Indian Journal of Dental Research

: 2020  |  Volume : 31  |  Issue : 2  |  Page : 305--311

Abfraction: Etiopathogenesis, clinical aspect, and diagnostic-treatment modalities: A review

Anand N Badavannavar1, Sneha Ajari2, Krishna U S. Nayak3, Shahnawaz Khijmatgar4,  
1 Department of Orthodontics, KLE VK Institute of Dental Sciences, KLE Academy of Higher Education and Research, Belgaum, Karnataka, India
2 Department of Oral Pathology,KLE VK Institute of Dental Sciences, KLE Academy of Higher Education and Research Belgavi, Karnataka, India
3 A.B Shetty Memorial Institute of Dental Sciences, Nitte (Deemed to be University), Mangalore, Karnataka, India
4 Department of Oral Biology and Genomic Studies, A B Shetty Memorial Institute of Dental Sciences, Nitte (Deemed to be University), Mangalore, Karnataka, India

Correspondence Address:
Dr. Shahnawaz Khijmatgar
Department of Oral Biology and Genomic Studies, A B Shetty Memorial Institute of Dental Sciences, Nitte (Deemed to be University), Mangalore, Karnataka - 575 018


Background: Abfraction is a loss of tooth structure along the gingival margin and manifests with different clinical appearances. It has multifactorial etiology and may occur due to normal and abnormal tooth function and may also be accompanied by pathological wear, such as abrasion and erosion. The theory behind the abfraction is that the tooth flexure in the cervical area is caused due to occlusal compressive forces and tensile stresses. This results in the fractures in the hydroxyapatite (HA) crystals. It is also caused by the low packing density of the Hunter–Schreger band (HSB) at the cervical area. Unfortunately, there is a lack of evidence regarding the outcome of abfraction with or without intervention. The aim of this review is to collect clinical information from the literature and discuss the etiology, pathogenesis, clinical representation, and management. Also, search databases for clinical studies that describe the role of sclerotic dentine in non-carious cervical lesions (NCCLs) are becoming a clinical challenge. Methods: The literature was searched that described the etiology, pathogenesis, clinical representation, and management of the abfraction lesions. Also, a specific question regarding the formation of sclerotic dentin in the NCCL lesion was described and searched for evidence that challenges etching, bonding, and successfully restoring NCCLs. The databases PUBMED, SCOPUS, MEDLINE, WEB of SCIENCE, and EMBASE were searched using the key terms. The inclusion criteria were the randomized controlled clinical trial, cohort studies, and cross-sectional studies that aimed at determining the role of sclerotic dentine in NCCLs and its effect on etching, bonding. Results: One clinical study was retrieved according to the PRISMA flowchart and PICO format. The longer etching time, total-etch adhesive system, and EDTA pre-treatment of the sclerotic dentin of cervical wedge-shaped defects could improve the bonding strength in lesions like NCCL's. Conclusion: In conclusion, clinical challenges that occur due to NCCLs are better managed by a proper understanding of factors like etiopathogenesis, ultra-structure of enamel, and dentine and their effect on the bonding of restorations of the tooth.

How to cite this article:
Badavannavar AN, Ajari S, Nayak KU, Khijmatgar S. Abfraction: Etiopathogenesis, clinical aspect, and diagnostic-treatment modalities: A review.Indian J Dent Res 2020;31:305-311

How to cite this URL:
Badavannavar AN, Ajari S, Nayak KU, Khijmatgar S. Abfraction: Etiopathogenesis, clinical aspect, and diagnostic-treatment modalities: A review. Indian J Dent Res [serial online] 2020 [cited 2020 Jul 9 ];31:305-311
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Full Text


Abfraction, as defined by Grippo, is 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.[1] The term is derived from the Latin words 'ab,' or away, and 'fractio,' or breaking by J. O. Grippo.[2],[3],[4] It is also known as non-carious cervical lesion (NCCL), stress-induced cervical lesion and is usually observed on the buccal surface at the cement-enamel junction (CEJ) of teeth, with prevalence ranging from 27 to 85%.[5],[6] This tooth structure loss, being independent of the bacterial process, is routinely and commonly seen in dental clinical practice these days.[7],[8],[9] Resulting from excessive non-axial forces from the masticatory system, malpositioned teeth, and bruxism, this lesion causes flexure of teeth that leads to disruption of the prismatic structure at the site of least resistance, namely, the tooth cervix.[3] The concept of abfraction is completely theoretical and paucity of experimental evidence demands the proper understanding of its historical background, complex terminologies, and biomechanics involved which in turn reflects the diagnosis, treatment planning, and management of such cases for successful clinical practice. This concise review covers this entire above-mentioned concept from one vantage point.


