Abstract

Previous experiments show that nerves have effect on the emigration of immunocompetent cells during acute neurogenic inflammation. The present study aims to determine whether the sympathetic or sensory nerves are responsible for emigration of CD43+ and I‐A antigen‐expressing cells in the dental pulp after electrical tooth stimulation. Wistar rats were used. Experimental rats (n = 6) had the right superior cervical ganglion removed (SCGx), whereas control rats (n = 6) had sham surgery. Fourteen days later, electrical stimulation of the right maxillary 1st molar was performed in both groups for 20–25 s every 5th min for a total period of 4 h. Changes in pulpal blood flow (PBF) were recorded with a laser Doppler flowmeter. All rats were transcardiacally perfused and processed for immunohistochemistry using antibodies against neuropeptides and immune cells. Intermittent electrical stimulation consistently increased PBF and depleted sympathetic and sensory neuropeptides in the dental pulp. The increase in PBF gradually decreased and approached control values at the end of the 4 h stimulation period. A significant increase in the number of I‐A antigen‐expressing dendritic cells was found in both the SCGx (P < 0.001) and control rats (P < 0.007). In contrast, tooth stimulation did not increase the number of CD43+ cells in the SCGx rats compared to the unstimulated contralateral control molar. Significantly more CD43+ PMN cells (P < 0.01) were found in the control rats after stimulation. It is concluded that stimulation of sympathetic nerves causes recruitment of CD43+ PMN cells, whereas stimulation of sensory nerves causes emigration of I‐A antigen‐expressing dendritic cells in the dental pulp.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.