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The loss of tooth structure can be classified into two categories: loss occurring from disease or loss from a non-disease source. The majority of tooth structure loss from disease is a result of microbiological activity (caries). Non-disease-related tooth structure loss may be divided into the sub-categories attrition, abrasion, and erosion.1
Attrition is defined as the loss of tooth structure (enamel and dentin) resulting from tooth-to-tooth contact. Tooth structure loss from abrasion is usually mechanical in nature, whereas, in the case of erosion, the loss of tooth structure is through chemical action.2
This article will focus on tooth structure loss by erosion-its etiology, diagnosis, and management.
Dental erosion has been defined by several researchers as a chemical process that involves the dissolution of tooth structure (enamel and dentin) by acids originating from sources that are not derived from a bacterial source.3 Others have included in their definition that dental erosion is an irreversible loss of dental hard tissues accompanied by softening of the eroded surface due to an acid attack; the eroded, softened surfaces are further subject to abrasives forces.4,5 When dental hard tissues are exposed to an acidic environment (intrinsic or extrinsic) that exceeds the buffering capability of the saliva, simultaneous dissolution of hydroxyapatite and fluorohydroxyapatite results in tooth structure loss in layers.5 When the rate of demineralization surpasses the rate of remineralization, erosion occurs. At a pH of 5.2 to 5.5, the outer layer of hydroxyapatite will begin to dissolve; fluorohydroxyapatite begins to dissolve at pH 4.5. Weaker acids are capable of demineralizing dentin at a pH of 6.9.6
Dental Erosion Classifications
There have been several classifications of dental erosion throughout history, beginning with the Knight Tooth Wear Index7 in 1984 to as recent as the year 2020. The earlier classifications did not share similar testing parameters, making comparisons difficult. The Tooth Wear Evaluation System (TWES) introduced in 2015 graded the severity of dental erosion on a numeric scale of 0 (indicating no wear) to 4 (indicating extreme wear). The newest classification incorporates the original TWES system and also includes more detailed grading, designates etiological factors more closely, and records pathological symptoms.8
Extrinsic Causes
Extrinsic causes of erosion originate from outside of the oral cavity and can be categorically divided into dietary and environmental causes. Extrinsic dietary acid sources are numerous but include various beverages, fresh and dried fruits, sour-flavored confections, medications, and nutritional supplements. The list of highly acidic beverages continues to grow in the market place and includes carbonated drinks, sports drinks, iced teas, flavored waters, juices, fruit-flavored drinks, powdered drinks, beer, and wine. Some brands of bottled waters are in the pH range of 5 to 5.5, which have the potential to affect exposed root structure. Reddy et al9 compiled the assessed pH of 379 beverages and categorized them as juices, carbonated soft drinks, flavored waters, teas, and energy drinks. The beverages were subdivided by their erosive potential ranging from extremely erosive to minimally erosive.
Food sources include fresh fruits, jams, jellies, and sauces. Some examples are apples, cranberry sauce, cherries, raspberries, apricots, and various fruit jams/jellies. Vinegar-based salad dressing, condiments such as ketchup and mayonnaise,10 pickled foods in vinegar, and refined grain products (baked goods, fast food, and white bread) are also acidic.12 Other extrinsic sources include frequent use of aspirin, cough suppressant syrups, and iron and vitamin C chewable supplements.
These are examples that many people do not associate with having erosive properties. Rinsing with a mouthwash after tooth brushing is an everyday common routine for many people. However, it is important to understand the acidity levels of a number of commercial mouthwashes when making recommendations to patients. Most popular mouthwashes have a pH below 6.5. In fact, a majority of brands are below 5.5, with the lowest at 3.3, which is the same pH as many carbonated soft drinks.12
Acids are added to beverages to achieve the desired tastes, to balance the sweetness of the sugar and act as preservatives. For example, malic acid (pH 3.3), which is found in apples, pears, and cherries, is added to non-carbonated beverages to enhance the flavor. It is also added to sweeten carbonated beverages. Phosphoric acid (pH 2.1) is added to cola beverages to increase the tartness and to improve the self-life. Citric acid (pH 3.2) is naturally occurring in citrus beverages. This provides the tangy flavor and functions as a preservative. It is also the most damaging acid due to its chelating capacity of seizing calcium from the saliva and teeth and forming a complex calcium citrate. As much as 30% of salivary calcium can be complexed by citric acid in fruit juices while reducing the buffer capacity of saliva.13 Studies have shown citric acid to be the most erosive.14,15 Plain carbonated water (seltzer water), which may seem to have little erosive effect, converts to carbonic acid (pH 4.68) when consumed. Beverages containing "natural flavorings" (such as flavored seltzer water) do not need to state the origins of those flavors. A single flavor could contain up to 100 different sources. The FDA lumps 3,000-plus chemical food additives under the term "natural flavorings." All citrus and fruit-flavored seltzer water beverages contain citric acid.16
Frequent consumption of acidic foods and beverages plays a greater role in dental erosion than the total intake.17 For example, soft-drink consumption has increased 300% in the last 20 years. The serving size has also increased. The average serving size of a soft drink in the 1950s was 7 ounces, increased to 12 ounces in the 1960s, and rose again to 20 ounces in the 1990s.10 Even 32-ounce sizes ("The Big Gulp") and larger are now available.
