website: AADR 37th Annual Meeting

ABSTRACT: 0490  

Nerve Density in Normal and Carious/Non-Painful Human Dental Pulp

A.A. WOOD, G.M. PERRY, and M.A. HENRY, University of Texas - San Antonio / Health Science Ctr, USA

Dental pulp contains many nociceptors and represents a valuable model system to evaluate peripheral pain mechanisms. The results of animal studies have demonstrated a sprouting of pulpal nerve fibers following dental injury, but the relationship of this sprouting to pain is mostly unknown. The evaluation of pulpal nerve fibers in normal human teeth and teeth with caries where the presence of absence of pain can be documented prior to extraction should help clarify the possible relationship of nerve sprouting to pain. Objective: Quantify and compare the staining intensity/density of nerve fibers within the odontoblastic layer of normal, fully erupted wisdom teeth that lack caries to that seen in non-painful molars with caries that extend into the dentin. Methods: Sections from normal and non-painful/carious dental pulp (n=9 in each group) were processed with the indirect immunofluorescence method and evaluated with confocal microscopy following triple-labeling with antibodies against N52 and GAP-43 (to identify nerve fibers) and TO-PRO-3 (as a nuclear marker to identify the odontoblastic layer). Z-series of images were obtained for each sample from the odontoblastic layer near the lesion in teeth with caries and of a comparable region in teeth without caries. Images were evaluated with NIH ImageJ to determine the staining intensity/density of nerve fibers within this region. Results: The staining intensity and nerve fiber density were both significantly greater (p<0.05 and p<0.01, respectively; Students unpaired t-test) within the odontoblastic layer of non-painful carious teeth when compared to normal wisdom teeth that lacked caries. Conclusion: Nerve sprouting in human teeth with caries occurs in the absence of pain and this finding suggests that sprouting does not lead to the activation of acute pain mechanisms, but rather may be related to reparative processes.

This work was supported by NIDCR, T-32 Grant #DE014318/COSTAR Program and NIDCR #DE015576/M.Henry

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