website: AADR 37th Annual Meeting

ABSTRACT: 0493  

b1 Adrenergic Receptor Expression on Human Dental Pulp Neurons

A. MAGGIO, J. VELA, G.M. PERRY, M.A. HENRY, and K.M. HARGREAVES, University of Texas - San Antonio / Health Science Ctr, USA

Objectives: Sympathomimetic amines are used in dentistry as part of local anesthetic solutions. Although most of their properties are attributed to vascular actions, the demonstration of adrenergic receptors on trigeminal neurons would be consistent with an additional direct neuronal site of action. In this study, we tested the hypothesis that the b1 adrenergic receptor (b1AR) is expressed on human trigeminal neurons.

Methods: Following IRB approved human consent, molar teeth with a clinical diagnosis of normal pulp (n=12) or painful/irreversible pulpitis (n=8) were extracted and processed with the indirect immunofluorescence method. Pulpal sections were stained using antibodies against b1AR (Santa Cruz Biotechnology), and N52 (Sigma)/CGRP (Peninsula Labs) to identify neuronal profiles. Confocal laser microscopy (Nikon C1si) was used to acquire images in three areas (upper coronal, lower coronal, and radicular) of each sample. The expression level of b1 adrenergic receptor on neuronal profiles was calculated with ImageJ. Data were analyzed by unpaired t-test.

Results: b1AR is co-expressed with N52/CGRP in human dental pulp neurons within both normal and irreversible pulpitis samples. Moreover, the percent of neuronal area that expresses b1AR is significantly greater in irreversible pulpitis samples when compared to normal samples (32.49±8.00% of neuronal area vs 14.03±3.34%; p<0.05).

Conclusion: Demonstration of b1AR on pulpal neurons is consistent with a potential direct site of action of sympathomimetic amines on certain trigeminal neurons. Moreover, the increase associated with the inflammatory (irreversible pulpitis) lesion during inflammation indicates that this receptor system undergoes profound upregulation where it may contribute to the activation of pulpal pain mechanisms.

Supported in part by NIDCR F30DE17307, R01DE015576, and T32DE14318

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