Abstract
We propose a new theory for enamel cupping lesions formation. At early stages, naturally formed cupping lesions showed increased porosity at two structural prismatic traits: the central cone extending into the enamel-dentine junction and the type-I Hunther-Schreger bands (HSB), suggesting them to be the main drivers for cupping lesion formation and development. In addition, these lesions were circumscribed by type-II HSBs, which present lower surface porosity and higher resistance to wear. This theory was verified in in vitro observations, where both the central cone and the type-I HSB of cuspal enamel showed higher susceptibility to wear, potentially elucidating the mechanisms involved on cupping lesion formation.
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