Tooth Wear: Erosion, Attrition, Abrasion, and Abfraction
Jul 27

Jul 27

Tooth Wear: Erosion, Attrition, Abrasion, and Abfraction

Category: Restorative Dentistry | Keywords: tooth wear, erosion, attrition, abrasion, abfraction, non-carious tooth surface loss, TWES, restorative management

1. Introduction

Non-carious tooth surface loss (TSL), commonly termed tooth wear, is an increasingly prevalent condition in contemporary dental practice. Unlike caries, which is a bacterially mediated disease, tooth wear represents the cumulative, irreversible loss of dental hard tissues through chemical and mechanical processes that do not involve bacteria. Epidemiological studies indicate that the prevalence of moderate-to-severe tooth wear in adults has increased substantially over the past two decades, with estimates ranging from 3% in young adults to 30–45% in older populations. The modern diet—rich in acidic beverages and characterized by increased life expectancy of the natural dentition—has transformed tooth wear from a geriatric concern to a condition affecting all age groups. This review provides a comprehensive classification of the four types of tooth wear, their etiologies, clinical diagnostic features, and evidence-based management strategies.

2. Classification and Definition of Tooth Wear Types

2.1 The Quadripartite Classification

Type Mechanism Etiological Agent Key Clinical Features
Erosion Chemical dissolution of dental hard tissues by acids Dietary acids, gastric acid (reflux/vomiting), environmental acids Smooth, polished, cupped lesions; enamel thinning; restoration "proudness"; broad concave defects on occlusal surfaces (perimolysis)
Attrition Mechanical wear due to tooth-to-tooth contact Bruxism, clenching, functional occlusal contacts Well-defined, matching wear facets on opposing teeth; flattened cusps and incisal edges; enamel and dentin wear at equal rates
Abrasion Mechanical wear due to foreign objects or substances Aggressive toothbrushing, abrasive toothpaste, occupational habits, oral jewelry V-shaped or wedge-shaped notches at cervical margins; sharp, well-defined margins; more severe on prominent teeth (canines, premolars); often unilateral (handedness)
Abfraction Biomechanical loading-induced flexure and microfracture Eccentric occlusal forces, parafunction, cervical stress concentration Deep, narrow, wedge-shaped cervical defects; may be subgingival; affects single teeth or teeth in heavy occlusion; associated with occlusal interferences
Clinical pearl: Tooth wear is rarely monofactorial. Most patients exhibit a combination of two or more mechanisms (e.g., erosion creating a susceptible surface that is subsequently worn by attrition or abrasion). The clinical challenge is identifying the dominant etiological factor(s) to direct preventive and restorative therapy.

3. Dental Erosion: The Chemical Component

3.1 Etiology and Sources of Acid

Extrinsic acids (dietary):

  • Carbonated beverages (pH 2.3–3.5): cola, lemon-lime sodas, energy drinks
  • Fruit juices (pH 2.8–4.0): orange, apple, grapefruit, lemon, cranberry juices
  • Citrus fruits: lemons (pH 2.0–2.6), oranges, grapefruits
  • Vinegar-based foods: salad dressings, pickles
  • Wine (pH 2.8–3.8) and alcoholic mixers
  • Medications: chewable vitamin C tablets (ascorbic acid), aspirin, iron tonics, hydrochloric acid replacement therapy

The critical pH for enamel dissolution is approximately 5.5; for dentin, dissolution begins at approximately pH 6.2–6.7, making dentin more susceptible to erosion than enamel. The erosive potential of an acidic substance depends not only on pH but also on titratable acidity (buffering capacity), calcium and phosphate concentration (degree of saturation with respect to hydroxyapatite), and frequency and duration of exposure.

