Denervation-induced changes in cell proliferation in the rat molar after wounding

Abstract

The dental pulp has the capacity to initiate and maintain repair after trauma. The purpose of the present study was to quantitatively analyze the role of the peripheral nervous system in regulation of pulpal cell proliferation in response to wounding. Six groups often rats were used in these studies. There was one baseline group (wounded, but innervation intact) and five resection groups. The resection groups included rats with unilateral superior cervical ganglionectomy (SCG), unilateral inferior alveolar nerve resection (IAN), unilateral chorda tympani (CT) resection, IAN + SCG, or a complete unilateral nerve resection (IAN + SCG + CT). One millimeter of enamel and dentin was removed from the first mandibular molar on the experimental (resected) side. Therefore, each rat had an experimental and control molar. Rats were killed at various intervals from day 0 to day 15 after wounding and received 0.5 ΜCi/g b.wt. 3 H-thymidine 1 hour before death. For the baseline (innervation intact) data a peak in 3 H-thymidine incorporation occurred at 5 days after wounding. In the resected groups, there was a general increase in the number of labeled cells at the zero time point, and a suppression of the 5-day peak with a delay in the proliferative response to wounding. The SCG + IAN-resected group maintained the lowest number of labeled cells throughout the entire experimental period compared to the experimental baseline data and the two controls. At the initial and termination points the SCG + IAN-resected groups demonstrated the highest number of labeled cells. The baseline data indicate that the maximal response to wounding occurs at day 5. Denervation results in a delay of the cell proliferative response to wounding with the most dramatic delay occurring in the IAN + SCG-resection group. The results indicate that the autonomic and sensory components of the peripheral nervous system may interact in regulating the proliferative response of pulpal cells to wounding.