTORIAL EVENT
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 ABSTRACT
 DEFINITION AND CONCEPTS IN...
 EVIDENCE IN SUPPORT OF...
THE RESTORATIVE CHALLENGE
 CONCLUSIONS
 REFERENCES
 
The theory of abfraction is based primarily on a few early engineering models. Experimental and clinical evidence are needed to show if and how this phenomenon occurs. Over the past 20 years, however, relatively few articles providing evidence have been published on this topic. An in vitro experiment56 serendipitously revealed cervical notches on a few teeth while the investigators were studying the effect of stress corrosion on enamel. The study design, however, was confounded by the effect of chemical erosion, and the investigators did not consider the history of the specimens. A case report57 documented a multifactorial etiology of abrasion, erosion and abfraction in a woman with linear enamel hypoplasia. A longitudinal case study58 of a person showed a direct correlation between occlusal wear and the growth of noncarious cervical lesions. The illustrations in that case depicted gingival recession that also may have been a factor associated with the increase in the size of the lesions. While case reports do provide important information, they generally do not provide evidence of a causal relationship.

A survey59 documented patients exhibiting wedge-shaped defects assumed to be stress-induced, without accounting for other possible etiologies such as toothbrush abrasion and erosion. In particular, a toothbrush bristle may penetrate subgingivally60 and a cementoenamel gap junction may occur61,62 that may make the dentin more susceptible to tooth wear. Since experimental toothbrush abrasion also produces V-shaped defects,63 subgingival wedge-shaped lesions may not be a particular characteristic of abfraction. Moreover, other surveys64,65 concluded that cervical lesions indeed may have a multifactorial etiology, with erosion as the primary etiology in conjunction with stress and abrasion or with toothbrush abrasion as the primary etiologic factor.66

More definitive data are needed to support abfraction as a distinct clinical entity or a primary factor in cervical lesions.

An exploratory study67 supported a multifactorial concept in noncarious cervical lesions, though the design did not include controls. In addition, a case-controlled study68 suggested that multiple mechanisms may operate in the initiation and progression of lesions. The study’s authors noted that since measures were obtained post hoc, factors associated with initiation of noncarious cervical lesions may differ from factors associated with progression. For example, factors such as brushing, diet and occlusion mechanism do not have substantial interaction and may act independently or at different points in the development of noncarious cervical lesions. Consequently, the authors advocated using the term "noncarious cervical lesion" since "abrasion" or "erosion" implies a single etiology. This study provides the strongest evidence of a multifactorial etiology to date. Other studies69,70 related to abfraction consisted of surveys of dentists to determine how they classified and managed noncarious cervical lesions, but the studies did not provide causal evidence.

The data supporting the abfraction hypothesis remain tenuous, and more definitive data are needed to support abfraction as a distinct clinical entity or a primary factor in cervical lesions. Since evidence points to a multifactorial etiology in the development of noncarious cervical lesions, the role of abfraction as a sole phenomenon is uncertain. That is, the observation that occlusal stresses may be associated with noncarious cervical lesions may not necessarily prove that occlusal loading is the primary factor involved in the creation of those lesions. Longitudinal clinical trials and intervention studies are needed to show the effects of occlusal therapy on noncarious cervical lesions.


   THE RESTORATIVE CHALLENGE
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 ABSTRACT
 DEFINITION AND CONCEPTS IN...
 EVIDENCE IN SUPPORT OF...
 THE RESTORATIVE CHALLENGE
CONCLUSIONS
 REFERENCES
 
A number of reviews and studies have reported controversies regarding restoration of Class V cervical lesions. The choice of technique and materials has been studied, compared and analyzed with regard to restoration failure and retention. Clinicians may attribute restorative failure to the tooth flexure theory and stress at the cervical area, since the same forces acting on enamel and dentin at the CEJ may cause the restorative material to undergo debonding, marginal leakage and loss of retention.48,71–76 Indeed, the authors of a two-year clinical study reported the association of occlusion, tooth location and the patient’s age with loss of retention of different restorative materials, and they supported the role of the tooth flexure theory in restoration retention.77

While some authors feel strongly that the tooth flexure theory is pivotal, others point to technique, material shrinkage, marginal leakage and the bonding agent’s properties as other possible causes for retention failure.78–83 Some investigators conclude that etched sclerotic dentin located at cervical lesions is more resistant to demineralization than is nonsclerotic dentin and, therefore, may make dentin less receptive to dentin-bonding systems.84–87

More in vitro investigations on the restoration of noncarious cervical lesions are needed. One controlled study found that cervical lesions and their restorations had no effect on the fracture resistance of teeth under compressive loading.88 This study, however, did not show whether restorations failed due to tooth flexure.