The concept that occlusal loading could cause cervical stress and loss of cervical tooth structure began to evolve in the late 1970s.[10],[11],[12] This lead to the origin of NCCLs, when W.D. Miller in 1907, published a paper on experiments and observations on tooth wear variously designated as erosion, abrasion, chemical abrasion, denudation, etc., His studies reported that erosion was caused by weak acids or gritty tooth powders, or by both. In the early 1980s, McCoy[10],[11],[12],[13],[14] questioned the role of toothbrush abrasion in the etiology of what previously had been referred to as “cervical erosion.” Later the work by McCoy[10] and Lee and Eakle[11] proposed that bruxism produced lateral forces that may be the primary cause of angled notches at the CEJ. J. O. Grippo[3] in 1991 stated that static or cyclic forces created tooth loss at the cervical area and the term called abfraction evolved. He concluded that the flexure resulted in damage to the enamel rods at the CEJ resulting in their loosening and consequent flaking away of the tooth structure. Grippo finally suggested that abfraction is the basic cause of all NCCLs, whereas Lee and Eakle[11] proposed a multifactorial etiology, with a combination of occlusal stress, abrasion, and erosion. Spranger[15] supported the multifactorial etiology of the cervical lesions and 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.


The contradictory and complexity of terminologies for abfraction used to reflect that the exact etiology for abfraction remains obscure. Grippo (1992) defined abfraction as a pathological loss of tooth substance caused by biomechanical loading forces. This results in flexure and failure of enamel and dentin at a location away from the loading. He first used the term abfraction to refer to a process of cervical tooth structure loss, based on work completed by McCoy[10] and Lee and Eakle.[11] Miller et al.[13] stated that NCCLs are also called abfractions. However, this statement is inappropriate as NCCLs have a variety of possible etiologies, of which abfraction may be the primary one. It is also important to differentiate the term 'stress corrosion' from 'abfraction'. Stress corrosion refers to the synergistic effects of stress and corrosion acting simultaneously.[16] Recently, new terms have been introduced to describe tooth wear. Biodental engineering factors have defined it as the effect of piezoelectricity at the cervical area, and 'stress corrosion' has been used to describe a multifactorial physiochemical degradation of the CEJ area.[17],[18]

Theory of abfraction

The theory of abfraction is based primarily on the relationship between occlusal loading and stress concentration in the cervical region of tooth. Various research on this relationship concludes that teeth do flex in the cervical region under bruxing loads, but none seems to cite actual damage caused only by this loading alone but hypothesized that this deformation was occurring in combination with the abrasive or erosive component as well.[19] Hence, studies from various data have proposed a combination of occlusal stress, parafunction, abrasion, and erosion in the development of lesions, leading to a conclusion that the progression of abfraction may be multifactorial.[15],[20] Recent studies by T.C. Abrahamsen[21] have shown that toothpaste (not the toothbrush) is abrasive enough to cause this type of damage if the patient is too aggressive in brushing the teeth in a very hard and vigorous “sawing” motion. Abrahamson suggested that the term “toothbrush abrasion” be replaced with the term “toothpaste abuse”.[11],[21] His studies, using mechanical “tooth brushing” machines, concluded that the toothbrush alone does not cause this type of tooth damage, but the addition of toothpaste to the bristles does. Toothbrushes without toothpaste do cause soft tissue damage and indeed, overly vigorous tooth brushing without toothpaste leads to gingival recession.[21] Grippo suggested the tooth flexure theory: the presence of class V non-carious lesions in some teeth but adjacent teeth (not subjected to lateral forces) are unaffected; the lesions progress around restorations that remain intact and under the margins of complete crowns, the lesions are rarely seen on the lingual aspect of mandibular teeth.[1] All these studies being theoretical, lack experimental evidences and thus the theory of abfraction is not yet proven. There were few conflicting evidence against the theory of abfraction: in case of abfraction, the most commonly damaged surface is the buccal surface of the tooth, while the lingual surface is less affected. If flexure of the teeth is responsible, there would be equal damage to both buccal and lingual surfaces. Also, there was a lack of evidence of these lesions in prehistoric skulls. These lesions later became evident in the 16th century in historic skulls after the invention of tooth powders and toothbrushes. Not all persons with the lesions demonstrate occlusal wear (indicating bruxing habit), and not all persons with severe occlusal wear exhibit NCCLs.