Intrinsic acids (gastric):

  • Gastroesophageal reflux disease (GERD): Affects 10–20% of the Western population; nocturnal reflux is particularly damaging due to reduced salivary flow during sleep
  • Eating disorders: Anorexia nervosa and bulimia nervosa; perimolysis (palatal erosion from frequent vomiting) is a pathognomonic sign. Prevalence of dental erosion in patients with eating disorders: 35–70%
  • Rumination syndrome: Involuntary regurgitation of recently ingested food
  • Pregnancy-related vomiting: Hyperemesis gravidarum
  • Chronic alcoholism: Gastritis and repeated vomiting

3.2 Clinical Appearance and Staging

Erosive lesions present as smooth, glazed, "melted" surfaces with loss of surface characteristics (perikymata on enamel). A hallmark sign is the presence of "cupping" or "cratering" on occlusal surfaces—concave defects where dentin has been preferentially dissolved, surrounded by a raised enamel rim. Another pathognomonic feature is restoration "proudness," where existing amalgam or composite restorations stand above the surrounding tooth structure due to preferential erosion of enamel and dentin around the restoration.

The Basic Erosive Wear Examination (BEWE) provides a simple, validated scoring system:

BEWE Score Clinical Appearance Management
0 No erosive tooth wear Routine maintenance
1 Initial loss of surface texture Preventive counseling; dietary analysis; fluoride therapy; review at 2 years
2 Distinct defect, hard tissue loss <50% of surface area As above plus: study casts to monitor progression; consider composite build-ups; review at 6–12 months
3 Hard tissue loss ≥50% of surface area As above plus: restorative intervention indicated; may require full-mouth rehabilitation

4. Attrition: The Tooth-to-Tooth Component

4.1 Etiology

Attrition is the physiological and/or pathological wear of tooth structure resulting from direct tooth-to-tooth contact. Physiological attrition accompanies normal mastication and aging, with average vertical tooth wear of approximately 10–40 μm per year. Pathological attrition is driven primarily by bruxism (sleep and awake), defined as repetitive jaw muscle activity characterized by clenching or grinding of teeth.

Sleep bruxism affects approximately 8–16% of the adult population and is classified as a sleep-related movement disorder. It is characterized by rhythmic (phasic) or sustained (tonic) masticatory muscle activity during sleep, with forces that can exceed 700 N—far exceeding the forces generated during conscious mastication (50–150 N). Awake bruxism affects approximately 20–30% of adults and is associated with stress, anxiety, and concentration.

4.2 Clinical Features

  • Well-defined, polished, highly faceted wear surfaces on opposing teeth that match precisely when the mandible is manipulated into the excursive position that produced them
  • Symmetric distribution, typically most severe on anterior teeth (incisal edges) and canines
  • Enamel and dentin wear at approximately equal rates, unlike erosion where dentin wears preferentially
  • May result in loss of occlusal vertical dimension (OVD)
  • Associated signs: masseter hypertrophy, linea alba, scalloped tongue, masticatory muscle pain/tenderness upon waking
  • Distinction from erosion: attrition facets are flat and sharply defined, while erosive lesions are concave and smooth

4.3 Management Principles

Management is predominantly preventive: occlusal splint therapy (hard stabilization splint) worn at night to protect teeth from bruxism forces; stress management and behavioral modification for awake bruxism; and restorative intervention only when wear compromises function, esthetics, or pulp vitality. The decision to restore attrited teeth requires careful consideration of the remaining tooth structure, the space available for restorative materials (minimum 1.5–2.0 mm occlusal clearance), and the presence of active parafunctional habits that threaten restoration longevity.

5. Abrasion: The Foreign Object Component

5.1 Etiology

Abrasion results from the frictional wear of tooth structure by exogenous materials. The most common cause is overly aggressive toothbrushing (horizontal scrubbing technique) with abrasive toothpaste, resulting in cervical wedge-shaped lesions. The relative dentin abrasivity (RDA) of toothpastes ranges from 30 (low abrasion) to >200 (high abrasion); whitening and tartar-control toothpastes typically have higher RDA values (100–200) than standard fluoride toothpastes (RDA 70–100).

