You must be signed in to read the rest of this article.
Registration on CDEWorld is free. Sign up today!
Forgot your password? Click Here!
The loss of dental tissue in the cervical region of the tooth is an increasingly common finding in clinical practice, with prevalence rates of up to 85% in some populations.1-4 Despite noncarious cervical lesions (NCCLs) affecting a majority of the populations and requiring dentists to regularly contend with this common pathology in patients, there remains disagreement over the mechanisms and factors involved in the etiology and progression of these lesions.5-11 Moreover, concern exists regarding the durability of restorative materials and successful control and treatment of this pathology.12-14
Prior to the concepts of modern dentistry, which have embraced theory and clinical guidelines based on scientific evidence, the etiology of the loss of enamel and dentin located near the cementoenamel junction (CEJ) was focused solely on friction caused by excessive toothbrush/dentifrice abrasion on teeth.15,16Some clinicians attributed NCCLs exclusively to the degradation of tooth structure as a result of acids derived from exogenous and endogenous sources.17,18
Zsigmondy in 1894 first described NCCLs as "keilformige defekte" (wedge-shaped lesions),19 and in 1932 Kornfeld referred to these lesions as "cervical erosions."20The term "noncarious cervical lesion" seems to have first appeared in Shore's book, Temporomandibular Joint Dysfunction and Occlusal Equilibration, published in 1976.21As for thesignificance of stress in theetiology of NCCLs, Korber in 1962 described and computed the elastic deformation of teeth.22 He stated that horizontal forces applied to teeth give rise to flexion-causing tension and compression in the cervical region. Lukas and Spranger investigated horizontal loading of teeth during lateral movements of the mandible and, like Korber, found that both torsion and translation (twisting and straight-line movement) occurred at the cervical area.23 Brady and Woody did an exhaustive electron microscopic investigation of NCCLs.24 McCoy in 1982 and shortly thereafter Lee and Eakle were the first Americans to publish and lecture on the significance of stress occurring in the cervical area.25,26
In 1991, Grippo coined the term "abfraction," which designated the loss of tooth substance in areas of stress concentration promoted by dental flexure.27 Abfraction in the formation of NCCLs is due to the stresses resulting from biomechanical loading forces exerted on teeth (static, as in deglutition and clenching, or cyclic, as in mastication or parafunction) that can cause enamel, dentin, and cementum to break away.6,8,26,27 The use of the term "abfraction" to describe the manifestations of stress in areas of stress concentration prompted the publishing of numerous articles that created contention by refuting the role of stress in the etiology of NCCLs.6,10,11,27
While the origin and development of NCCLs has been vigorously debated, it appears these anomalies are related to three distinct and fundamental etiological mechanisms, namely stress, biocorrosion, and friction (Figure 1),10,28,29 which are defined as follows:
• Stress-manifests as abfraction caused by stress-strain concentration from pathologic occlusion and parafunction
• Biocorrosion-the chemical, biochemical, and electrochemical degradation of tooth substance caused by endogenous and exogenous acids, proteolytic agents, and piezoelectric effects on dentin
• Friction-tooth substance wear caused by toothbrush/dentifrice abrasion
Thus, this article aims to contribute to the theoretical knowledge base of the etiology of the stress-strain mechanism, explaining how this process influences the origin and development of NCCLs. It will also discuss the significance of stress acting in concert with biocorrosion and friction as cofactors in the etiology of NCCLs.
