website: 86th General Session & Exhibition of the IADR

ABSTRACT: 1693  

Response of Microvasculature of the Dental Pulp in Advanced Caries

N. HUNTER1, M. RAGHUNATH BANAVAR1, M. NADKARNI1, and H. ZOELLNER2, 1Westmead Center for Oral Health, Sydney, NSW, Australia, 2Westmead Centre for Oral Health, Sydney, NSW, Australia

Objective:

It is now recognised that dentinal caries is associated with complex consortia of anaerobic bacteria. Mechanisms of pathogenicity including pulpal pathology remain unknown. In studies at the Institute of Dental Research four categories of pulpal response were noted in relation to advancing caries. One type manifests vascular activity in the form of extensive deposition of basement membrane proteins that can occupy the majority of the pulpal tissue. As the relationship of the encroaching microflora to this response is preserved in a spatial context, the objective of the study was to define the vascular changes in relation to groups of bacteria localised by in situ hybridization analysis.

Methods:

Bacteria corresponding to the implicated groups identified will be localised in 1 micrometer resin sections and identified by fluorescent-labelled oligonucleotide probes based on 16S rRNA sequences. The endothelial response will be monitored for genes encoding basement membrane (type IV collagen) and leukocyte adhesion proteins (P-selectin).

Results:

Quantitative analysis of excavated dentine indicated that this profile of vascular response was linked to Porphyromonas endodontalis, Peptostreptococcus micros, Fusobacterium sp. and Prevotella sp. In situ hybridization will be used to localise these species within the lesion and to relate these to vascular responses assessed both by immunohistochemistry and in situ hybridization.

Conclusion:

The analysis of the spatial distribution of bacteria in relation to vascular activity will form the basis of in vitro models aimed at dissecting the mechanism of the response.

The research is supported by National Institutes of Health, USA grants 1 RO1 DE015272-03.

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