Some medications are considered xerogenic in nature and cause a dry mouth, which, in turn, limits the buffering effect of saliva. Medications that have anticholinergic and sympathomimetic actions-like tricyclic antidepressants, antipsychotics, and atropinic drugs as well as decongestants, bronchodilators, and anti-hypertensive drugs-all diminish salivary flow.18 Illegal drugs such as methamphetamine (hydrochloric salt) and cocaine (hydrochloride salt) cause a decline in the pH in the mouth when they are smoked or applied to the gingival tissue. These drugs, as well as ecstasy and heroin, increase sugar cravings and heighten anxiety, leading to bruxism.18
Environmental extrinsic causes include exposure to unmanaged chlorinated swimming pool water, battery manufacturing plants, and acidic fumes in mines.10
Intrinsic Causes
Intrinsic erosion is a result of endogenous acids in the oral cavity. These acids result from regurgitation, which allows stomach acids (pH 1.5 to 3.5)19 to come in contact with the teeth. This is often secondary to conditions such as gastroesophageal reflux disease (GERD), anorexia nervosa, and bulimia nervosa.
Mechanics of Erosion
The acquired pellicle is an organic, non-bacterial, protein film that covers hard and soft oral tissues. An acid must diffuse through the acquired pellicle before it can attack the enamel. Once contact is made between the acid and the enamel, the hydrogen ion component of the acid will start to dissolve the outer enamel layer. The acid continues to dissolve the enamel prism sheath followed by the prism core leaving a honeycomb appearance.3 If the acidic environment continues, further dissolution of the interprismatic areas of enamel will occur.
When acidic materials are introduced into the oral cavity (referred to as an acid challenge), there is a reflective response by the salivary glands to increase the flow of saliva in order to dilute or clear the acids. Salivary components include sodium, calcium, potassium, magnesium, bicarbonates, and urea that help to neutralize the acid and return the pH to normal. This mechanism is referred to as the buffering capacity of saliva.20
The immediate effect of an acid challenge results in a loss of minerals to a depth of a few micrometers (0.0001 millimeters), known as enamel softening. The outer softened layer can be easily removed by tooth brushing with or without a dentifrice. Since this layer may be removed with tooth brushing, it is advised to wait 30 to 60 minutes after an acid challenge occurs before brushing. Waiting will allow the normal buffering actions of the salvia to neutralize the acid and remineralize the softened layer.21
Changes to salivary flow and salivary contents will have an effect on its buffering capacity. Changes to the calcium and phosphate content of foods and beverages can affect the erosive potential of acids.13 West et al22 found the addition of calcium to a low-pH blackcurrant juice drink reduced the erosive ability of the drink. It has been shown that calcium-enriched orange juices and sports drinks have little erosive effect. Lussi and Jaggi reported that yogurt has a pH of 4.0 but had little erosive effect due to its high calcium and phosphate level.13
DIAGNOSIS
In the early stages of dental erosion, the clinician may have difficulty diagnosing the problem due to limited clinical signs and symptoms as reported by the patient. The first signs of erosion may visually appear as even, shiny surfaces.23 As the erosion progresses, clinical signs become more evident that include the appearance of irregular and rough edges of the teeth. For example, chronic regurgitation displays a typical distribution of erosive tooth loss that appears as saucer-like lesions on the occlusal surfaces of premolars and molars. These are referred to as perimolysis.10 The regurgitation pathway of hydrochloric acid over the dorsum of the tongue affects maxillary and mandibular teeth differently. The erosive effects can be seen on the palatal and occlusal surfaces on all of the maxillary teeth. Whereas, the erosive effects seen on the mandibular premolars and molars are confined to the occlusal and buccal surfaces only.