Recent reviews and technique articles have detailed tooth preparation procedures, choice of restorative materials and their benefits, esthetic considerations and analyses of properties of current and new restorative materials.43,71,89–91 Restorative materials, however, are being introduced constantly.

Cervical lesions occur in a variety of forms depending on the type and severity of the etiologic factor, and not all lesions require restorations.89 The decision to restore noncarious cervical lesions is based on the desire to strengthen the tooth and decrease the theoretical stress concentration and flexure, mitigate lesion progression, prevent hypersensitivity and pulp involvement, improve oral hygiene and enhance esthetics.30,49,89 Treatment measures43,71,89–92 have included resin-based composites, glass ionomers or a combination of the techniques.78,93–95 Other treatment possibilities include metal restorations for posterior teeth, dentin-bonding agents96–98 and copal varnishes, fluoride therapy and desensitizing agents, nightguard and occlusal adjustments, dietary modification and oral habit cessation. In tandem with cervical restoration, gingival recession and mucogingival defects may be corrected by root coverage procedures using grafting techniques (free and connective-tissue grafts) and nongrafting procedures (rotational and coronally advanced flaps, guided tissue regeneration) or a combination of these methods.99,100

There is little direct evidence supporting abfraction as the primary factor in causing noncarious cervical lesions, but there is some evidence to show otherwise.

Many variables may confound cervical restoration failure, and controlled experimental and clinical trials remain elusive. Nevertheless, experiments should be designed to assess how tooth flexure by itself affects restoration failure.


   CONCLUSIONS
TOP
 ABSTRACT
 DEFINITION AND CONCEPTS IN...
 EVIDENCE IN SUPPORT OF...
 THE RESTORATIVE CHALLENGE
 CONCLUSIONS
REFERENCES
 
The theory of abfraction is based on a limited number of engineering studies consisting of FEA analysis and photoelastic methods. Those techniques demonstrated theoretical stress concentrations at the cervical areas of teeth on application of a mostly static load. Some clinicians and authors have proposed that tensile and compressive stresses play a primary role in causing enamel and dentin fracture—mainly creating wedge-shaped cervical lesions—while abrasion and erosion play a secondary role. Those early stress studies analyzed the tooth by itself, or just the crown and a portion of the root. More recent investigations, however, have considered the role of the periodontal ligament and alveolar bone and emphasized the effect they have on stress distribution and data analysis. These studies have exposed some limitations of previous studies and have provided additional data that may cast reservations on the fundamental basis of abfraction.

Although some clinical studies have associated occlusion with noncarious cervical lesions or cervical restoration failure, it should be emphasized that noncarious cervical lesions may occur as part of a multifactorial event whose mechanism is not elucidated completely yet. Moreover, the association of occlusal loading factors and noncarious cervical lesions may not necessarily support a causal relationship. Therefore, there is little direct evidence supporting abfraction as the primary factor in causing noncarious cervical lesions, but there is some evidence to show otherwise. Additional research is needed to assess more definitively the mechanism through which noncarious cervical lesions are initiated and propagated, as well as the potential role of abfraction in noncarious cervical lesions and restorations. Ideally, such investigations would include intervention studies with occlusal therapy to show that eliminating occlusal loading factors prevents formation or progression of cervical lesions or loss of restorative material.



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  		Dr. Litonjua was a periodontics resident, Department of Periodontics and Endodontics, State University of New York at Buffalo, when this article was written. He now is a clinical research assistant, Department of Periodontics and Endodontics, State University of New York at Buffalo, 250 Squire Hall, 3435 Main St., Buffalo, N.Y. 14214-3008, e-mail "laldmd{at}yahoo.com". Address reprint requests to Dr. Litonjua.

 


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  		Dr. Andreana is a clinical assistant professor, Department of Periodontics and Endodontics, State University of New York at Buffalo, and is manager, Applied Testing Center, Ivoclar Vivadent, Amherst, N.Y.

 


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  		Mr. Bush is the director, South Campus Instrumentation Center, State University of New York at Buffalo.

 


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  		Dr. Cohen is a professor and the director, Postgraduate Periodontics, Department of Periodontics and Endodontics, State University of New York at Buffalo.

