The Effect of Tooth Pulp Inflammation on Trigeminal Fos Expression

Objectives: We have previously carried out detailed characterisation and identification of Fos expression within the trigeminal nucleus after tooth pulp stimulation in ferrets. The aim of this study was to determine the effect of pulpal inflammation on the excitability of central trigeminal neurones following ferret tooth pulp stimulation. Methods: Fifteen adult ferrets were prepared under anaesthesia (ketamine 25 mg/kg, xylazine 2 mg/kg: i.m.) to allow tooth pulp stimulation, recording from the digastric muscle and i.v. injections at a subsequent experiment. In nine animals pulpal inflammation was induced, by introducing human caries into a deep buccal cavity. Five days later animals were re-anaesthetised (alphaxalone/alphadolone, induction: 6 mg/kg, maintenance: 6-8 mg/kg/h i.v.) and treated with vehicle (0.85% saline). The teeth were then stimulated at ten times the threshold of the jaw-opening reflex for ninety minutes (n = 7). In five inflamed and three non-inflamed control animals no stimuli were applied. At 120 minutes from the start of the experiment all animals were perfused with fixative and brainstems processed for Fos immunohistochemistry. Tooth pulps were also collected and labelled using an antibody raised against the common leucocyte marker CD45, to confirm the degree of pulpal inflammation. Results: Stimulation of all tooth pulps induced ipsilateral Fos expression caudally in subnucleus caudalis (Vc) and rostrally in subnucleus oralis (Vo). All non-stimulated animals showed negligible Fos labelling with no differences between inflamed and non-inflamed groups. Following tooth pulp stimulation, Fos expression in vehicle treated animals was greater in animals with inflamed teeth than in animals with non-inflamed teeth, with the greatest effect seen in Vc (P = 0.02). Conclusion: These results suggest that inflammation increases the number of trigeminal brainstem neurones activated by tooth pulp stimulation; this may be mediated by peripheral or central mechanisms. (Supported by GlaxoSmithKline, UK).