The authors wish to respond to Dr. Linn’s insightful comments regarding tooth surface lesions. We are in agreement with his finding that cervical lesions occur more frequently on the facial surfaces of teeth than on the lingual surfaces. We also agree that toothbrush and toothpaste abuse may be significant factors in the development of cervical lesions as indicated in our article. Furthermore, the use of excessive dentifrice also may be a significant factor, as Dr. Linn points out.
Were toothbrush abrasion and dentifrice abrasion the sole causes of cervical lesions, we would anticipate this site to be at the facially most prominent tooth structure, just as Dr. Linn does. This would lead us to seek most lesions at the buccal height of contour of the tooth. Instead, we find the lesions generally at the cervical enamel, which is relatively difficult to reach with the toothbrush and dentifrice.
How can this be reconciled?
The multifactorial concept delineated in our article explains this most clearly as the joint action of various etiologic agents that usually are required to induce an actual clinical lesion. Thus, abrasion-causing wear may be combined with the effects of flexure (abfraction) on the highly vulnerable, very thin and brittle cervical enamel rods. In addition, these mechanisms may be synergistically joined by the many sources of acid (corrosion) operating in the mouth.
Palamara and colleagues1 found that, in a mild acid medium, "loaded teeth showed a loss of enamel 10 times greater than unloaded teeth." Furthermore, they also found that "regardless of the presence or absence of a load, during acid dissolution (corrosion), greater volume loss occurred in the cervical area than in the middle third of the tooth." Thus, it would appear that the cervical area is both chemically and structurally vulnerable to the effects of the pathodynamic mechanisms, as indicated in our Figures 9 and 10.
That some bruxers, or some with "traumatic occlusion," show no lesions may be readily explained by the multifactorial concept of their etiology. If other etiologic factors (corrosion, abrasion or attrition) are not present, then stress or flexure alone may be inadequate to produce clinically detectable cervical lesions.
In addition, the significance of predisposing factors, such as the structure and composition of teeth, also has been indicated in our article. Tooth mobility and saliva (quantity, quality and location) are modifying factors that may be protective for the teeth. Conversely, a very watery saliva may permit rapid attrition of the teeth. The greater salivary flow in the lingual area, as opposed to the buccal vestibule of the mouth, provides buffering and a mucinous coating to protect the lingual surfaces of teeth against the endogenous and exogenous acidic corrodents that are significant contributors to the odontolytic processes under discussion.
Furthermore, bruxism may rapidly wear away the cuspal inclines of posterior teeth. The resulting flat, horizontal occlusal surfaces would direct occlusal stress, in the long axis of the teeth, thus minimizing lateral stress, which tends to flex teeth. This altered occlusal anatomy would thus minimize tooth flexure and diminish the likelihood of abfraction.
On the other hand, any situation that promotes lateral stress (for example, bruxism in the presence of occlusal interferences or steep guiding inclines) may increase the tendency toward abfraction, especially in conjunction with other etiologic factors.
We wish to thank Dr. Linn for affording us the opportunity to respond to his letter, and to clarify some points covered in our article.
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