To conclude, the concept of abfraction being theoretical should further raise opportunities for research in this area to impart the proper understanding of its exact etiology and thus prevention of such lesions occurring on tooth structure.


The etiopathogenesis of abfraction is quite convoluted, and various researchers have worked on the same to conclude its exact etiology. Lee and Eakle in 1984 have postulated that abfraction has a multifactorial etiology, with a combination of occlusal stress, abrasion, and erosion. This occlusal stress can be tensile stress (occurring along the horizontal axis) or compressive stress (occurring along the long axis of the tooth). In normal occlusion, these stresses are directed towards the apical area of the tooth. But, in the case of occlusal interferences, premature contacts, bruxism, clenching, and malocclusions that act as stressors, these stresses are directed in the lateral direction towards the CEJ. The alternating tensile and compressive stress (cyclic nonaxial) causes tooth cusp flexure resulting in the concentration of stress at CEJ and separation of hydroxyapatite bonds in enamel causing fracture and breakdown of tooth structure.[11],[22],[23] It has also been suggested that when the tooth is subjected to tensile and compressive stress, the electric potential gradient formed also leads to loss of tooth structure.[24] Gibbs et al. found that when a tooth is hyperoccluded, the masticatory forces transmitted to this tooth are only approximately 40 percent of maximal bite force.[25] Suit et al. inferred that tooth contact occurs on average for only 194 milliseconds during mastication and 683 milliseconds during swallowing. The lateral damaging forces thus produce compressive stress on the side towards which the tooth bends and tensile stress on the other side. These stresses create micro-fractures in the enamel or dentine at the cervical region.[26] Mc Coy postulated that alternating tensile and compressive stresses cause weakening of enamel and dentin and when this cyclic tension and compression reach a fatigue limit; there occurs cracking and breakdown of tooth structure. The tensile stresses created at CEJ pull apart enamel prisms and increases susceptibility to chemical erosion.[10] Based on the structure, the enamel is weak in tension, and thus the tensile forces may disrupt hydroxyapatite (HA) crystals, allowing water and other small molecules to penetrate between the prisms and prevent reestablishment of interprismatic bonds on the release of the stress.[27] This process renders these HA crystals more susceptible to chemical and mechanical destruction and thus results in abfraction. Ultimately, the enamel breaks away at the cervical margin and exposes the dentin, in which the process continues.[5]

Clinical features

Abfraction lesions, primarily at the cervical region of the dentition, are typically wedge-shaped, with sharp internal and external line angles.[5] This being a theoretical phenomenon, the size, shape, and location of these lesions are dictated by the direction, magnitude, frequency, duration, and location of forces that arise when teeth come in contact.[28] Lee and Eakle first described the characteristics of the lesions resulting from tensile stresses. They concluded that an abfraction lesion should be located at or near the fulcrum in the region of greatest tensile stress concentration, be wedge-shaped, and display a size proportional to the magnitude and frequency of tensile force application.[11] They proposed that the direction of the lateral forces acting on a tooth determines the location of the lesion.

The most common tooth to be involved are anterior and premolar teeth because of a smaller size of the teeth and are more frequently found on the buccal or lingual surfaces due to the direction of occlusal or incisal loads, the angling and asymmetry of the tooth buccal-lingual plane, and its relationship with the supporting alveolar bone.[28],[29],[30] Amongst the premolars, the mandibular premolars have the highest risk for developing these defects, followed by the maxillary premolars. The reason behind this being the anatomical location of the furcation adjacent to the cervical region marked grooves on root and crown, as well as cervical constriction of the crown and low crown volume makes premolars more susceptible to abfraction.[31],[32],[33]


