INTRODUCTION: Odontogenic ameloblast-associated protein (ODAM) has been shown to be specifically expressed in ameloblasts and odontoblasts and has been suggested to play a role in the mineralization of the enamel, possibly through the regulation of matrix metalloproteinase 20. However, its function in dentin is not clear. The purpose of this study was to evaluate the effect of ODAM on tertiary dentin formation. METHODS: MDPC-23 odontoblastic cells were cultured, and the effect of recombinant ODAM (rODAM) on mineralized nodule formation was evaluated. Pinpoint pulp exposures were made in rat teeth and then capped with rODAM mixed with a carrier (rODAM group), carrier only (Carrier group), or white mineral trioxide aggregate (WMTA group). After 1, 2, and 4 weeks, odontoblasts and tertiary dentin were investigated histologically and immunohistochemically. RESULTS: Nodule formation in MDPC-23 cells was enhanced by rODAM treatment. Odontoblasts were polarized and showed a palisade arrangement in the remaining pulp from the rODAM group, but not the Carrier or WMTA groups. In the WMTA group, extensive tertiary dentin along the entire pulp-dentin border obliterated the pulp chamber. In contrast, in the rODAM group, limited reaction of odontoblasts resulted in normal pulp tissue appearance without excessive tertiary dentin formation and obliteration of the pulp cavity. In the Carrier and WMTA groups, bone sialoprotein was immunostained in most of the tertiary dentin, whereas in the rODAM group, dentin sialoprotein expression was immunostained primarily in newly formed reactionary dentin. CONCLUSIONS: These results suggest that rODAM accelerates reactionary dentin formation close to the pulp exposure area, thereby preserving normal odontoblasts in the remaining pulp.
INTRODUCTION:Odontogenic ameloblast-associated protein (ODAM) has been shown to be specifically expressed in ameloblasts and odontoblasts and has been suggested to play a role in the mineralization of the enamel, possibly through the regulation of matrix metalloproteinase 20. However, its function in dentin is not clear. The purpose of this study was to evaluate the effect of ODAM on tertiary dentin formation. METHODS: MDPC-23 odontoblastic cells were cultured, and the effect of recombinant ODAM (rODAM) on mineralized nodule formation was evaluated. Pinpoint pulp exposures were made in rat teeth and then capped with rODAM mixed with a carrier (rODAM group), carrier only (Carrier group), or white mineral trioxide aggregate (WMTA group). After 1, 2, and 4 weeks, odontoblasts and tertiary dentin were investigated histologically and immunohistochemically. RESULTS: Nodule formation in MDPC-23 cells was enhanced by rODAM treatment. Odontoblasts were polarized and showed a palisade arrangement in the remaining pulp from the rODAM group, but not the Carrier or WMTA groups. In the WMTA group, extensive tertiary dentin along the entire pulp-dentin border obliterated the pulp chamber. In contrast, in the rODAM group, limited reaction of odontoblasts resulted in normal pulp tissue appearance without excessive tertiary dentin formation and obliteration of the pulp cavity. In the Carrier and WMTA groups, bone sialoprotein was immunostained in most of the tertiary dentin, whereas in the rODAM group, dentin sialoprotein expression was immunostained primarily in newly formed reactionary dentin. CONCLUSIONS: These results suggest that rODAM accelerates reactionary dentin formation close to the pulp exposure area, thereby preserving normal odontoblasts in the remaining pulp.