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Tooth Surface Lesions Part I


Carious and noncarious tooth surface lesions have been described in the literature for almost 150 years. Their etiology was unexplainable, however, some of the theories proposed for causation included a disease inherent inside the tooth or in the composition of saliva and friction of the lips, friction of folds of the mucous membranes, exfoliation, acids or acids in combination with mechanical agents, electrolytic action, defective development, and resorption.1,2 Miller suggested that these erosive lesions had “a multiplicity of names, not one of which is fitted to all of the conditions and phenomena present.”2 


Classification of Noncarious Lesions 

Miller’s scientific classification system categorized the forms of tooth substance loss as abrasion, attrition, and erosion.2 An additional category, initially reported by McCoy and defined by Grippo, was coined “abfraction,” derived from Latin roots meaning away and breaking.3 Additionally, erosion, is defined as “the progressive loss of a material from a solid surface due to mechanical interaction between that surface and a fluid, a multicomponent fluid, impinging liquid or solid particles.” This effect does not occur on teeth in the oral cavity,4 however, and should be replaced with the term corrosion to indicate the chemical dissolution of teeth. Although the original classification provided some insight into the understanding of the etiology and treatment of these lesions, several other concomitanteffects (eg, biochemical, biomechanical, and bioelectric processes) may be responsible for the development of noncarious tooth surface lesions.5 Today’s nomenclature for the classification of hard tissue lesions includes four recognized categories that are defined and described as follows.

Abrasion is defined as frictionbetween a tooth and an exogenous agent that causes wear of tooth substance. This wear can be caused by friction from the food bolus and is called masticatory abrasion or from abnormal mechanical forces (eg, improper toothbrushing, improper use of dental floss and toothpicks, biting fingernails, holding nails between the teeth).3,6,7 

Attrition is friction between teeth that results in physiologic wear of tooth substance caused by normal tooth-to-tooth contact (ie, incisal, occlusal, and interproximal wear from mastication,3,6 bruxism, and clenching5).

Corrosion is the loss of tooth substance from an intrinsic or extrinsic origin caused from chemical or electrochemical action. The intrinsic form (endogenous source) of corrosion can be caused by regurgitation of gastric acids as in habitual vomiting associated with bulimia, anorexia nervosa, and pregnancy morning sickness.3,7 The external form (exogenous source) can be caused by diet (eg, carbonated soft drinks, candies that contain phosphoric or citric acid, citrus fruits or juices, baby bottle syndrome3,7) or from occupational tooth corrosion (ie, airborne acids such as industrial chemicals and chlorinated swimming pool water).7 

Abfraction is the microstructural loss of tooth substance by biomechanical loading forces in areas of stress concentration, primarily in the cervical area due to eccentric loading. It can occur on the occlusal or incisal surfaces where stress is concentrated at the areas of contact.

There are three basic physical and chemical mechanisms that are responsible for these hard tissue lesions: friction, corrosion, and stress.7 The exogenous form of friction (abrasion) and the endogenous form (attrition) manifest as wear defects. The exogenous and endogenous forms of corrosion manifest as chemical or electrochemical degradation lesions, and the exogenous and endogenous form of stress lead to dental manifestations of microfracture and abfraction lesions.4,7 These mechanisms can occur coactive as synergistic, sequential, or alternative interactions. Since a particular lesion can result from one or more of these mechanisms, the criteria used for a differential diagnosis must be based on direct clinical examination, a comprehensive review of the patient’s medical and dental history, an inspection of the patient’s occlusion for symptoms and clinical signs of trauma, and the morphologic characteristics of the lesion.5 


Morphological Characteristics 

Since each of the aforementioned noncarious lesions has a specific morphological characteristic, a description of the characteristics of each can provide useful information for identification during differential diagnosis. The morphologic characteristics of cervical lesions produced by abrasive forces generally have sharply defined margins and a hard smooth surface that may exhibit scratching (Figure 1A).Cervical abrasion is commonly produced by improper brushing techniques, and interproximal lesions are caused by friction from objects such as toothpicks. These abrasive lesions are generally free of plaque and are not discolored.8 

