Changes in Pulpal Nociceptors after Tooth Injury

Exposure of dentin and tooth pulp due to caries or gingival recession is frequently associated with pain and increased sensitivity to environmental stimuli. Our working hypothesis is that pulpal injury changes the populations of specific neuronal subtypes within the pulp, and the expression of nociceptive channels and receptors expressed by them. Objectives: We propose to i) identify neuronal subtypes in dental pulp from animals with tooth injury and uninjured controls. We will use neuronal markers for identification of various subtypes of nociceptors to determine their populations in injured and naive rat pulp. ii) We will determine the co-expression of mas-related gene (Mrg) proteins, and cold-sensitive transient receptor potential (TRP) channels on various subtypes of pulpal nociceptors. Mrgs encode a family of G protein-coupled receptors (GPCRs) believed to be associated with nociceptive actions. TRP channels are a family of receptors that act as noxious stimuli detectors. Experimental methods: Rats were subjected to pulp injury of two maxillary molars, and maxillary regions including the injured molars were dissected and preserved for immunohistochemical staining. Fixed tissues were demineralized, and sectioned. Tissue sections will be incubated with antibodies directed against neuronal and nociceptive molecules to establish their cellular and subcellular distribution. Results: The results will indicate which types of pulpal nociceptors express the selected Mrg proteins and TRP channels, as well as levels of expression of Mrg proteins and TRP channels in dental pulp following tooth injury. Conclusions: Analysis of the data will provide information about the distribution of neuronal nociceptors in dental pulp and provide insights into the mechanisms that contribute to dental pain after tooth injury. Identification and characterization of neuronal populations altered by pulp injury is important for developing new pharmaceuticals selectively targeting pain transduction mechanisms in the pulp. (Partially funded by Odontographic Society of Chicago Research and Education Foundation Award)