Tooth Surface Lesions Part I
Diagnosis
Douglas A. Terry, DDS
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.
Conclusion
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.
References
- Darby ET. Dental erosion and the gouty
diathesis: Are they usually associated? Dent
Cosmos 1892;34:629-640.
- 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.
- Grippo JO. Abfractions: A new classification
of hard tissue lesions of teeth. J
Esthet Dent 1991;3(1):14-19.
- Grippo JO, Simring
M. Dental “erosion” revisited. J Am Dent Assoc 1995;126(5);619-630.
- Lambrechts P, Van Meerbeek B, Perdigão J, et al. Restorative therapy for erosive
lesions. Eur J Oral Sci
1996;104(2):229-240.
- Eccles JD. Tooth surface loss from abrasion,
attrition, and erosion. Dent Update.
1982;9(7):373-381.
- 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.
- Kaidonis JA, Townsend GC, Richards LC.
Abrasion: An evolutionary and clinical view. Austral Prosthod J
1992;6:9-16.
- 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.
- Tyas MJ. The class
V lesion—Aetiology and restoration. Austral
Dent J 1995;40(3):167-170.