Treatment Strategies for Noncarious Cervical Lesions

Although their etiology appears multifactorial, documenting these lesions’ signs and symptoms can help clinicians determine appropriate therapy

Anoncarious cervical lesion (NCCL) is a small saucer- or notch-shaped loss of tooth structure at the cementoenamel junction that is most commonly found on the tooth’s facial surface (Figure 1). These lesions are not at increased risk of caries because they are generally accessible for self and professional cleaning. Typically presenting in middle-age to older adults, NCCL prevalence is highly variable and ranges from 5% to 90%.1–5 Evidence suggests their cause is multifactorial: Abfraction due to occlusal stress, erosive tooth wear or a combination of factors are all possible etiologies.6,7 Although NCCLs don’t necessarily require restoration, patients often seek treatment based on a desire for improved esthetics. The decision to manage and restore NCCLs depends on the theory assumed responsible for their origin.8

Originally, NCCLs were attributed to excessive abrasion caused by harsh toothbrushing and/or the use of abrasive dentifrices. Although brushing with proper technique does not produce mechanical damage, excessive brushing force and highly abrasive toothpastes can cause permanent wear of dentin.9 Generally, this problem is associated with poor oral hygiene methods, such as horizontal brushing along the cervical margins in line with the margins of gingival tissue. While aggressive brushing and abrasive toothpaste may seem like logical causes, several factors shed doubt on these explanations. One is that NCCLs often appear on a single tooth, which would be difficult to produce with brushing motions directed across the full dentition. Additionally, NCCLs have been observed in a nonbrushing population of lepers who experienced acidic food exposure, parafunction and some xerostomia.10 These lesions have also been noted in ancient teeth found in archeological digs from five geographical sites.11 Finally, NCCLs are generally not sensitive, which seems counterintuitive if they were caused by continued abrasion of the dentin.2

FIGURE 1. Schematic of a saucer-shaped noncarious cervical lesion that is thought to be slowly progressing toward a notch-shaped lesion. COURTESY OF THE JOURNAL OF THE AMERICAN DENTAL ASSOCIATION

A second theory is that NCCLs are caused by the tensile stress created by occlusion. Although this theory was first described in 1984,12 it did not receive much attention until 1991, when Grippo coined the term “abfraction” to describe this phenomenon.13 Abfractions are presumed to arise in the presence of heavy working contacts and associated occlusal stress.14,15 According to this theory, teeth under stress experience compression on lingual surfaces and tension on buccal surfaces. Over time, the tension leads to micromorphological fatigue and contributes to loss of superficial tooth structure during mastication and/or brushing. Tooth stress occurs with normal occlusion, but is greatest in patients with malocclusion. This often is seen in combination with occlusal wear facets.

Chewing and swallowing produce several thousand loading cycles each day, causing minor fatigue damage that accumulates over the years. The first visual evidence is a saucer-shaped lesion. Although NCCLs occur on facial surfaces because the normal loading of teeth causes flexure patterns with tension on the facial surface, this process has not been well documented.6,16,17 Lesions can be artificially produced in the laboratory, but there has been no monitoring of lesion development over an extended period due to the cost of this type of clinical trial.

EROSIVE FACTORS

Erosion — the degradation of tooth structure due to physicochemical action of acidic or corrosive agents — is an etiologic factor in the development of NCCLs.18,19 There are two types of erosion: intrinsic and extrinsic. Intrinsic erosion stems from gastric acid contacting the oral cavity and teeth, such as occurs in gastroesophageal reflux. Extrinsic erosion is caused by the regular exposure to acidic foods and beverages. Many foods and beverages have low pH, including fruit, soft drinks, sports drinks, juices, vinegar, salad dressing and white wine.20 Lesions from extrinsic erosion tend to occur on the labial surfaces of anterior teeth and buccal or occlusal surfaces of posterior teeth.21 Erosion softens the surface enamel, which, when subjected to abrasion or abfraction, causes further progression of the lesion. The main signs are cupping of cusp tips, loss of dental anatomy, and restorations “standing proud” due to the erosive loss of enamel surrounding the restoration. Clinicians should look for early signs of erosion so preventive strategies can be initiated and the need for extensive restorative care avoided.

It is equally possible that NCCLs occur when components of these theories occur together. In addition, patients’ risk levels can change over time.1 If superficial tooth structure is weakened by micromorphological fractures and erosion, for example, abrasion from brushing and dentifrice can contribute to loss of dentinal structure. Ultimately, the very nature of NCCLs makes them difficult to study because their etiology may differ from the factors that cause their progression.

