Histological evaluation of direct pulp capping with DSP-derived synthetic peptide in beagle dog
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Abstract
Abstract
The purpose of this study was to investigate the pulpal response to direct pulp capping with dentin sialo-protein (DSP) -derived synthetic peptide in teeth of dogs, and to compare its efficacy to capping substances Ca(OH)2 and white mineral trioxide aggregate (WMTA). A total of 72 teeth of 6 healthy male beagle dogs were used. The mechanically exposed pulps were capped with one of the following: (1) DSP-derived synthetic peptide (PEP group); (2) Ca(OH)2 (CH group); (3) a mixture paste of peptide and Ca(OH)2 (PEP+CH group); or (4) white MTA (WMTA group). The access cavity was restored with a reinforced glass ionomer cement. Two dogs were sacrificed at each pre-determined intervals (2 weeks, 1 month, and 3 months). After the specimens were prepared for standard histological processing, sections were stained with hematoxylin and eosin. Under a light microscope, inflammatory response and hard tissue formation were evaluated in a blind manner by 2 observers. In the PEP group, only 3 of 17 specimens showed hard tissue formation, indication that the DSP-derived synthetic peptide did not induce proper healing of the pulp. Compared with the CH group, the PEP group demonstrated an increased inflammatory response and poor hard tissue formation. The CH and WMTA groups showed similar results for direct pulp capping in mechanically exposed teeth of dogs.

Pulp capping with PEP at 2 weeks. Although the pulp capping material was impacted into the pulp, newly formed hard tissue barrier was observed. Incisal portion of the pulp from the impacted site (left portion in the figure) showed degeneration of the pulp.

Pulp capping with CH at 2 weeks. Newly formed hard tissue barrier was observed and odontoblast-like cells arranged beneath it. Although hemorrhage was seen, a few inflammatory cells were found.

Pulp capping with PEP+CH at 2 weeks. Hard tissue formation was rare. Inflammatory cells infiltrated around the impacted capping material.

Pulp capping with WMTA at 2 weeks. Among the dentin debris, scattered hard tissue was formed. Infiltration of inflammatory cells under odontoblast cell layer and dilatation of blood vessels were observed.

Pulp capping with PEP at 1 month. Many inflammatory cells infiltrated around the exposed site. There was no hard tissue formation even around the dentin debris.

Pulp capping with CH at 1 month. The thickness of hard tissue increased, compared with that of 2 weeks. In newly formed hard tissue, dentinal tubule-like structures were observed.

Pulp capping with PEP+CH at 1 month. Newly formed hard tissue grew mainly around the fragments of dentin. Dilatation of blood vessels was observed.

Pulp capping with WMTA at 1 month. Newly formed hard tissue grew into a complete bridge. They include the fragments of dentin that were pushed into the pulp during cavity preparation.

Pulp capping with PEP at 3 months. Inflammatory response persisted at the exposed site. The newly formed hard tissue were related to the dentin debris.

Pulp capping with CH at 3 months. There was a complete dentin bridge and normal pulp tissue organization beneath the exposed site. There were vacuole-like structure, cells and dentin chips inside a dentin bridge.

Pulp capping with PEP+CH at 3 months. No hard tissue formation was observed. Inflammatory response of the pulp persisted.

Pulp capping with WMTA at 3 months. There was a thick hard tissue barrier, that did not include a cell body and had no tubular structure, across the exposed site.
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