 


   FOOTNOTES
 

Dr. Tobias is a clinical instructor, Department of Restorative Dentistry, State University of New York at Buffalo.


The authors thank Dr. Norman D. Mohl for his comments and suggestions for this article and to Ms. Noreen M. Fitzpatrick for the artwork.


   REFERENCES
TOP
 ABSTRACT
 DEFINITION AND CONCEPTS IN...
 EVIDENCE IN SUPPORT OF...
 THE RESTORATIVE CHALLENGE
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  1. American Academy of Periodontology. Glossary of periodontal terms. 4th ed. Chicago: American Academy of Periodontology; 2001:1.

  2. Graf H, Grassl H, Aeberhard H-J. A method of measurement of occlusal forces in three directions. Helv Odont Acta 1974;18:7–11.

  3. Brunski JB. Biomechanics of oral implants: future research directions. J Dent Educ 1988;52:775–87.[Abstract]

  4. Haraldson T, Carlsson GE, Ingervall B. Functional state, bite force and postural muscle activity in patients with osseointegrated oral implant bridges. Acta Odontol Scand 1979;37:195–206.[Medline]

  5. Proffit WR, Fields HW, Nixon WL. Occlusal forces in normal- and long-face adults. J Dent Res 1983;62:566–70.[Abstract/Free Full Text]

  6. Linderholm H, Wennström A. Isometric bite force and its relation to general muscle force and body build. Acta Odontol Scand 1970; 28:679–89.[Medline]

  7. Gibbs CH, Mahan PE, Lundeen HC, Brehnan K, Walsh EK, Holbrook WB. Occlusal forces during chewing and swallowing as measured by sound transmission. J Prosthet Dent 1981;46:443–9.[Medline]

  8. Gibbs CH, Mahan PE, Mauderli A, Lundeen HC, Walsh EK. Limits of human bite strength. J Prosthet Dent 1986;56:226–9.[Medline]

  9. Graf H, Zander HA. Tooth contact patterns in mastication. J Prosthet Dent 1963;13:1055–66.

  10. Garner LD, Kotwal NS. Correlation study of incisive biting forces with age, sex, and anterior occlusion. J Dent Res 1973;52:698–702.[Abstract/Free Full Text]

  11. Craig RG, Peyton FA, Johnson DW. Compressive properties of enamel, dental cements, and gold. J Dent Res 1961;40:936–45.[Free Full Text]

  12. Peyton FA, Mahler DB, Hershenov B. Physical properties of dentin. J Dent Res 1952;31:366–70.[Free Full Text]

  13. Craig RG, Peyton FA. Elastic and mechanical properties of human dentin. J Dent Res 1958;37:710–8.[Free Full Text]

  14. Bowen RL, Rodriquez MS. Tensile strength and modulus of elasticity of tooth structure and several restorative materials. JADA 1962;64:378–87.[Medline]

  15. Lehman ML. Tensile strength of human dentin. J Dent Res 1967;46:197–201.[Free Full Text]

  16. Sano H, Ciucchi B, Matthews WG, Pashley DH. Tensile properties of mineralized and demineralized human and bovine dentin. J Dent Res 1994;73:1205–11.[Abstract/Free Full Text]

  17. Carvalho RM, Santiago SL, Fernandes CA, Suh BI, Pashley DH. Effects of prism orientation on tensile strength of enamel. J Adhes Dent 2000;2:251–7.[Medline]

  18. Lertchirakarn V, Palamara JE, Messer HH. Anisotropy of tensile strength of root dentin. J Dent Res 2001;80:453–6.[Abstract/Free Full Text]

  19. Rasmussen ST, Patchin RE, Scott DB, Heuer AH. Fracture properties of human enamel and dentin. J Dent Res 1976;55:154–64.[Abstract/Free Full Text]

  20. Spears IR, van Noort R, Crompton RH, Cardew GE, Howard IC. The effects of enamel anisotropy on the distribution of stress in a tooth. J Dent Res 1993;72:1526–31.[Abstract/Free Full Text]

  21. Powers JM, Craig RG, Ludema KC. Frictional behavior and surface failure of human enamel. J Dent Res 1973;52:1327–31.[Abstract/Free Full Text]

  22. Neumann HH, DiSalvo NA. Compression of teeth under the load of chewing. J Dent Res 1957;36:286–90.[Free Full Text]

  23. McCoy G. The etiology of gingival erosion. J Oral Implantol 1982;10:361–2.[Medline]

  24. McCoy G. On the longevity of teeth. J Oral Implantol 1983; 11:248–67.[Medline]

  25. Hood JA. Experimental studies on tooth deformation: stress distribution in Class V restorations. N Z Dent J 1972;68:116–31.[Medline]