The Abfraction Concept and Development of the Term
As mentioned, abfraction is the pathologic loss of tooth tissue microstructure in areas of stress concentration caused by eccentric occlusal loading forces. A subset designation of NCCLs, these lesions occur mostly at the CEJ, wherein flexure can lead to a disruption of the extremely thin layer of enamel prisms and cause microfracture of the cementum and dentin.6,8,9 NCCLs are related to the direction, magnitude, frequency, duration, and location of the occlusal load resulting in varying shapes of lesions in the cervical region.8 Abfractive lesions have been said to be due to flexure and ultimate fatigue of enamel and dentin at a location away from the point of loading when supportive alveolar bone exists.27
American scholars have shown an interest in this pathology since the 1970s and 1980s.24-29According to Grippo's aforementioned 1991 publication, abfraction occurs when excessive non-axial or eccentric occlusal forces are applied to teeth, promoting cusp flexion and resultant stress concentration in the cervical area, which causes ultimate material fatigue to susceptible teeth at locations away from the point of loading.27 In addition to their varying shapes,27 a common feature of many abfractive lesions is the morphology of wedge-shaped lesions that have well-defined, angled flat walls and can also occur in the subgingival region.8,28,30-32
The occlusal forces of 66.5 pounds (30 kg) during swallowing and 58.7 pounds (27 kg) during chewing represent averages of only 41% and 36%, respectively, of the average maximum biting strength of 162 pounds (73 kg).33 Furthermore, the length of time in which the teeth remain in contact during intercuspation is only about 194 milliseconds during chewing and a surprisingly much higher 683 milliseconds during swallowing.34 It is thought that magnitudes of forces during bruxism are much higher than those loads found during normal functional activity.35 Thus, one may presume that occlusal parafunction is more prone to promote tooth substance loss in the cervical region than physiological processes.6,28 Waugh reported Eskimos have above-average bite strength and recorded one individual having a bite strength of 348 pounds (158 kg).36
Dentin has varying micro- and macrostructure and can support major stress concentration more so than enamel. This assertion was a main point of criticism represented in the abfraction concept.37 Neither Michael et al31 nor other critical authors ever considered that abfractions commonly occur when a biocorrodent is working synergistically with effects from stress.9,38-43
Frictional effects from toothbrushing and dentifrice use have been proposed as contributory to NCCL development and/or maturation. The present author could not find any in vivostudies to support or refute the view that modern soft-bristle toothbrushes with low abrasive index dentifrices contribute to abfraction/NCCL development or maturation. However, in a population with Hansen's disease who did not brush their teeth, NCCLs were present.2 This population group regularly consumed acids in their diet, which are noted in Figure 1 as an example of exogenous biocorrosion. Also, a study of a Mexican population from the late 19th century, which pre-dates toothbrushing or dentifrices for personal oral hygiene, found prominent NCCLs that were probably related in their etiologies more so to stress conditions rather than biocorrosion or friction.44
One could presume that with good personal dental hygiene efforts, vigorous toothbrushing would remove softened dentin or fractured enamel hydroxyapatite. It must be understood that soft-tissue damage from abrasion precedes hard-tissue loss in a given location. Effects from abrasion on exposed surfaces vary depending on the integrity/resistance of the surface, the frequency of abrasion, and the direction of force application. A more traditional series of abfractions from chronic occlusal sequelae without the influence of abrasion from toothbrushing is illustrated in Figure 2.
Abfraction advancement can be affected by altered friction occurring from toothbrush/dentifrice abrasion, acids in one's diet, reflux conditions, or stress in occlusal contact.45 All of these incidents have an effect on teeth and in the formation of NCCLs resulting from stress and strain. However, NCCLs can be regarded as unavoidable for many, if not most, people.
Gastroesophageal reflux (GER) disease (GERD), silent GERD, and other anorexic conditions produce loss of hard tissue on lingual surfaces due to acidic or protease challenges over time. GER applies to conditions when an incidental ocassion of reflux action occurs, such as drinking too much alcohol, or an event of undiagiosed food allergy. It is of interest that Fauchaud in the 1700s did not appreciate the differences between the chemical effects of biocorrosion and the effects of friction, which is a physical mechanism.28,46 He was attempting as a physician to explain oral or systemic conditions using terms available at that time. Chronicity is a key factor separating a pathologic state from more normal health. Figure 3 illustrates a patient with anorexia nervosa, which is an example of chronic endogenous biocorrosion.
Cervical Dentin Hypersensitivity
It is clinically notable that the terms "dentin hypersensitivity" and "cervical dentin hypersensitivity" (CDH) do not apply to the same dental pulp pain. Dentin hypersensitivity is self-limiting over a week or two following tooth preparation, crown cementation, or restoration placement from a transient pulpitis. CDH, however, will remain active for a long period of time unless occlusal therapy is provided and/or biocorrosive effects are reduced.47-49 CDH commonly occurs before or during the development of visible/detectable NCCLs. The "hydrodynamic theory" for open dentin tubules proposed by Brännström in the early 1960s is what led to the development of desensitizing materials that are commonly promoted in current-day dentifrices.50 It is the present author's view that etiologic conditions must be evaluated/determined prior to treatment.
Results of the Review
Multifactorial etiologic conditions for NCCLs have been reported, primarily from occlusal stress and biocorrosive conditions. The presence of CDH, a pulp pain, must not be ignored as it could be a precursor to development of NCCLs, yet it does not present during all formations of NCCLs. Nonvital or minimized dentin tubule openings into the oral environment will produce different responses to indices (stimuli) of air, cold, tactile stimulation, electrical stimulation, acid exposure, and combinations thereof. Therefore, CDH is not always present during the process of the formation of abfractive lesions, which are a subset of NCCLs. Dental physicians must determine etiologic factors prior to treatment, in the author's opinion.
Treatment options are best selected with informed consent of the patient and with the clinician following secure identification of causative conditions. Treatments may include direct composites, direct-indirect restorations, veneers, and full- or partial-coverage prostheses. Glass-ionomers may be used as a temporary measure to block the sharp pain of CDH, but their esthetic shortcomings relegate their use as a temporary measure.