CLINICAL CONSIDERATIONS

The way in which NCCLs are restored and managed depends on lesion etiology. If the patient presents with NCCLs adjacent to each other, some dentinal hypersensitivity and a horizontal toothbrushing pattern, toothbrush abrasion is the likely cause. Treating and managing lesions caused by abfraction requires more care. If patients present with lesions on single teeth, obvious wear facets and/or no sensitivity, for example, ab­fraction may be the cause. In this case, modification of the existing occlusion should be considered prior to lesion restoration. One option is to improve anterior guidance with crowns or veneers, thus eliminating or reducing lateral excursive contacts on posterior teeth. A thorough risk/benefit analysis is advised before initiating such treatment. The impact of using nightguards and bite splints to reduce the risk of NCCLs among individuals with malocclusion has not yet been reported in the literature. However, these treatments would not necessarily affect normal daytime occlusal patterns or stress.

If clinical signs point to erosion as the primary etiology, the nature of erosion — intrinsic or extrinsic — will help determine treatment. In the case of lesions on facial surfaces due to extrinsic erosion, a dietary analysis is warranted. The key is to provide the patient with an effective protocol to avoid acidic challenges or minimize erosive tooth wear after an acidic challenge. Such an approach may include rinsing with water, followed by rinsing with sodium bicarbonate and an over-the-counter fluoride mouthrinse. Eating cheese after an acidic challenge is useful because it stimulates salivary flow and buffering capacity, and cheese’s relatively high (6 to 7.4) pH helps neutralize acidity.22

RESTORATIVE CARE

If the lesions are esthetically displeasing, become detrimental to pulp health, or if the patient experiences dentinal hypersensitivity, NCCLs should be restored. The goal is to relieve or eliminate the events contributing to lesion formation so they do not return after restoration.18 Evidence suggests that materials with a low elastic modulus that will accommodate tooth flexure — such as microfilled, nanohybrid or nanofilled composite resin, glass ionomer or resin modified glass ionomer — may be good choices for restoring NCCLs.23 The restoration may involve a regular composite, low modulus composite, flowable composite or a flowable composite liner. While low modulus materials or liners are intended to accommodate tooth flexure, the evidence does not indicate that using these materials is necessary.24

The way in which noncarious cervical lesions are restored and managed depends on lesion etiology

During restoration, the enamel margins of the lesion are typically roughened with a flame-shaped diamond to ensure a bevel. Staining or leakage along the composite border may become difficult to remove during hygiene procedures. Clinicians should consider placing mechanical retention in preparation to restore NCCLs, and not rely on adhesives alone. If the tooth is being crowned, a porcelain-fused-to-metal or all-ceramic crown can be extended to include the lesion boundaries. If occlusal stresses are contributing to abfraction and they persist, the lesions will become refocused at the border of the crown and begin to produce a more apical NCCL. The tooth can be removed from occlusion at the obvious contacts to reduce stress. The occlusion can also be shifted from group function to canine guidance. However, most of these effects are temporary.

Generally, NCCLs are not sensitive, as their slow progression provides enough time for a vital pulp to lay down sclerotic dentin that occludes the dentinal tubules, thus preventing rapid fluid movement and hypersensitivity. If possible, these surfaces should not be disturbed by explorers, manual scalers or power scalers during routine dental procedures.

All NCCLs should be clinically documented with photographs of the shape and size of the lesions on facial surfaces, as well as any clues to their presence, such as occlusal wear facets on teeth. A periodontal probe can be used to estimate the widths and depths of tooth surface NCCLs. Comparison of diagnostic casts fabricated from impressions made at different intervals over several years may also be a valuable management tool.

CONCLUSION

In summation, NCCLs can arise from toothbrush and dentifrice abrasion, abfraction, erosive tooth wear or multifactorial causes. They are restored for reasons of esthetics, dentinal hypersensitivity or if there is pathological progression toward a vital pulp. Generally, tooth stress needs to be mitigated to reduce or eliminate factors that contribute to ongoing lesion development.


KEY TAKEAWAYS

  • Noncarious cervical lesions (NCCLs) can arise from excessive toothbrush force, dentifrice abrasion, abfraction, erosive tooth wear or a combination of these factors.
  • Although NCCLs don’t necessarily require restoration, patients often seek treatment to help improve esthetics.
  • The way in which NCCLs are restored and managed depends on etiology, but the very nature of these lesions makes them difficult to study because their etiology may differ from the factors that cause lesion progression.
  • Lesions from extrinsic erosion, which is caused by regular exposure to acidic foods and beverages, tend to occur on the labial surfaces of anterior teeth and buccal or occlusal surfaces of posterior teeth.21
  • Dental teams should look for early signs of erosion so preventive strategies can be initiated and the need for extensive restorative care avoided.
  • If the lesions are esthetically displeasing, become detrimental to pulp health, or if the patient experiences dentinal hypersensitivity, NCCLs should be restored.
  • Clinicians should consider placing mechanical retention in preparations to restore NCCLs, and not rely on adhesives alone. • Materials with a low elastic modulus that will accommodate tooth flexure — such as microfilled, nanohybrid or nanofilled composite resin, glass ionomer or resin modified glass ionomer — are often a good choice for restoring NCCLs.23