Careful and complete anamnesis is crucial to establishing the diagnosis of abfraction. Evaluation of any systemic pathologies such as gastroesophageal reflux disease, eating disorders, dietary habits, and parafunctional habits play a role in diagnosis. As abfraction is multifactorial, evaluation of all contributing factors should be done to differentiate abfraction from other NCCLs. The pointing clue towards diagnosis was characteristic wedge-shaped lesions and associated contributing factors such as erosion, abrasion, etc., Sometimes the clinical manifestations of these lesions may alter from the characteristic wedge-shaped to more saucer-shaped with blunt angles and broader outlines when exposed to these contributing factors. Additional hallmark feature for diagnosis is that these lesions may appear deeper than wider depending upon the stage of progression and related etiological factors. Tooth Wear Index proposed by Smith and Knight is the most accepted index to categorize tooth wear in the cervical region and it is as follows: The classifications on this index are as follows:

0 = no change in contour;

1 = minimal loss of contour;

2 = defect <1 mm deep;

3 = defect 1 mm to 2 mm deep;

4 = defect >2 mm deep, or pulp exposure, or exposure of secondary dentin.


The most important criterion for restoration is that of retention. Clinical studies have shown that restorations of abfraction lesions have a higher percentage of failure in the cervical area due to popping out effect caused by parafunctional habits. As these lesions implicate enamel and dentine margins, they represent a challenge to the dental profession.[34] When abfraction lesion is less than 1 mm in depth 22, only monitoring at regular intervals is enough. Restoring these lesions improves the maintenance of oral hygiene of the patient. It also helps in decreasing thermal sensitivity, improving esthetics, and strengthening the teeth.

Along with restoration, a variety of treatment strategies have also been proposed like occlusal adjustments, occlusal splints, elimination of parafunctional habits, altering toothbrushing techniques, etc.[1],[35],[36] For restoring abfractions, various materials have been tried to date. These include glass-ionomer cement (GICs), resin-modified GICs (RMGICs), polyacid-modified resin-based composites (compomers), composite resins and a combination of the techniques.[37],[38],[39] Tyas et al. said that RMGIC should be the first preference. RMGIC/GIC liner or base with resin composite should be used wherever aesthetics is concerned.[40] Two different techniques either etch-and-rinse technique or self-etch technique have been employed for restoring these lesions. The main reason for the failure of restoration is difficulty in gaining and maintaining a good seal between the restoration and tooth at the margin. The retention rate for restorations with a lower elastic modulus may be significantly better than a material with a higher elastic modulus.[41] Heymann et al. reported the association of occlusion, tooth location, patient's age with loss of retention while others blame technique, marginal shrinkage, properties of bonding agent, and inadequate adhesive resin thickness for the retention loss.[42],[43],[44],[45],[46],[47]

Sclerotic dentin is a form of dentin that causes apatite crystals and collagen fibers to appear in dentinal tubules due to external stimuli. It occurs as a result of a protective mechanism in teeth, mainly in older individuals and is found in the apical third of the roots.[48],[49] The formed dentin as a result of stimuli like attrition, abrasion, and erosion becomes harder than normal dentin. It has more mineral density.[48],[49] Restoration of these lesions with the dental materials is a challenging task. In restorations like where bonding is required, the material should be able to bond to sclerotic dentin. The bonding varies in the region of normal dentin and that compared to sclerotic dentin. Sclerotic hyper-mineralized dentine contains a low protein and lack in the sponge-like organic matrix that is needed for resin interdiffusion network. A lightly stoned fine diamond instrument should be used to achieve bonding in sclerotic dentin. The smear layer thus produced consists essentially of a gelatinous surface layer of coagulated protein, 0.5 to 1.5 microns in thickness, which is thought to enhance the efficacy of the dentin bond by creating a 'high energy' surface layer relatively free of dentinal fluid contamination.[50] Regional tensile bond strength showed that the overall bond strength to natural sclerotic dentin is about 20% lower than sound cervical dentin.[51]

Evidence for challenges in etching, bonding, and successfully restoring NCCL lesions