  26. Selna LG, Shillingburg HT, Kerr PA. Finite element analysis of dental structures: axisymmetric and plane stress idealizations. J Biomed Mater Res 1975;9:237–52.[Medline]

  27. Yettram AL, Wright KW, Pickard HM. Finite element stress analysis of the crowns of normal and restored teeth. J Dent Res 1976; 55:1004–11.[Abstract/Free Full Text]

  28. Lee WC, Eakle WS. Possible role of tensile stress in the etiology of cervical erosive lesions of teeth. J Prosthet Dent 1984;52:374–80.[Medline]

  29. Grippo JO. Abfractions: a new classification of hard tissue lesions of teeth. J Esthet Dent 1991;3:14–9.[Medline]

  30. Grippo JO. Noncarious cervical lesions: the decision to ignore or restore. J Esthet Dent 1992;4(supplement):55–64.[Medline]

  31. Palamara D, Palamara JE, Tyas MJ, Messer HH. Strain patterns in cervical enamel of teeth subjected to occlusal loading. Dent Mater 2000;16:412–9.[Medline]

  32. Rees JS. The role of cuspal flexure in the development of abfraction lesions: a finite element study. Eur J Oral Sci 1998;106:1028–32.[Medline]

  33. Goel VK, Khera SC, Ralston JL, Chang KH. Stresses at the dentinoenamel junction of human teeth: a finite element investigation. J Prosthet Dent 1991;66:451–9.[Medline]

  34. Takahashi N, Kitagami T, Komori T. Behaviour of teeth under various loading conditions with finite element method. J Oral Rehabil 1980;7:453–61.[Medline]

  35. Thresher RW, Saito GE. The stress analysis of human teeth. J Biomech 1973;6:443–9.[Medline]

  36. Atmaram GH, Mohammed H. Estimation of physiologic stresses with a natural tooth considering fibrous PDL structure. J Dent Res 1981;60:873–7.[Abstract/Free Full Text]

  37. Kuroe T, Itoh H, Caputo AA, Nakahara H. Potential for load-induced cervical stress concentration as a function of periodontal support. J Esthet Dent 1999;11:215–22.[Medline]

  38. Rees JS. An investigation into the importance of the periodontal ligament and alveolar bone as supporting structures in finite element studies. J Oral Rehabil 2001;28:425–32.[Medline]

  39. Korioth TW, Hannam AG. Deformation of the human mandible during simulated tooth clenching. J Dent Res 1994;73:56–66.[Abstract/Free Full Text]

  40. Meredith N, Setchell DJ, Swanson SA. The application of thermoelastic analysis to study stresses in human teeth. J Oral Rehabil 1997;24:813–22.[Medline]

  41. Morin DL, Douglas WH, Cross M, DeLong R. Biophysical stress analysis of restored teeth: experimental strain measurement. Dent Mater 1988;4:41–8.[Medline]

  42. Goel VK, Khera SC, Singh K. Clinical implications of the response of enamel and dentin to masticatory loads. J Prosthet Dent 1990; 64:446–54.[Medline]

  43. Gallien GS, Kaplan I, Owens BM. A review of noncarious dental cervical lesions. Compendium 1994;15:1366–74.[Medline]

  44. Lambert RL, Lindenmuth JS. Abfraction: a new name for an old entity. J Colo Dent Assoc 1994;72:31–3.[Medline]

  45. Levitch LC, Bader JD, Shugars DA, Heymann HO. Non-carious cervical lesions. J Dent 1994;22:195–207.[Medline]

  46. Owens BM, Gallien GS. Noncarious dental "abfraction" lesions in an aging population. Compend Contin Educ Dent 1995;16:552–62.[Medline]

  47. Spranger H. Investigation into the genesis of angular lesions at the cervical region of teeth. Quintessence Int 1995;26:149–54.[Medline]

  48. Lee WC, Eakle WS. Stress-induced cervical lesions: review of advances in the past 10 years. J Prosthet Dent 1996;75:487–94.[Medline]

  49. Osborne-Smith KL, Burke FJ, Wilson NH. The aetiology of the non-carious cervical lesion. Int Dent J 1999;49:139–43.[Medline]