Attrition lesions usually occur on the occlusal surfaces, incisal edges, lingual surfaces of maxillary anterior teeth, and labial surfaces of mandibular anterior teeth. The teeth are worn in the shape of flat facets that can be attributed to the functional movements of the dentition (Figure 1B). Attrition can also occur on proximal surfaces as a result of the anterior component of force, where small horizontal and vertical movements of teeth occur during function, thus causing frictional wear.3,8 

The extrinsic form of corrosion, caused by ingestion of acidic foods, beverages, and medications, is generally U-shaped or disc-shaped, broad, and shallow. These often have poorly defined margins, and the adjacent enamel is smooth, shiny, and free of developmental ridges. The extrinsic form of corrosion results from exogenous acids such as dietary acids, fruit juices, and ascorbic acid, and is generally located on the facial surfaces of the anterior teeth (Figure 2).7 The intrinsic form of corrosion, caused by the reflux of gastric contents or regurgitation, is generally located on the lingual and incisal surfaces of maxillary anterior teeth and appear as flattened wear. These lesions usually are free from plaque accumulation unless sensitivity prevents adequate oral hygiene.9 Another intrinsic form of surface loss that is caused by corrodents produced by bacterial plaque is called biocorrosion or caries. The etiology of caries is a process that involves acidogenic and proteolytic mechanisms (Figure 3A).7 

Abfraction lesions typically are irregular V- or wedge-shaped cervical lesions. The shape of the lesion depends on the relative areas of compression and tension exerted by occlusal forces. If the cusp is put into a state of tension, the resultant cervical lesion will be wedge-shaped; conversely, if the cervical region is subjected to compressive stresses, the lesion will be more concave or saucer-shaped. Circular occlusal lesions also can develop in the enamel and dentin to form occlusal cusp tip invaginations (Figure 3B).3 

After considering all factors related to tooth substance loss from abrasion, attrition, corrosion, abfraction, or a combination of these processes, a differential diagnosis should be developed prior to restorative treatment. This differential diagnosis provides information for determining etiology and can require additional information such as oral hygiene routine, medical and dental factors, abnormal oral habits, and occlusal idiosyncrasies.5,6,10 The information acquired during the differential diagnosis can provide a methodical approach for preventive and restorative therapy.



Consideration of the etiology and morphological characteristics of these lesions can provide information not only for identification, but more importantly for prevention of the lesions, tissue preservation, and perpetuation of the longevity of a selected restorative therapy. Part II of this discussion will describe preventative measures for management of these tooth surface lesions, while providing a perio-aesthetic approach for the restorative treatment of these lesions and recession-type defects.




  1. Darby ET. Dental erosion and the gouty diathesis: Are they usually associated? Dent Cosmos 1892;34:629-640.
  2. Miller WD. Experiments and observation on the wasting of tooth tissue variously designated as erosion, abrasion, chemical abrasion, denudation, etc. Dent Cosmos 1907;49:1-23.
  3. Grippo JO. Abfractions: A new classification of hard tissue lesions of teeth. J Esthet Dent 1991;3(1):14-19.
  4. Grippo JO, Simring M. Dental “erosion” revisited. J Am Dent Assoc 1995;126(5);619-630.      
  5. Lambrechts P, Van Meerbeek B, Perdigão J, et al. Restorative therapy for erosive lesions. Eur J Oral Sci 1996;104(2):229-240.
  6. Eccles JD. Tooth surface loss from abrasion, attrition, and erosion. Dent Update. 1982;9(7):373-381.
  7. 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.
  8. Kaidonis JA, Townsend GC, Richards LC. Abrasion: An evolutionary and clinical view.           Austral Prosthod J 1992;6:9-16.
  9. Zipkin I, McClure FJ. Salivary citrate and dental erosion; procedure for determining citric acid in saliva; dental erosion and citric acid and saliva. J Dent Res 1949;28(6):613-626.
  10. Tyas MJ. The class V lesion—Aetiology and restoration. Austral Dent J 1995;40(3):167-170.



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