Abfractions are a dental flexure subset of NCCLs, also resulting from biocorrosive conditions and manifested as hard-tissue loss. CDH often precedes the visual presence of NCCLs and is primarily a result of chronic occlusal loading and biocorrosion. In vivo research is indicated to determine if frictional contributions from toothbrushing and/or dentifrice abrasion play a role in the development of CDH and/or NCCLs.
About the Author
Thomas A. Coleman, DDS
Retired clinician after nearly 40 years practicing dentistry in Vermont, New York, and New Mexico
Queries to the author regarding this course may be submitted to email@example.com.
1. Levitch LC, Bader JD, Shugars DA, Heymann HO. Non-carious cervical lesions. J Dent. 1994;22(4):195-207.
2. Faye B, Kane AW, Sarr M, et al. Noncarious cervical lesions among a non-toothbrushing population with Hansen's disease (leprosy): initial findings. Quintessence Int. 2006;37(8):613-619.
3. Afolabi AO, Shaba OP, Adegbulugbe IC. Distribution and characteristics of non carious cervical lesions in an adult Nigerian population. Nig Q J Hosp Med. 2012;22(1):1-6.
4. Que K, Guo B, Jia Z, et al. A cross-sectional study: non-carious cervical lesions, cervical dentine hypersensitivity and related risk factors. J Oral Rehabil. 2013;40(1):24-32.
5. Bergstrom J, Eliasson S. Cervical abrasion in relation to toothbrushing and periodontal health. Scand J Dent Res. 1988;96(5):405-411.
6. Grippo JO, Simring M, Schreiner S. Attrition, abrasion, corrosion and abfraction revisited: a new perspective on tooth surface lesions. J Am Dent Assoc. 2004;135(8):1109-1118.
7. Wood I, Jawad Z, Paisley C, Brunton P. Non-carious cervical tooth surface loss: a literature review. J Dent. 2008;36(10):759-766.
8. Michael JA, Townsend GC, Greenwood LF, Kaidonis JA. Abfraction: separating fact from fiction. Aust Dent J. 2009;54(1):2-8.
9. Senna P, Del Bel Cury A, Rösing C. Non-carious cervical lesions and occlusion: a systematic review of clinical studies. J Oral Rehabil. 2012;39(6):450-462.
10. Grippo JO, Oh DS. A classification of the mechanisms producing pathological tissue changes. J Med Eng Technol. 2013;37(4):259-263.
11. Silva AG, Martins CC, Zina LG, et al. The association between occlusal factors and noncarious cervical lesions: a systematic review. J Dent. 2013;41(1):9-16.
12. Soares PV, Santos-Filho PC, Soares CJ, et al. Non-carious cervical lesions: influence of morphology and load type on biomechanical behaviour of maxillary incisors. Aust Dent J. 2013;58(3):306-314.
13. Soares PV, Souza LV, Verissimo C, et al. Effect of root morphology on biomechanical behaviour of premolars associated with abfraction lesions and different loading types. J Oral Rehabil. 2014;41(2):108-114.
14. Soares PV, Machado AC, Zeola LF, et al. Loading and composite restoration assessment of various non-carious cervical lesions morphologies - 3D finite element analysis. Aust Dent J. 2015;60(3):309-316.
15. Radentz WH, Barnes GP, Cutright DE. A survey of factors possibly associated with cervical abrasion of tooth surfaces. J Periodontol. 1976;47(3):148-154.
16. Sangnes G. Traumatization of teeth and gingiva related to habitual tooth cleaning procedures. J Clin Periodontol. 1976;3(2):94-103.
17. Hurst PS, Lacey LH, Crisp AH. Teeth, vomiting and diet: a study of the dental characteristics of seventeen anorexia nervosa patients. Postgrad Med J. 1977;53(620):298-305.
18. White DK, Hayes RC, Benjamin RN. Loss of tooth structure associated with chronic regurgitation and vomiting. J Am Dent Assoc. 1978;97(5):833-835.
19. Zsigmondy U. Uber die keilformigen Defecte an den Facialfalachen der Zahnhalse. Ungar Vjherschr Zahnartze. 1894;1:439-442.
20. Kornfeld B. Preliminary report of clinical observations of cervical erosions, a suggested analysis of the cause and the treatment for its relief. Dental Items of Interest. 1932;54(12):905-909.
21. Shore NA. Temporomandibular Joint Dysfunction and Occlusal Equilbration. 2nd ed. Philadelphia, PA: Lippincott; 1976.
22. Korber KH. Die elastische deformierrung menschlicher zahne. Dtsch Zahnarztl Z. 1962;17:691-698.
23. Lukas D, Spranger H. Experimentelle untersuchungen uber die horizonalbelastung des zahnes bei definierten unterkiefer lateralbewegungen. Dtsch Zahnarztl Z. 1973;28:755-758.