  50. Grippo JO, Masi JV. Role of biodental engineering factors (BEF) in the etiology of root caries. J Esthet Dent 1991;3:71–6.[Medline]

  51. Grippo JO, Simring M. Dental ‘erosion’ revisited. JADA 1995; 126:619–30.[Abstract/Free Full Text]

  52. McCoy G. Dental compression syndrome: a new look at an old disease. J Oral Implantol 1999;25:35–49.[Medline]

  53. McCoy G. TMJ disorders and their relationship to occlusion and dental compression syndrome. Dent Today 1997;16:86.[Medline]

  54. McCoy G. Dysfunction of the human mastication system. Dent Today 1997;16:94–9.[Medline]

  55. McCoy G. Taking responsibility for occlusion. Dent Today 1996; 15:92–3.[Medline]

  56. Whitehead SA, Wilson NH, Watts DC. Development of noncarious cervical notch lesions in vitro. J Esthet Dent 1999;11:332–7.[Medline]

  57. Boston DW, al-bargi H, Bogert M. Abrasion, erosion, and abfraction combined with linear enamel hypoplasia: a case report. Quintessence Int 1999;30:683–7.[Medline]

  58. Pintado MR, Delong R, Ko CC, Sakaguchi RL, Douglas WH. Correlation of noncarious cervical lesion size and occlusal wear in a single adult over a 14-year time span. J Prosthet Dent 2000;84:436–43.[Medline]

  59. Braem M, Lambrechts P, Vanherle G. Stress-induced cervical lesions. J Prosthet Dent 1992;67:718–22.[Medline]

  60. Waerhaug J. Effect of toothbrushing on subgingival plaque formation. J Periodontol 1981;52:30–4.[Medline]

  61. Muller CJ, van Wyk CW. The amelo-cemental junction. J Dent Assoc S Afr 1984;39:799–803.[Medline]

  62. Schroeder HE, Scherle WF. Cemento-enamel junction: revisited. J Periodontal Res 1988;23:53–9.[Medline]

  63. Björn H, Lindhe J. Abrasion of dentine by toothbrush and dentifrice: a methodological study. Odontol Revy 1966;17:17–27.[Medline]

  64. Khan F, Young WG, Shahabi S, Daley TJ. Dental cervical lesions associated with occlusal erosion and attrition. Aust Dent J 1999; 44:176–86.[Medline]

  65. Young WG, Khan F. Sites of dental erosion are saliva-dependent. J Oral Rehabil 2002;29:35–43.[Medline]

  66. Piotrowski BT, Gillette WB, Hancock EB. Examining the prevalence and characteristics of abfractionlike cervical lesions in a population of U.S. veterans. JADA 2001;132:1694–701.[Abstract/Free Full Text]

  67. Mayhew RB, Jessee SA, Martin RE. Association of occlusal, periodontal, and dietary factors with the presence of non-carious cervical dental lesions. Am J Dent 1998;11:29–32.[Medline]

  68. Bader JD, McClure F, Scurria MS, Shugars DA, Heymann HO. Case-control study of non-carious cervical lesions. Community Dent Oral Epidemiol 1996;24:286–91.[Medline]

  69. Bader JD, Levitch LC, Shugars DA, Heymann HO, McClure F. How dentists classified and treated non-carious cervical lesions. JADA 1993;124:46–54.[Abstract]

  70. Lyttle HA, Sidhu N, Smyth B. A study of the classification and treatment of noncarious cervical lesions by general practitioners. J Prosthet Dent 1998;79:342–6.[Medline]

  71. Vandewalle KS, Vigil G. Guidelines for the restoration of class V lesions. Gen Dent 1997;45:254–60.[Medline]

  72. Lambrechts P, Braem M, Vanherle G. Buoncore memorial lecture: evaluation of clinical performance for posterior composite resins and dentin adhesives. Oper Dent 1987;12:53–78.[Medline]

  73. Douglas WH. Clinical status of dentine bonding agents. J Dent Res 1989;17:209–15.

  74. Neo J, Chew CL. Direct tooth-colored materials for noncarious lesions: a 3-year clinical report. Quintessence Int 1996;27:183–8.[Medline]

  75. Van Meerbeek B, Braem M, Lambrechts P, Vanherle G. Evaluation of two dentin adhesives in cervical lesions. J Prosthet Dent 1993;70:308–14.[Medline]

  76. Powell LV, Johnson GH, Gordon GE. Factors associated with clinical success of cervical abrasion/erosion restorations. Oper Dent 1995;20:7–13.[Medline]