Early signs of erosion on posterior teeth may appear as small pits on the cusp tips.3 If abrasive forces in the form of parafunctional habits are introduced, the occlusal wear could accelerate. In long standing cases, the presence of occlusal restorations may start to appear more prominent, as if the fillings were "extruding" in an occlusal direction. As clinical signs become more pronounced, the patient may become symptomatic and report having hot and cold temperature as well as sweet sensitivities.
A systematic approach can aid the clinician in diagnosing dental erosion. First, the patient must understand and take ownership of the problem before the clinician presents a treatment plan. The examination should include visual and tactile tests.24 Visually, the dimension and severity of the erosive damage must be documented. The clinician must also notate the presence of erosive signs and describe the dimension and severity.24 A tactile test will provide activity and risk assessment. A 12 surgical blade may be used to score or scratch a line in an eroded area as a baseline indicator. Further, an impression is taken of the tooth and a stone cast poured as a reference. The patient returns in 1 to 4 weeks and another impression is taken. A comparison under magnification of the two stone models accurately details the erosive activity of the teeth.
Another modality used for assessing the progression of erosive tooth loss is photography. Photographs that are compared between recall appointments and/or the comparisons of study casts will show the progression of tooth erosion. Evaluating the occlusal and proximal enamel thickness on bitewing radiographs is also an effective aid in diagnosing erosion.
Management of Erosive Tooth Loss
As previously mentioned, the first step in managing dental erosion is the patient awareness of the problem and their commitment in following a treatment plan. A thorough history of risk factors must be documented. The clinician must identify the etiologic source(s) of the acids, whether they are extrinsic, intrinsic, or both. Dietary counseling is essential. Many foods and beverages may not seem to be damaging in the patient's mind, however, educating them about the acid levels in the foods and beverages that they consume may be very insightful and prompt them to make dietary modifications.
Introducing a xylitol-containing chewing gum, mints, candy or water can also help to mitigate an acid challenge event. Studies have shown that xylitol suppresses dental caries by inhibition of glucosyltranferases in cariogenic bacteria.25-27 The FDA and the European Union have officially recognized the oral health benefits of xylitol. Chewing xylitol-containing gum has been shown to be the best vehicle to deliver xylitol to the oral cavity.28 However, a recommendation of xylitol-based products should include a strong warning that xylitol will cause life-threatening toxicoses in dogs.29,30
Behavior control is essential in minimizing or preventing dental erosion. As an example, many people carry and consume containers of water daily. Plain water is not an issue; however, if a slice of lemon, lime, or other citrus is added to the water, this lowers the pH of the beverage. Sipping acidic water throughout the day results in a greater frequency of acid challenges. Parents of young adults, particularly teens with eating disorders, should be made aware that their child has an issue. It is imperative that the problem be addressed and that the child receives psychological counseling.
Oral hygiene habits must also be evaluated. A homecare regimen should include proper brushing and flossing techniques in addition to using a mouthwash that has a pH greater than 7. Using bioactive glass-containing dentifrices benefits the early symptoms of dentin hypersensitivity. The active ingredient in these dentifrices, fluoro calcium phosphosilicate, has been shown to provide a better treatment response to dentinal hypersensitivity due to an early onset of relief compared to other dentifrices.31
Statistics have shown that some patients do not follow all recommendations for improving their general health. In respect to the elimination of all acidic beverages for patients with erosive tooth structure loss, acid neutralizing strategies may be introduced. Drinking more plain water, especially after meals, using a straw when drinking acidic beverages, and following up by drinking plain water after consuming an acidic drink will all assist in reducing acid levels. Interestingly, ending a meal by eating cheese also reduces acid.