Four possible factors that might influence the overall decrease in bond strength in natural cervical sclerotic lesions are: a) weakening of the bonds that occur due to the presence of a hybridized intermicrobial matrix and along with entrapped bacteria; b) Quality of self-etching primer to etch through a thick hypermineralized surface layer; c) presence of a layer of possibly re-mineralized, denatured collagen at the base of the hypermineralized surface layer; and d) retention of acid-resistant sclerotic casts that obliterate the tubular lumina and prevent effective resin tag formation.[51] To increase the bonding to the sclerotic dentin, removal of surface layers of sclerotic dentin or conditioning with stronger acids is recommended in NCCLs.[52] However, there is high heterogeneity in the studies that have been published, and therefore need additional clinical trials to determine the best dentin treatment option in NCCLs.[53] Studies by Karan K (2012), Liu KL (2016), and Li TT (2015) concluded that longer etching time, total-etch adhesive system, and EDTA pre-treatment of the sclerotic dentin of cervical wedge-shaped defects could improve the bonding strength in lesions like NCCLs.[54],[55],[56] J.W.V. Van Dijken (2000) used N = 148 class V restorations in N = 60 patients of NCCLs and restored with EBS/Pertac Hybrid, Prisma TPH, and GIC Fuji II LC materials. The authors found that N = 30 restorations (21.1%) were lost during follow-up and the restorations placed in sclerotic lesions were lost in 32.4%.[57] Another study by same author J.W.V. Van Dijken (2013) found that after 5 years of follow-up, 2-hydroxyethyl methacrylate (HEMA) free adhesives performed good and were durable and only 22 restorations were failed due to retention. All restorations performed better in NCCLs.[58] The reason for this finding may be due to the hydrolytic property of HEMA material. In the study by Burrow and Tyas (2012),[59] 11 subjects were enrolled and 60 NCCLs were restored. The study aimed to determine the retention ability of the restorations in NCCLs using all-in-one adhesive systems. The authors found 98% survival rates after a follow-up of 3 years.[59] Esra Can Say (2014) found that clinical performance of self-etch adhesive with or without selective acid etching enamel margins was acceptable.[60] The studies by Ritter AV (2008) and Van landuyt KL (2014)[61],[62] showed the opposite results as findings do not support that NCCLs affect the adhesive capacity of the materials [Table 1], [Figure 1].[61],[62]{Table 1}{Figure 1}

 Level of Evidence

Although, there are seven clinical studies that demonstrated the effect of retension, adhesion and restoration in NCCLs that contribute to a high level of evidence but due to the quality of studies (level of bias) and heterogeneity among published studies it is not possible to have meta-analysis. It becomes elusive to conclude the effectiveness of adhesive materials in NCCL's. Therefore, the level of evidence is low.


