Inflammatory Lesions of the Tooth Pulp Induce Changes in Brainstem Neurons of the Rat Trigeminal Subnucleus Oralis

Abstract

Neuroplastic changes are known to occur in the CNS in response to injury of peripheral nerves. Previous investigation has demonstrated neuroplasticity in second-order neurons of the subnucleus oralis (SO) of the trigeminal (V) nuclear complex in association with aseptic injury to the tooth pulp. A question arises, therefore, as to whether similar changes occur in response to injury associated with inflammation induced by tooth pulp infection. The effects of tooth pulp infection on the mechanoreceptive fields (RFs) of SO neurons were examined in rats. Infection was established by exposure and removal of the coronal pulp of the mandibular first molar, which was left open to the oral environment for 7 (n = 5) or 28 (n = 6) days. Neurons in SO were then electrophysiologically characterized in chloralose/urethane-anesthetized rats. The RF and the response properties of 118 low-threshold mechanoreceptive (LTM) neurons from seven-day-old rats and 149 LTM neurons from 28-day-old rats were compared with those of 204 LTM neurons tested in 11 untreated (control) rats. Significant differences were noted in RF size and location when control, seven-day-old, and 28-day-old groups were compared. Radiographic examination revealed inconsistencies among examiners in the interpretation of periapical lesions < 2 mm in diameter and general agreement in the identification of periapical lesions > 2 mm in diameter. Histological examination of teeth with pulp exposure revealed superficial necrosis and inflammation without periapical extension in the seven-day-old animals and total pulp necrosis with periapical inflammation, abscess formation, and alveolar bone resorption in the 28-day-old animals. The results indicate that neuroplastic changes in LTM oralis neurons can develop subsequent to tooth pulp infection and that there may be a correlation between the incidence of these changes and the extension of the attending inflammation from the pulp to the dental supporting tissues.