Hygienists provide ongoing care based on the needs of the patient. SPT extends beyond basic preventive care and involves a higher level of services aimed at controlling chronic periodontal disease. Patients undergoing supportive periodontal therapy should perceive a difference.27
Restorative Management
Detection of caries normally leads the clinician, without hesitation, to initiate corrective therapy. In the case of young patients with dental erosion, many clinicians prefer to observe or "watch" the situation until the patient is a bit older. The literature supports that the use of direct observation to monitor the progression of erosive tooth structure loss is unreliable.32-34 Some clinicians may not feel comfortable in proposing extensive rehabilitation for younger patients who are asymptomatic and unaware of their dental condition.34 In the case of very young patients, deciduous teeth have a thinner layer of enamel, and therefore, are predisposed to rapid erosion which exposes the underlying dentin and the possibility of dental pulp exposure.35 The sooner a course of therapy can be initiated, the more conservative treatment options may be successful.
A conservative approach to restoring a compromised dentition is paramount. The amount of erosive tooth structure loss will determine the extent of the restorative management. In the case of eroded palatal surfaces of maxillary anterior teeth, the amount of interocclusal space dictates the treatment approach. If more than a millimeter of space is available, direct composite veneers may be placed lingually. In more severe, long-standing cases, with the entire palatal enamel missing and the mandibular anterior teeth super-erupted and yielding no interocclusal space, increasing the vertical dimension may be necessary. Early detection and treatment of dental erosion obviously diminishes the need for complex restorative care.
Long standing erosive and/or abrasive activity can result in non-carious cervical lesions (NCCLs) presenting as a layer of pathologically altered dentin. This dentin, referred to as pathologic sclerotic dentin, has a hypermineralized layer. The layer consists of dentinal tubules that are partially or completely obliterated.36,37 Restorative treatment for pathologic sclerotic dentin with conventional acid etching steps and adhesive bonding strategies has its shortcomings due to the continued presence of tubule obliteration as well as the hypermineralized surface layer, which resists the etching action of both self-etching primers and phosphoric acid.38,39 It has been shown that acid conditioners and adhesive resins have variable degrees of penetration into a sclerotic dentin surface.40
There have been several suggested approaches when bonding to sclerotic dentin. These techniques include the use of a rotary bur, an air abrasion with aluminum oxide to remove the hypermineralized layer, or the use of a stronger concentration of phosphoric acid (45% - 50%) with incorporating a longer etch time.41 Wang et al compared the micro-tensile bond strength of self-etching adhesive resin to sclerotic dentin and found using 35% phosphoric acid for 30 seconds followed by an application of either 5% or 10% sodium hypochlorite for 60 seconds increased the bond strength.42 The study found that 35% phosphoric acid demineralized the collagen fibers, decalcified the superficial layer, and diminished the sclerotic casts obliterating the dentinal tubules. The sodium hypochlorite acted to disolve and remove the exposed dentinal collagen. They also reported that this conditioning protocol resulted in an alteration of the microstructure and created a fresh apatite surface.
Martini et al studied the effect of ethylene diamine tetra-acetic acid (EDTA) in conditioning sclerotic dentin for 2 minutes or 30 seconds with a sonic device oscillating at a frequency of 170 Hz.They found an increase in bond strength while using a self-etching adhesive.43
Finally, Yu et al reported that mechanical roughening did not show a significant difference for self-etching and etch & rinse adhesives. They found that increasing the acid concentration and etching time did not improve self-etching adhesives and showed only a slight increase in bond strength with etch & rinse adhesives. Their recommendation was to use an adhesive that contains a functional monomer and has the ability to bond to calcium salts, such as 10-methacryloxydecyl dihydrogen phosphate (MDP) or dipentaerythritol penta-acrylate phosphate (PENTA). The study also recommended that the acid etching be confined to the enamel just slightly coronal to the lesion (selective etching).44
Conclusion
The extrinsic and intrinsic causes of dental erosion have been described. Dietary causes can be overlooked by dentists and dental hygienists in routine recall visits. Dental offices could develop a protocol for screening and classifying patients as high, medium, or low risk. Thorough examination of dietary habits should also be explored and suggestions be made to counter the erosion progress. Documentation on patients who exhibit early signs of erosive tooth structure loss should also occur. If these clinical signs worsen, restorative measures should then be instigated. Dental erosion can be as destructive to tooth structure as dental caries. Prevention through patient education can be our best asset in curtailing this damaging process.
References
1. Bartlett DW, Shah P. A critical review of non-cariouscervical (wear) lesions and the role of abfraction, erosion,and abrasion. J Dent Res. 2006;85(4):306-312.
