Abfraction lesions are angular, wedge-shaped defects found at the cervical region of teeth and are caused by mechanical overloading initiated by cuspal flexure. Clinically, these lesions are more prevalent on the labial aspect of maxillary incisors. The aim of this study was to provide a biomechanical explanation for this clinical variation. Two-dimensional plane strain finite element models of an maxillary incisor, canine and first premolar were developed and the cervical stress profiles were examined along a horizontal plane 1.1 mm above the amelo-cemental junction. The local X (horizontal) stress on the labial/buccal side was 176.4 MPa for the incisor, 57.8 MPa for the premolar, and 3.4 MPa for the canine. Similarly, the maximum labial/buccal principal stress was 181.4 MPa for the incisor, 25.2 MPa for the premolar, and 66.8 MPa for the canine. The labial/buccal stress profile in the cervical region of an maxillary incisor was always greater than that found in an maxillary canine or premolar tooth. These findings provide a biomechanical explanation for the clinical variation seen in the prevalence of cervical abfraction lesions.

Many workers have suggested that abfraction lesion formation is caused by the physical overloading of enamel. However, an alternative mechanism, involving undermining of the cervical enamel along the amelodentinal junction (ADJ), may be a more realistic explanation. The aim of this study was to examine what effect undermining of the buccal cervical enamel would have on the stress distribution in upper teeth. Two-dimensional plain strain finite element meshes of an upper incisor, canine and first premolar and the supporting periodontal ligament and alveolar bone were developed. Each tooth was loaded with an oblique 100 N load, and the nodal maximum principal stresses (MPS) along a buccal horizontal sampling plane 1.1 mm above the amelo-cemental junction was measured. A discontinuity between the cervical enamel and dentine elements was then introduced (0.1 mm wide) using gap elements. The vertical extent of this defect varied from 0.1 to 0.5 mm. The value of the MPS varied from 1.8 to 209 Mpa, and the lowest values were found for the intact teeth (range 0.6-30.3 MPa). The discontinuity caused a dramatic increase in the numerical values of the MPS, and in many instances these exceeded the known failure stress for enamel.

The aim of this study was to compare the erosive susceptibility of cuspal and cervical enamel from human premolar and molar teeth. Small blocks of cervical and cuspal enamel were immersed in either orange juice or Coca-Cola at 37 degrees C and the surface enamel loss was measured by surfometry at 1, 2, 3 and 4 h. Additionally, once-hourly enamel loss was measured, specimens were placed in an ultrasonic bath containing water and ultrasonicated for 5 s to determine the degree of surface demineralization. A further set of enamel specimens were prepared that had 100 microm of the enamel surface removed. This was done to remove the hypermineralized surface enamel layer. Surface enamel loss in orange juice at 4 h, following ultrasonication, ranged from 13.2 to 16.9 microm. The surface enamel loss in Coca-Cola at 4 h, following ultrasonication, ranged from 21.7 to 27.5 microm. Subsurface enamel loss in orange juice at 4 h, following ultrasonication, ranged from 10.7 to 16.1 microm. The subsurface enamel loss in Coca-Cola for 4 h, following ultrasonication, ranged from 36.8 to 37.2 microm. Overall, little difference was found in the erosive susceptibility of cervical and cuspal enamel to the effects of orange juice or Coca-Cola.