Dr. Staninec has raised points important for understanding the nature of noncarious cervical lesions, or NCCLs. In response to his first two questions, our literature review did not yield any reports describing controlled clinical or experimental trials investigating the point of initiation or confinement of lesions. Consequently, further studies are needed to elucidate the mechanisms associated with lesion formation and propagation.
His third question on the occurrence of subgingival lesions is a very interesting topic, since abfraction proponents have presented such lesions as evidence in support of the tooth flexure theory.1 Our review of literature yielded one clinical survey documenting only one instance of a subgingival lesion from an unspecified number of cases.1 Since one histological study has shown that toothbrush filaments may penetrate subgingivally, gingival recession and root exposure may not be entirely necessary for subgingival lesion formation.2
Subgingival lesions also may arise from anatomical variations. Microscopic analyses have shown that, in some cases, a gap with exposed dentin may exist at the cementoenamel junction.3,4 In addition, repeated scaling and root planing also may remove tooth structure.5–7 Therefore, gingival recession and root exposure may not always be necessary for the presence of subgingival lesions.
Dr. Lee argues that NCCLs are not due to "a sole single cause." He also notes that a vast majority of NCCLs could be adequately explained by stress damage, toothbrush abrasion or a combination of both of these factors. Indeed, we emphasized throughout the article that the etiology is most likely multifactorial and may include conditions such as toothbrush abrasion, erosion and occlusal loading, or a combination of those factors.
In any event, we believe that the conclusions stated in our article are entirely consistent with the 2003 American Academy of Operative Dentistry recommendations for clinical practice.8
We believe that a complete understanding of the etiology and the relative contribution of each potential factor has not been definitively determined. This is apparent from the numerous published articles that are speculative about the etiology of NCCLs, many of them using anecdotal information or case reports to support their conclusions.
Consequently, controlled clinical trials are needed to more fully elucidate the mechanisms associated with lesion formation and propagation, as we noted in our article. Such studies would facilitate evidence-based treatment decisions.
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