24. Brady JM, Woody RD. Scanning microscopy of cervical erosion. J Am Dent Assoc. 1977;94(4):726-729.
25. McCoy G. The etiology of gingival erosion. J Oral Implantol. 1982;10 (3):361-362.
26. Lee WC, Eakle WS. Possible role of tensile stress in the etiology of cervical erosive lesions of teeth. J Prosthet Dent. 1984;52(3):374-380.
27. Grippo JO. Abfractions: a new classification of hard tissue lesions of teeth. J Esthet Dent. 1991;3(1):14-19.
28. Grippo JO, Simring M, Coleman TA. Abfraction, abrasion, biocorrosion, and the enigma of noncarious cervical lesions: a 20-year perspective. J Esthet Restor Dent. 2012;24(1):10-23.
29. Grippo JO, Coleman TA, Messina AM, Oh DS. A literature review and hypothesis for the etiologies of cervical and root caries. J Esthet Restor Dent. 2018;30(3):187-192.
30. Lee WC, Eakle WS. Stress-induced cervical lesions: review of advances in the past 10 years. J Prosthet Dent. 1996;75(5):487-494.
31. Michael JA, Kaidonis JA, Townsend GC. Non-carious cervical lesions on permanent anterior teeth: a new morphological classification. Aust Dent J. 2010;55(2):134-137.
32. Hur B, Kim HC, Park JK, Versluis A. Characteristics of non-carious cervical lesions-an ex vivo study using micro computed tomography. J Oral Rehabil. 2011;38(6):469-474.
33. Gibbs CH, Mahan PE, Lundeen HC, et al. Occlusal forces during chewing and swallowing as measured by sound transmission. J Prosthet Dent. 1981;46(4):443-449.
34. Gibbs CH, Mahan PE, Mauderli A, et al. Limits of human bite strength. J Prosthet Dent. 1986;56(2):226-229.
35. Suit SR, Gibbs CH, Benz ST. Study of gliding tooth contacts during mastication. J Periodontol. 1976;47(6):331-334.
36. Waugh LM. Dental obervations among Eskimo. VII: Survey of mouth condtions, nutritional study, and gnathodynamometer data, in most primitive and populous native villages in Alaska. J Dent Res. 1937;16:355-356.
37. Xu HH, Smith DT, Jahanmir S, et al. Indentation damage and mechanical properties of human enamel and dentin. J Dent Res. 1998;77 (3):472-480.
38. Aubry M, Mafart B, Donat B, Brau JJ. Brief communication: study of noncarious cervical tooth lesions in samples of prehistoric, historic, and modern populations from the south of France. Am J Phys Anthropol. 2003;121(1):10-14.
39. Litonjua LA, Andreana S, Bush PJ, et al. Noncarious cervical lesions and abfractions: a re-evaluation. J Am Dent Assoc. 2003;134(7):845-850.
40. Estafan A, Furnari PC, Goldstein G, Hittelman EL. In vivo correlation of noncarious cervical lesions and occlusal wear. J Prosthet Dent. 2005;93(3):221-226.
41. Bartlett 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(4):306-312.
42. Wood ID, Kassir AS, Brunton PA. Effect of lateral excursive movements on the progression of abfraction lesions. Oper Dent. 2009;34(3):273-279.
43. Tripathi P, Chopra D, Bagga S. Abfraction myth or reality. J Dent Med Sciences. 2014;13(2):70-73.
44. Ritter AV, Grippo JO, Coleman TA, Morgan ME. Prevalence of carious and non-carious cervical lesions in archaeological populations from North America and Europe. J Esthet Restor Dent. 2009;21(5):324-334.
45. Christensen GJ. What causes changes in occlusion? Dental Economics. 2013;103(7):24-29.
46. Fauchaud P. The Surgeon or Treatise on the Teeth. Lindsay L, translation from 1746. 2nd ed. London, England: Butterrweorth; 1946:20,21,40,46,47.
47. Coleman TA, Kinderknecht KE. Cervical dentin hypersensitivity. Part I: The air indexing method. Quintessence Int. 2000;31(7):461-465.
48. Coleman TA, Grippo JO, Kinderknecht KE. Cervical dentin hypersensitivity. Part II: Associations with abfractive lesions. Quintessence Int. 2000;31(7):466-473.
49. Coleman TA, Grippo JO, Kinderknecht KE. Cervical dentin hypersensitivity. Part III: Resolution following occlusal equilibration. Quintessence Int. 2003;34(6):427-434.
50. Brännström M. Dentinal and pulpal response. III. Application of an air stream to exposed dentine, long observation periods. An experimental study. Acta Odontol Scand. 1960;18(3):235-252.