website: AADR 37th Annual Meeting

ABSTRACT: 0357  

Molecular structural alterations of the dentin in non-carious cervical lesions

K. KARAN, X. YAO, C. XU, J.D. EICK, M.P. WALKER, and Y. WANG, University of Missouri -Kansas City, kansas City, USA

Objective: The molecular structural nature of the dentin in non-carious cervical lesions (NCCLs) is poorly understood. This investigation characterized the morphological and chemical structure including inhomogeneities, composition, mineral crystallinity, collagen organization of normal dentin and affected dentin substrates within NCCLs using SEM and Raman microspectroscopic mapping/imaging. Methods: Five extracted human pre-molars affected with NCCLs were selected and cavities matching the natural lesion with respect to size and location were prepared on the lingual/palatal surface of each tooth to serve as the control. The specimens were sectioned to expose the gingival and occlusal margins of the NCCLs and the control cavities. Micro-Raman spectra and imaging acquired at 1.5 micron spatial resolution at positions perpendicular to the lesion surfaces. The same specimens were also imaged with SEM. Results: The spectra comparison showed that the relative carbonate content was decreased dramatically in the NCCL-affected dentin as compared to normal dentin. In addition, the mineral phosphate peak shifted from 959 to 965cm-1 with a decrease in peak width, indicating changes in composition and crystallinity. The mineral/matrix ratios were 4.36±1.13 and 3.74±0.78 for NCCL-affected and normal dentin, respectively. Differences in collagen secondary structure were also noted. Raman images based on the above parameters/ratios showed a 20-30 micron thick heterogeneous hypermineralized layer with complicated structure, which was confirmed by SEM observations. Conclusions: Distinct differences in mineral and matrix are noted in affected dentin of NCCLs. Further studies are required to understand the role that these differences play in bonding to these clinically-relevant substrates. Supported by NIH K25 DE015281, R03 DE15735 and K23 DE01623.

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