  77. Heymann HO, Sturdevant JR, Bayne S, Wilder AD, Sluder TB, Brunson WD. Examining tooth flexure effects on cervical restorations: a two-year clinical study. JADA 1991;122:41–7.[Medline]

  78. Brackett WW, Gilpatrick RO, Browning WD, Gregory PN. Two-year clinical performance of a resin-modified glass-ionomer restorative material. Oper Dent 1999;24:9–13.[Medline]

  79. Hansen EK. Five-year study of cervical erosions restored with resin and dentin-bonding agent. Scand J Dent Res 1992;100:244–7.[Medline]

  80. Sidhu SK. A comparative analysis of techniques of restoring cervical lesions. Quintessence Int 1993;24:553–9.[Medline]

  81. van Dijken JW. Clinical evaluation of four dentin bonding agents in class V abrasion lesions: a four-year follow-up. Dent Mater 1994; 10:319–24.[Medline]

  82. Maneenut C, Tyas MJ. Clinical evaluation of resin-modified glass-ionomer restorative cements in cervical ‘abrasion’ lesions: one-year results. Quintessence Int 1995;26:739–43.[Medline]

  83. Neo J, Chew CL, Yap A, Sidhu S. Clinical evaluation of tooth-colored materials in cervical lesions. Am J Dent 1996;9:15–8.[Medline]

  84. Marshall GW, Chang YJ, Saeki K, Gansky SA, Marshall SJ. Citric acid etching of cervical sclerotic dentin lesions: an AFM study. J Biomed Mater Res 2000;49:338–44.[Medline]

  85. Duke ES, Lindemuth J. Variability of clinical dentin substrates. Am J Dent 1991;4:241–6.[Medline]

  86. Hörsted-Bindslev P, Knudsen J, Baelum V. 3-year clinical evaluation of modified Gluma adhesive systems in cervical abrasion/erosion lesions. Am J Dent 1996;9:22–6.[Medline]

  87. Heymann HO, Bayne SC. Current concepts in dentin bonding: focusing on dentinal adhesion factors. JADA 1993;124:26–36.[Abstract]

  88. Osborne-Smith KL, Burke FJ, McFarlane T, Wilson NH. Effect of restored and unrestored non-carious cervical lesions on the fracture resistance of previously restored maxillary premolar teeth. J Dent 1998;26:427–33.[Medline]

  89. King PA. Adhesive techniques. Br Dent J 1999;186:321–6.[Medline]

  90. Tyas MJ. The class V lesion: aetiology and restoration. Aust Dent J 1995;40:167–70.[Medline]

  91. Leinfelder KF. Restoration of abfracted lesions. Compendium 1994;15:1396–1400.[Medline]

  92. Coleman TA, Grippo JO, Kinderknecht KE. Cervical dentin hypersensitivity, part II: association with abfractive lesions. Quintessence Int 2000;31:466–73.[Medline]

  93. Tyas MJ, Burrow MF. Clinical evaluation of a resin-modified glass ionomer adhesive system: results at three years. Oper Dent 2001;26:17–20.[Medline]

  94. Brackett WW, Browning WD, Ross JA, Gregory PN, Owens BM. 1-year clinical evaluation of Compoglass and Fuji II LC in cervical erosion/abfraction lesions. Am J Dent 1999;12:119–22.[Medline]

  95. Gladys S, Van Meerbeek B, Lambrechts P, Vanherle G. Evaluation of esthetic parameters of resin-modified glass-ionomer materials and a polyacid-modified resin composite in class V cervical lesions. Quintessence Int 1999;30:607–14.[Medline]

  96. Burrow MF, Tyas MJ. 1-year clinical evaluation of one-step in non-carious cervical lesions. Am J Dent 1999;12:283–5.[Medline]

  97. Swift EJ Jr, Perdigão J, Heymann HO, et al. Eighteen-month clinical evaluation of a filled and unfilled dentin adhesive. J Dent 2001;29:1–6.[Medline]

  98. van Dijken JW. Clinical evaluation of three adhesive systems in class V non-carious lesions. Dent Mater 2000;16:285–91.[Medline]

  99. Toffenetti F, Vanini L, Tammaro S. Gingival recessions and non-carious cervical lesions: a soft and hard tissue challenge. J Esthet Dent 1998;10:208–20.[Medline]

  100. Cuenin M, Clem B. Periodontal and restorative treatment of the class V lesion. Gen Dent 1993;41:252–4.[Medline]




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