To conclude, proper understating of the etiopathogenesis and careful evaluation can help in successful diagnosis and effective treatment planning of such lesions. Further clinical studies are needed to determine the best possible solution to manage sclerotic dentin in NCCL's.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Grippo JO. Noncarious cervical lesion the decision to ignore or restore. J Esthet Dent 1992;4(Suppl):55-64.
2Braem M, Lambrechts P, Vanherle G. Stress-induced cervical lesions. J Prosthet Dent ;67:718-22.
3Grippo JO. Abfractions: A new classification of hard tissue lesions of teeth. J Esthet Dent 1991;3:14-9.
4Litonjua LA, Andreana S, Bush PJ, Tobias TS, Cohen RE. Non carious cervical lesions and abfractions: A re-evalution. J Am Dent Assoc 2003;134:845-50.
5Barttlet DW, Shah P. A critical review of non-carious cervical (wear) lesions and the role of abfraction, erosion, and abrasion. J Dent Res 2006;85:306-12.
6Levitch LC, Bader JD, Shugars DA, Heymann HO. Non-carious cervical lesions. J Dent 1994;22:195-207.
7Borcic J, Anic I, Urek MM, Ferreri S. The prevalence of non-carious cervical lesions in permanent dentition. J Oral Rehabil 2004;31:117-23.
8Reyes E, Hildebolt C, Langenwalter E, Miley D. Abfractions and attachment loss in teeth with premature contacts in centric relation: Clinical observations. J Periodontol 2009;80:1955-62.
9Rees JS. The effect of variation in occlusal loading on the development of abfraction lesions: A finite element study. J Oral Rehabil 2002;29:188-93.
10McCoy G. The etiology of gingival erosion. J Oral Implantol 1982;10:361-2.
11Lee WC, Eakle WS. Possible role of tensile stress in the etiology of cervical erosive lesions of teeth. J Prosthet Dent 1984;52:374-80.
12Brady JM, Woody RD. Scanning microscopy of cervical erosion. J Am Dent Assoc 1977;94:726-9.
13Miller N, Penaud J, Ambrosini P, Bisson-Boutelliez C, Briancon S. Analysis of etiologic factors and periodontal conditions involved with 309 abfractions. J Clin Periodontol 2003;30:828-32.
14McCoy G. On the longevity of teeth. J Oral Implantol 1983;11:248-67.
15Spranger H. Investigation into the genesis of angular lesions at the cervical region of teeth [review]. Quintessence Int 1995;26:149-54.
16Grippo JO, Simring M. Dental 'erosion' revisited. J Am Dent Assoc 1995;126:619-20.
17Grippo JO, Masi JV. Role of biodental engineering factors (BEF) in the etiology of root caries. J Esthet Dent 1991;3:71-6.
18Grippo JO, Masi JV. The role of stress corrison and piezoelectricity in the formation of root caries. 13th bioengineering conference, University of Pennsylyania, Philadelphia, PA. Foster RR, ed 1987;vol 1:93-5.
19mhtml: file//F/abfraction pub -theory ofabfraction.
20Lee WC, Eakle WS. Stress-induced cervical lesions: Review of advances in the past 10 years. J Prosthet Dent 75:487-94.
21Abrahamsen TC. The worn dentition – Pathognomonic patterns of abrasion and erosion. Int Dent J 2005;55:268-76.
22Grippo JO, Simring M, Schreiner S. Attrition, abrasion, corrosion and abfraction revisited: A new perspective on tooth surface lesions. J Am Dent Assoc 2004;135:1109-18.
23Rees JS. A Review of biomechanics of abfraction. Eur J Prosthodont Restor Dent 2000;8:139-44.
24Marino AA, Gross BD. Piezoelectricity in cementum, dentine and bone. Arch Oral Biol 1989;34:507-9.
25Gibbs 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.
26Suit SR, Gibbs CH, Benz ST. Study of gliding contacts during mastication. J Periodontology 1976;47:331-4.
27Powers JM, Craig RG, Ludema KC. Frictional behavior and surface failure of human enamel. J Dent Res 1973;52:1327-31.
28Piotrowski BT, Gillette WB, Hancock EB. Examining the prevalence and characteristics of abfraction like cervical lesions in a population of US veterans. J Am Dent Assoc 2001;132:1694-701.
29Khan F, Young WG, Shahabi S, Daley TJ. Dental cervical lesions associated with occlusal erosion and attrition. Aust Dent J 1999;44:176-86.
30Borcic J, Anic I, Smojver I, Catic A, Miletic I, Ribaric PS. 3D finite element model and cervical lesion formation in normal occlusion and in malocclusion. J Oral Rehabil 2005;32:504-10.
31Soares PV, Souza LV, Veríssimo C, Zeola LF, Pereira AG, Santos-Filho PC, et al. Effect of root morphology on biomechanical behaviour of premolars associated with abfraction lesions and different loading types. J Oral Rehabil 2014;41:108-14.
32Benazzi S, Grosse IR, Gruppioni G, Weber GW, Kullmer O. Comparison of occlusal loading conditions in a lower second premolar using three-dimensional finite element analysis. Clin Oral Investig 2014;18:369-75.
33Katranji A, Misch K, Wang H. Cortical bone thickness in dentate and edentulous human cadavers. J Periodontol 2007;78:874-8.