2. Urzua I, Cabello R, Rodriguez G, et al. Absence of non-carious cervical lesions (NCCLs) in a Chilean pre-Columbian sample with severe occlusal tooth wear. Int J Odontostomat. 2015;9(1):59-64.
3. Sengupta A, Dental erosion etiology, diagnosis and management. ACTA Scientific Dent Sciences. 2018;2(11):43-48.
4. Lussi A. Erosive tooth wear - a multifactorial condition of growing concern and increasing knowledge. Monographs in Oral Sci. 2006;20:1-8.
5. Addy M, Hunter ML. Can tooth brushing damage your health? Effects on oral and dental tissues. International Dental Journal. 2003;53:177-186.
6. Singh ML, Kugel G, Papas A, Magnuson B. Non-carious lesions due to tooth surface loss: to restore or not to restore? Tufts University School of Dental Medicine. July 1, 2020. https://tufts.cdeworld.com/courses/21769-non-carious-lesions-due-to-tooth-surface-loss-to-restore-or-not-to-restore. Accessed April 1, 2021.
7. Imfeld T. Dental erosion. Definition, classification and links. Eur J Oral Sci. 1996;104(2):151-155.
8. Wetselaar P, Wetselaar-Glas MJM, et al. Diagnosing tooth wear, a new taxonomy based on the revised version of the Tooth Wear Evaluation System (TWES 2.0). J Oral Rehabil. 2020;47:703-712.
9. Reddy A, Norris DF, Momeni SS, et al. The pH of beverages in the United States. J Am Dent Assoc. 2016;147(4):255-263.
10. Santhiya B, Puranik MP, Uma SR. Risk factors, assessment and management of dental erosion in dental setting - a literature review. Inter J Applied Dent Sciences. 2019;5(2):28-36.
11. Scialla JJ, Anderson CA. Dietary acid load: a novel nutritional target in chronic kidney disease? Adv Chronic Kidney Dis. 2013;20(2):141-149.
12. Bolding LM, Masri R, Arola D, et al. Caries management by risk assessment (CAMBRA) and its effect on the surface roughness of various restorative materials. J Prosthet Dent. 2015;114(4):543-548.
13. Lussi A, Jaggi T. Erosion-diagnosis and risk factors. Clin Oral Investig. 2008;12(1):5-13.
14. Burato EM, Andrade L, Rath IBS, Tames DR. Evaluation of the erosive potential of the Brazilian sport drinks to the dental hard tissues. Rev ABO Nac. 2002;10:109-112.
15. Cai F, Manton DJ, Shen P, et al. Effect of addition of citric acid and casein phosphopeptide-amorphous calcium phosphate to a sugar-free chewing gum on enamel remineralization in situ. Caries Res. 2007;41:377-383.
16. U.S. Food & Drug Administration. Specific animal food labeling requirements. 21 CFR US Department of Health and Human Services. Protection of human subjects. 45 CFR §501.22. Updated April 1, 2020. https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/cfrsearch.cfm?fr=501.22. Accessed April 1, 2021.
17. O'Sullivan E, Milosevic A. UK national clinical guidelines in paediatric dentistry: diagnosis, prevention and management of dental erosion. International Journal of Paediatric Dentistry. 2008;18(Suppl. 1):29-38.
18. Grobler SR, Chikte U, Westraat J. The pH levels of different methamphetamine drug samples on the street market in Cape Town. ISRN Dent. 2011;2011:974768. doi:10.5402/2011/974768.
19. Lawrie JH, Forrest AP. The measurement of gastric acid. Postgrad Med J. 1965;41:408-417.
20. Li T, Fang Y, Zhu Y, et al. A small dose of arginine vasopressin in combination with norepinephrine is a good early treatment for uncontrolled hemorrhagic shock after hemostasis. J Surg Res. 2011;169(1):76-84. doi:10.1016/j.jss.2010.02.001.
21. Addy M, Shellis RP. Interaction between attrition, abrasion and erosion in tooth wear. Monogr Oral Sci. 2006;20:17-31.
22. West NX, Hughes JA, Parker DM, et al. Development of low erosive carbonated fruit drinks 2. Evaluation of an experimental carbonated black currant drink compared to a conventional carbonated drink. J Dent. 2003;31(5):361-365.