Other etiological factors include:

  • Occupational habits: Holding nails, pins, or sewing needles between teeth (seamstresses, carpenters); playing wind instruments; pipe smoking
  • Oral jewelry: Tongue piercings abrading palatal surfaces; lip piercings abrading labial/buccal surfaces
  • Improper use of interdental aids: Aggressive use of toothpicks or interdental brushes
  • Cultural practices: Chewing abrasive substances in certain cultures

5.2 Clinical Features

  • Characteristic wedge-shaped or V-shaped notches at the cementoenamel junction (CEJ)
  • Sharp, well-defined margins; affected dentin appears smooth, polished, and hard
  • More severe on prominent teeth (canines and premolars) which protrude facially and receive the greatest toothbrushing force
  • Frequently unilateral, with greater severity on the side contralateral to the patient's dominant hand (right-handed patients show more severe lesions on the left side)
  • Gingival recession commonly accompanies cervical abrasion due to the combination of abrasive and traumatic insult to the gingival margin
  • Distinction from abfraction: abrasion lesions tend to be broader and shallower; abfraction lesions are deeper, narrower, and more angular

6. Abfraction: The Biomechanical Component

6.1 Proposed Mechanism

Abfraction, a term introduced by Grippo in 1991, describes the loss of tooth structure at the cervical margin resulting from biomechanical loading forces. The hypothesis holds that eccentric occlusal forces generate tensile and compressive stresses at the cervical fulcrum, causing flexure of the tooth and disruption of the chemical bonds between enamel and dentin crystals. Over time, repeated flexure produces microfractures in the cervical enamel and dentin, which subsequently propagate and coalesce, resulting in wedge-shaped cervical defects. The lesion is theorized to be further propagated by the ingress of small molecules (water, acids) into the microfractures, preventing remineralization of the hydroxyapatite crystals.

6.2 Evidence and Controversy

The abfraction hypothesis remains controversial. Finite element analysis studies consistently demonstrate stress concentration at the cervical region under eccentric loading, supporting the theoretical feasibility of the mechanism. However, clinical evidence is largely circumstantial: abfraction lesions are more common in teeth with occlusal interferences or heavy excursive contacts, and they are more prevalent in bruxers. Critics argue that cervical lesions attributed to abfraction could be entirely explained by a combination of abrasion and erosion, and that the biomechanical component may serve to accelerate—rather than initiate—tooth loss in a surface already compromised by chemical and abrasive factors.

The current consensus, reflected in the 2017 European Federation of Conservative Dentistry guidelines, acknowledges abfraction as a contributing mechanism in the multifactorial etiology of non-carious cervical lesions, while emphasizing that clinical diagnosis of abfraction as a "pure" entity is challenging and often speculative.

6.3 Clinical Features

  • Deep, narrow, wedge-shaped or angular defects at the cervical margin, often extending subgingivally
  • Typically affect single teeth or groups of teeth subject to heavy eccentric occlusal forces
  • Sharp internal line angles and well-defined enamel margins
  • Often asymptomatic until dentin exposure occurs, at which point thermal sensitivity may result
  • May be associated with occlusal wear facets
  • Rapidly progressive when combined with erosive or abrasive co-factors

7. The Tooth Wear Evaluation System (TWES)

7.1 Rationale and Structure

The TWES, developed by Wetselaar and Lobbezoo, provides a comprehensive, modular diagnostic framework that integrates etiological assessment with quantitative wear scoring. The TWES comprises five modules:

  1. TWES 1: Screening module — Identifies patients with tooth wear requiring further evaluation. Uses a five-point ordinal scale (0–4) per sextant.
  2. TWES 2: Etiological module — Systematic assessment of chemical (dietary, gastric, environmental), mechanical (bruxism, oral habits, occupational), and chemical-mechanical interactions. Employs validated questionnaires (e.g., GERD-Q for reflux, Oral Behaviors Checklist for bruxism).
  3. TWES 3: Qualitative module — Detailed clinical photographs, diagnostic casts, and tooth-specific wear pattern analysis to characterize the distribution and morphology of wear lesions.
  4. TWES 4: Quantitative module — Objective measurement of tooth wear using 3D scanning and superimposition techniques to quantify volume loss over time (μm/year). Essential for monitoring progression and determining whether active wear requires intervention.
  5. TWES 5: Decision-making module — Integrates data from modules 1–4 to guide clinical decision-making along three pathways: monitoring, preventive intervention, or restorative intervention. Incorporates patient factors (esthetic demands, functional complaints, sensitivity) and tooth-level factors (remaining tooth structure, pulpal proximity, restorability).

8. Management Strategies: A Stepwise Approach

8.1 Step 1: Diagnosis and Etiological Identification

Comprehensive history (medical, dental, dietary, social, occupational), clinical examination, and application of the TWES or BEWE framework. Identify the dominant etiological factor(s). Photographic documentation and study casts for baseline comparison. If erosion is suspected, a 3–7 day diet diary and referral to a gastroenterologist for GERD evaluation may be indicated.

8.2 Step 2: Preventive Intervention

Preventive strategies target the specific etiology:

Etiology Preventive Interventions
Dietary erosion Dietary counseling; reduce frequency and duration of acid exposure; use a straw for acidic beverages; rinse with water or fluoride mouthwash after acid challenge; delay toothbrushing for ≥30 minutes post-acid exposure; neutralize oral pH with sugar-free gum or antacid tablets
Intrinsic erosion (GERD) Medical management of GERD (PPIs, H2 antagonists); elevate head of bed; avoid meals within 3 hours of bedtime; fluoride therapy
Attrition (bruxism) Occlusal splint (hard, full-arch, maxillary stabilization splint); stress management; sleep hygiene; botulinum toxin injection for severe, refractory sleep bruxism
Abrasion Correct toothbrushing technique (modified Bass technique); switch to low-abrasion toothpaste (RDA <70); soft-bristled toothbrush; eliminate causative habits
Abfraction Occlusal adjustment to eliminate eccentric interferences; occlusal splint to redistribute forces; address bruxism if present

8.3 Step 3: Monitoring and Reassessment

For mild-to-moderate tooth wear (BEWE 1–2), 6–12 month recall intervals with serial photography, study casts, or intraoral scanning to monitor progression. Objective measurement of wear rate using 3D superimposition techniques reveals whether wear is active or arrested. Stable wear that is not progressing, is not symptomatic, and does not compromise esthetics or function may require no restorative intervention—a management approach termed "monitoring and maintenance."

8.4 Step 4: Restorative Intervention

Restorative intervention is indicated when: (1) tooth wear is progressive despite preventive measures; (2) esthetics are compromised; (3) dentin hypersensitivity is unresponsive to desensitizing therapy; (4) tooth structure loss threatens pulp vitality or tooth integrity; or (5) functional impairment (mastication, phonetics) is present.

Restorative options, in order of increasing invasiveness:

  1. Direct composite resin restorations: The preferred approach for localized or moderate generalized wear. Advantages include conservatism (minimal or no tooth preparation), reversibility, repairability, and cost-effectiveness. Adhesive protocols (total-etch or self-etch) provide excellent bond strengths to both enamel and dentin. Dahl concept may be employed: a localized increase in OVD using anterior composite build-ups to create posterior interocclusal space through passive eruption, eliminating the need for posterior tooth preparation.
  2. Indirect restorations (onlays, crowns, veneers): Indicated for extensive wear (>50% of clinical crown) or when the quality of remaining tooth structure precludes direct composite restorations. Lithium disilicate (e.max) is the material of choice for anterior restorations; monolithic zirconia is preferred for posterior restorations in patients with ongoing parafunction.
  3. Full-mouth rehabilitation: Reserved for the most severe cases involving generalized, deep tooth wear affecting virtually all teeth, with loss of OVD, compromised function, and esthetic impairment. Requires comprehensive treatment planning including diagnostic wax-up, OVD determination, and phased treatment sequencing as described in a related article on full-mouth rehabilitation protocols.