34Brackett MG, Dib A, Bracket WW, Estrada BE, Reyes AA. One year clinical performance of a resin modified glass inomoer and a resin composite restorative material in unprepared class V restorations. Oper Dent 2002;27:112-6.
35Lyttle 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.
36Michael JA, Townsend GC, Greenwood LF, Kaidonis JA. Abfraction: separating fact from fiction, Aust Dent J 2009;54:2-8.
37Fruits TJ, Van Brunt CL, Khajotia SS, Duncanson MG Jr. Effect of cyclical lateral forces on microleakage in cervical resin composite restorations. Quintessence Int 2002;33:205-12.
38Li Q, Jepsen S, Albers HK, Eberhard J. Flowable materials as an intermediate layer could improve the marginal and internal adaptation of composite restorations in Class-V-cavities. Dent Mater 2006;22:250-7.
39Peaumans M, De Munck J, Landuyt V, Kanumilli P, Yoshida Y, Inoue S, et al. Restoring cervical lesions with flexible composites. Dent Mater 2007;23:749-54.
40Tay FR, Gwinnett AJ, Pang KM, Wei SH. Structural evidence of a sealed tissue interface with a total etch wet bonding technique in vivo. J Dent Res 1994;73:629-36.
41Van Meerbeek BV, De Munck J, Yoshida Y, Inoue S, Vargas M, Vijay P, et al. Buonocore memorial lecture. Adhesion to enamel and dentin: Current status and future challenges. Oper Dent 2003;28:215-35.
42Brackett 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.
43Hansen EK. Five-year study of cervical erosions restored with resin and dentin-bonding agent. Scand J Dent Res 1992;100:244-7.
44Sidhu SK. A comparative analysis of techniques of restoring cervical lesions. Quintessence Int 1993;24:553-9.
45Van Dijken JW. Clinical evaluation of four dentin bonding agentsin class V abrasion lesions: A four-year follow-up. Dent Mater 1994;10:319-24.
46Maneenut C, Tyas MJ. Clinical evaluation of resin-modified glassionomer restorative cements in cervical 'abrasion' lesions: One-year results. Quintessence Int 1995;26:739-43.
47Neo J, Chew CL, Yap A, Sidhu S. Clinical evaluation of toothcolored materials in cervical lesions. Am J Dent 1996;9:15-8.
48Berkovitz BK, Moxham BJ, Linden RW, Sloan AJ. Master Dentistry Volume 3 Oral Biology E-Book: Oral Anatomy, Histology, Physiology and Biochemistry. Elsevier HealthSciences; 2010.
49Kumar GS. Orban's Oral Histology and Embryology. Elsevier Health Sciences; 2014.
50Olgart L, Brännström M, Johnson G. Invasion of bacteria into dentinal tubules. Experiments in vivo and in vitro. Acta Odontol Scand 1974;32:61-70.
51Tay FR, Kwong SM, Itthagarun A, King NM, Yip HK, Moulding KM, et al. Bonding of a self-etching primer to non-carious cervical sclerotic dentin: Interfacial ultrastructure and microtensile bond strength evaluation. J Adhes Dent 2000;2:9-28.
52Kwong SM, Cheung GS, Kei LH, Itthagarun A, Smales RJ, Tay FR, Pashley DH. Micro-tensile bond strengths to sclerotic dentin using a self-etching and a total-etching technique. Dent Mater 2002;18:359-69.
53Rocha AC, Da Rosa WL, Cocco AR, Da Silva AF, Piva E, Lund RG. Influence of surface treatment on composite adhesion in non-carious cervical lesions: Systematic review and meta-analysis. Oper Dent 2018;43:508-19.
54Karan K, Yao X, Xu C, Wang Y. Chemical characterization of etched dentin in non-carious cervical lesions. J Adhes Dent 2012;14:315-22.
55Liu KL, Zhang XF, Wei X. Influence of different acid etching modes on bond strengths to non-carious sclerotic dentin. Shanghai Kou Qiang Yi Xue 2016;25:38-41.
56Li TT, Sun MM, Kang JT, Sun Z. Clinical research of EDTA pre-treatment on the bonding strength of resin. Shanghai Kou Qiang Yi Xue 2015;24:594-7.
57Van Dijken JW. Clinical evaluation of three adhesive systems in class V non-carious lesions. Dent Mater 2000;16:285-91.
58van Dijken JW. A randomized controlled 5-year prospective study of two HEMA-free adhesives, a 1-step self-etching and a 3-step etch-and-rinse, in non-carious cervical lesions. Dent Mater 2013;29:e271-80.
59Burrow MF, Tyas MJ. Comparison of two all-in-one adhesives bonded to non-carious cervical lesions—results at 3 years. Clin Oral Investig 2012;16:1089-94.
60Say EC, Yurdaguven H, Ozel E, Soyman M. A randomized five-year clinical study of a two-step self-etch adhesive with or without selective enamel etching. Dent Mater J 2014;33:757-63.
61Ritter AV, Heymann HO, Swift EJ Jr, Sturdevant JR, Wilder AD Jr. Clinical evaluation of an all-in-one adhesive in non carious cervical lesions with different degrees of dentin sclerosis. Oper Dent 2008;33:370-8.
62Van Landuyt KL, De Munck J, Ermis RB, Peumans M, Van Meerbeek B. Five-year clinical performance of a HEMA-free one-step self-etch adhesive in noncarious cervical lesions. Clin Oral Investig 2014;18:1045-52.