23. Lussi A, Jaeggi T, Zero D. The role of diet in the aetiology of dental erosion. Caries Res. 2004;38(Suppl 1):34-44. doi:10.1159/000074360.
24. Bartlett D, Ganss C, Lussi A. Basic Erosive Wear Examination (BEWE): a new scoring system for scientific and clinical needs. Clin Oral Investig. 2008;12(Suppl 1):S65-S68.
25. Devulapalle KS, Mooser G. Glucosyltransferase inactivation reduces dental caries. J Dent Res. 2001;80(2):466-469.
26. Bowen WH, Koo H. Biology of Streptococcus mutans-derived glucosyltransferases: role in extracellular matrix formation of cariogenic biofilms. Caries Res. 2011;45(1):69-86.
27. Benwait J, Isaac P, Ackerson L, K, Meurman J, H. Oral and systemic effects of xylitol consumption. Caries Res. 2019;53:491-501.
28. Llop MR, Jimeno FG, et al. Effects of xylitol chewing gum on salivary flow rate, pH, buffering capacity and presence of Streptococcus mutans in saliva. Eur J Paediatr Dent. 2010;11(11):9-14.
29. Murphy LA, Coleman AE. Xylitol toxicosis in dogs. Vet Clin North Am Small Anim Pract. 2012;42(2):307-312.
30. Helvey GA. Xylitol: Reducing caries in humans but toxic to dogs. Parkell Today. Feb 2017:11.
31. Aggarwal SD, Borkar A, Borse N, Acharya A. Comparative evaluation of fluoro calcium phosphosilicate, calcium sodium phosphosilicate, and strontium chloride hexahydrate containing dentifrice for the treatment of dentin hypersensitivity: A randomized single-blind study. J Int Oral Health. 2019;11:404-411.
32. Taylor DF, Bayne SC, Sturdevant JR, WilderAD. Comparison of direct and indirect methods for analyzing wear of posterior composite restorations. Dent Mater. 1989;5:157-160.
33. Leinfelder KF, Wilder AD Jr, Teixeira LC. Wear rates of posterior composite resins. J Am Dent Assoc. 1986;112:829-833.
34. Vailati F, Belser UC. Classification and treatment of the anterior maxillary dentition affected by dental erosion: The ACE Classification. Int J Periodontics Restorative Dent. 2010;30:599-571.
35. Taji S, Seow WK. A literature review of dental erosion in children. Aust Dent J. 2010;55(4):358-367.
36. Murakami C, Tello G, Abanto J, et al. Risk factors for erosive tooth wear in Brazilian preschool children. Caries Research. 2011;45:121-129.
37. Lopes CG, Baratieri CM, Baratieri LN, et al. Bonding to cervical sclerotic dentin: effect of acid etching time. J Adhes Dent. 2004;6:19-23.
38. Gwinnett AJ, Jandresen M. Micromorphological features of cervical erosion after acid conditioning and its relation with composite resin. J Dent Res. 1978;57:543-549.
39. Isokawa S, Kubota K, Kuwajima K. Scanning electron microscope study of dentine exposed by contact facets and cervical abrasion. J Dent Res. 1973;52:170-174.
40. Tay FR, Nawareg MA, Abuelenain D, Pashley DH. Cervical sclerotic dentin: Resin bonding. In: Goldberg M, ed. Understanding Dental Caries. Springer; 2016:97-125.
41. Kusunoki M, Itoh K, Takahashi Y, Hisamitsu H. Contraction gap versus shear bond strength of dentin adhesive in sound and sclerotic dentins. Dent Mater. 2006;25(3):576-583.
42. Wang J, Song W, Zhu L, et al. A comparative study of the microtensile bond strength and microstructural differences between sclerotic and normal dentine after surface pretreatment. BMC Oral Health. 2019;19(1):216. https://doi.org/10.1186/s12903-019-0899-x.
43. Martini EC, Parreiras SO, Gutierrez MF, et al. Effect of different protocols in preconditioning with EDTA in sclerotic dentin and enamel before universal adhesives applied in self-etch mode. Oper Dent. 2017;42(3):284-296.
44. Yu DH, Jia LL, Li JY. Effects of various surface treatments on the bonding efficacy of noncarious cervical sclerotic lesions. Hua Xi Kou Qiang Yi Xue Za Zhi. 2020;38(4):438-442. doi:10.7518/hxkq.2020.04.015.