9. The Role of OVD and the Dahl Concept

When tooth wear results in loss of OVD and insufficient restorative space, increasing OVD is often necessary. The Dahl concept, first described in 1975, provides a conservative approach whereby a localized increase in OVD creates posterior disclusion; over 3–6 months, passive eruption and intrusion of posterior teeth re-establish posterior contact while the anterior restorations remain in place. The Dahl concept achieves posterior restorative space without the need for posterior tooth preparation, making it the single most important technique in the conservative management of localized anterior tooth wear.

Success of the Dahl concept requires: (1) healthy periodontium; (2) adequate anterior tooth structure for adhesive bonding; (3) patient acceptance of the temporary posterior disclusion (typically 3–6 months); and (4) absence of active TMD. Posterior contact re-establishes in approximately 80–90% of cases; the remaining 10–20% require posterior restoration to close the residual space.

10. Prognosis and Long-Term Outcomes

With appropriate diagnosis, preventive intervention, and restorative management, the prognosis for tooth wear is generally favorable. A 2018 systematic review reported 5-year survival rates of 90–95% for direct composite restorations in tooth wear cases, with the primary failure mode being bulk fracture rather than secondary caries. Indirect ceramic restorations in wear cases exhibit 10-year survival rates exceeding 92%. Critical determinants of long-term success include: successful elimination or control of the underlying etiology (ongoing erosion or bruxism is a strong predictor of restoration failure), patient compliance with preventive measures (dietary modification, splint wear, oral hygiene), and regular maintenance and monitoring.

11. Conclusion

Tooth wear represents a growing clinical challenge driven by modern dietary patterns and an aging dentate population. Successful management hinges on accurate diagnosis of the dominant etiological mechanism(s)—erosion, attrition, abrasion, and abfraction—using systematic assessment tools such as the TWES and BEWE. The therapeutic philosophy is one of minimal intervention: prevention first, monitoring when wear is inactive, and progressive restoration—from direct composites through to full-mouth rehabilitation—only when necessary. The Dahl concept provides a powerful, conservative mechanism for managing localized anterior wear without posterior intervention. Finally, the multifactorial nature of tooth wear demands that clinicians address all contributing etiologies simultaneously; failure to do so is the most common cause of restorative failure in this patient population.

References

  1. Bartlett D, O'Toole S. Tooth wear: best evidence consensus statement. J Dent. 2019;87:7-8.
  2. Loomans B, et al. Severe tooth wear: European consensus statement on management guidelines. J Adhes Dent. 2017;19(2):111-119.
  3. Wetselaar P, Lobbezoo F. The tooth wear evaluation system: a modular clinical guideline for the diagnosis and management planning of worn dentitions. J Oral Rehabil. 2016;43(1):69-80.
  4. Grippo JO, et al. Attrition, abrasion, corrosion and abfraction revisited: a new perspective on tooth surface lesions. J Am Dent Assoc. 2004;135(8):1109-1118.
  5. Shellis RP, et al. Understanding the chemistry of dental erosion. Monogr Oral Sci. 2014;25:163-179.
  6. Lobbezoo F, et al. Bruxism defined and graded: an international consensus. J Oral Rehabil. 2013;40(1):2-4.
  7. Pintado MR, et al. Variation in tooth wear in young adults over a two-year period. J Prosthet Dent. 1997;77(3):313-320.
  8. Poyser NJ, et al. The Dahl concept: past, present and future. Br Dent J. 2005;198(11):669-676.
  9. Mesko ME, et al. Rehabilitation of severely worn teeth: a systematic review. J Dent. 2016;48:9-15.
  10. Lussi A, et al. Dental erosion—an overview with emphasis on chemical and histopathological aspects. Caries Res. 2011;45(S1):2-12.