REFERENCES

  1. Levitch LC, Bader JD, Shugars DA, Heymann HO. Non-carious cervical lesions. J Dent. 1994;22:195–207.
  2. Aw TC, Lepe X, Johnson GH, Mancl L. Characteristics of noncarious cervical lesions: a clinical investigation. J Am Dent Assoc. 2002;133:725–733.
  3. Borcic J, Anic I, Urek MM, Ferreri S. Prevalence of non-carious cervical lesions in permanent dentition. J Oral Rehabil. 2004;31:117–123.
  4. Pegararo LF, Scolaro JM, Conti PC, Telles D, Pegararo TA. Non-carious cervical lesions in adults — prevalence and occlusal aspects. J Am Dent Assoc. 2005;136:1694–1700.
  5. Lai ZY, Zhi QH, Zhou Y, Lin HC. Prevalence of non-carious cervical lesions and associated risk indicators in middle-aged and elderly populations in Southern China. Chin J Dent Res. 2015;18:41–50.
  6. Bartlett DW, Shah P. Critical review of non-carious cervical (wear) lesions and the role of abfraction, erosion, and abrasion. J Dent Res. 2006;85:306–312.
  7. Wood I, Jawab Z, Paisley C, Brunton P. Non-carious cervical tooth structure loss: a literature review. J Dent. 2008;36:759–766.
  8. Nascimento MM, Dilbone DA, Pereira PN, Duarte WR, Geraldeli S, Delgado AJ. Abfraction lesions: etiology, diagnosis, and treatment options. Clin Cosmet Investig Dent. 2016;8:79–87.
  9. Dzakovich JJ, Oslak RR. In vitro reproduction of noncarious cervical lesions. J Prosthet Dent. 2008;100:1–10.
  10. Faye B, Kane AW, Sarr M, Lo C, Ritter AV, Grippo JO. Non-carious cervical lesions among a non-toothbrushing population with Hansen’s disease (leprosy): initial findings. Quintessence Int. 2006;37:613–619.
  11. 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;21:324–334.
  12. Lee WC, Eakle WS. Possible role of tensile stress in the etiology of cervical erosive lesions of teeth. J Prosthet Dent. 1984;52:374–380.
  13. Grippo JO. Abfractions: a new classification of hard tissue lesions of teeth. J Esthet Restor Dent. 1991;3:14–19.
  14. Braem M, Lambrechts P, Vanherle G. Stress-induced cervical lesions. J Prosthet Dent. 1992;67:78–722.
  15. Sawlani K, Lawson NC, Burgess JO, et al. Factors influencing the progression of noncarious cervical lesions: a 5-year prospective clinical evaluation. J Prosthet Dent. 2016;115:571–577.
  16. Michael JA, Townsend GC, Greenwood LF, Kaidonis JA. Abfraction: separating fact from fiction. Aust Dent J. 2009;54:2–8.
  17. Senna P, Del Bel Cury A, Rosing C. Non-carious cervical lesions and occlusion: a systematic review of clinical studies. J Oral Rehabil. 2012;39:450–462.
  18. Lussi A, Jaeggi T. Dental Erosion — Diagnosis, Risk Assessment, Prevention, and Treatment. Hanover Park, Illinois: Quintessence Publishing; 2011.
  19. Lussi A, Schaffner M. Progression of and risk factors for dental erosion and wedge-shaped defects over a 6-year period. Caries Res. 2000;34:182–187.
  20. Jarvinen VK, Rytomaa, II, Heinonen OP. Risk factors in dental erosion. J Dent Res. 1991;70:942–947.
  21. Nunn JH. Prevalence of dental erosion and the implications for oral health. Eur J Oral Sci. 1996;104:156–161.
  22. Honório HM, Rios D, Júnior ES, de Oliveira DS, Fior FA, Buzalaf MA. Effect of acidic challenge preceded by food consumption on enamel erosion. Eur J Dent. 2010;4:412–417.
  23. Heymann HO, Sturdevant JR, Bayne S, Wilder AD, Sluder TB, Brunson WD. Examining tooth flexure effects. J Amer Dent Assoc. 1991;122:41–47.
  24. Heymann HO, Bayne SC. Current concepts in dentin bonding. J Am Dent Assoc. 1993;124:26–36.

The authors have no commercial conflicts of interest to disclose.

Featured photo by freemixer / istock / Getty Images Plus

From Decisions in Dentistry. April 2017;3(4):24–28.

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