Posts recentes

Verrucous Carcinoma and Spindle Cell Carcinoma

Verrucous Carcinoma and Spindle Cell Carcinoma

Squamous cell carcinoma is not a single, uniform disease, and two of its oral variants illustrate the extremes of its behavior. Verrucous carcinoma is a slow-growing, exophytic tumor that almost never metastasizes, while spindle cell carcinoma is an aggressive, sarcomatoid malignancy that can be ...

Pulp Polyp: Hyperplastic Pulpitis Presentation

Pulp Polyp: Hyperplastic Pulpitis Presentation

Most people expect a toothache to be the first sign of pulp disease, but some forms of pulpitis are surprisingly silent. A pulp polyp is the visible result of chronic hyperplastic pulpitis, a condition in which the dental pulp grows out of a large carious opening as a fleshy mass. Recognizing thi...

Pilocarpine and Cevimeline for Saliva Stimulation

Pilocarpine and Cevimeline for Saliva Stimulation

Dry mouth is not merely uncomfortable; it is a medical condition with real consequences for teeth, speech, swallowing and quality of life. When the salivary glands cannot produce enough saliva, medications called sialogogues can restore some of the missing fluid. Pilocarpine and cevimeline are th...

Pemphigus Vulgaris and Mucous Membrane Pemphigoid

Pemphigus Vulgaris and Mucous Membrane Pemphigoid

A blister in the mouth can be the first warning of a systemic autoimmune disease, and two disorders deserve particular attention in the dental chair: pemphigus vulgaris and mucous membrane pemphigoid. Both produce chronic oral ulceration, yet their immunologic targets, clinical behavior and long-...

Parulis and Oroantral Fistula: Fistula Signs

Parulis and Oroantral Fistula: Fistula Signs

When infection drains from a tooth, the body often creates a visible escape route, and the dentist must interpret these fistulous openings correctly. A parulis is the common gum boil that signals chronic periapical infection, while an oroantral fistula is a communication between the mouth and the...

Ossifying Fibroma and Cemento-Ossifying Fibroma

Ossifying Fibroma and Cemento-Ossifying Fibroma

Among the fibro-osseous lesions of the jaws, the ossifying fibroma holds a unique position because it is a true neoplasm, unlike the reactive cemento-osseous dysplasia discussed in an earlier article. It grows continuously, expands bone and requires surgical removal, and its cemental variant adds...

Orthokeratinized Odontogenic Cyst: Distinct Entity

Orthokeratinized Odontogenic Cyst: Distinct Entity

Not all keratocystic lesions of the jaw behave alike, and one of the most important distinctions in oral pathology separates the orthokeratinized odontogenic cyst from its better-known relative, the odontogenic keratocyst. Although the two lesions look similar under the microscope at first glance...

Necrotizing Ulcerative Periodontitis: Distinct Entity

Necrotizing Ulcerative Periodontitis: Distinct Entity

Periodontal disease is usually a slowly progressive infection, but a rare form called necrotizing ulcerative periodontitis destroys tissue with alarming speed. Unlike ordinary periodontitis, this condition produces necrotic, cratered papillae, deep pocketing and rapid bone loss, and it appears al...

Herpangina and Hand Foot Mouth Disease

Herpangina and Hand Foot Mouth Disease

Every parent has met the child who refuses to eat because of painful mouth sores, and most of these children have one of two viral illnesses: herpangina or hand, foot and mouth disease. Both are caused by enteroviruses, both produce fever and oral ulcers, and both are overwhelmingly common in you...

Cementoosseous Dysplasia: Florid and Focal Types

Cementoosseous Dysplasia: Florid and Focal Types

Cementoosseous dysplasia is one of the most common fibro-osseous lesions found on dental radiographs, yet it is also one of the most frequently misdiagnosed. The lesion replaces normal bone with cellular fibrous tissue and cementum-like material, and it appears in several forms that range from a ...